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Correlation of Intramyocardial Electrocardiograms with

Polarographic Oxygen and Contractility in the

Nonischemic and Regionally Ischemic Left Ventricle



E HAVE previously shown that the enicardial-surface electrocardiogram is an inadequate index of localized myocardial ischemia. While striking chanares of polaro-graphic oxygen and contractility regularly occur a few seconds after coronary arterial branch occlusion, epieardial electrocardio-graphic changes are delayed and sometimes absent.1 Intramyocardial electrocardiographic studies, on the other hand, reveal that local-ized ischemia disturbs myocardial electrical activity at least as early as either oxygena-tion or contractility, and over a more exten-sive area.

We have developed a technique for ampli-fication and recording of oxygen-reduction currents and electrocardiograms simultane-ously from the same lead-point2"4 in the myocardium. This technique was combined with motion-picture records of muscle con-traction5 and epicardial-surface color. Thus, simultaneous information about electrical ac-tivity, oxygenation, and contractility in lo-cally altered myocardium and adjacent, un-disturbed muscle became available. This makes possible, as we will show in the present paper, an assessment of the limitations of From the Edward B. Robinette Foundation, Department of Medicine, the Department of Pa-thology, and the Harrison Department of Surgical Eesearch, School of Medicine, University of Pennsyl-vania, Philadelphia, Pennsylvania.

Supported by Eesearch Grant H-398 from the National Heart Institute, National Institutes of Health, V. S. Public Health Service.

Dr. Katcher is a Postdoctoral Eesearch Fellow, National Heart Institute (HF-7812 C3).

Eeeeived for publication July 11, 1961.

epieardial heart-body leads, which are still indispensable links between open-chest situa-tions and the body-surface electrical phe-nomena of concern to the clinician. We con-sider such an assessment to be elementary for understanding the behavior of the heart muscle and the electrocardiogram in coronary heart disease.6


In 28 dogs, weighing 15 to 23 Kg., the heart was exposed under

morphine-Dial-urethane-pento-barbital anesthesia.7 A branch of the left anterior

descending coronary artery was isolated. Eight to 10 glass-insulated platinum electrodes were inserted in the left ventricle as previously


The construction of electrodes had been modified

from those used in our earliest work.7 The

rela-tively heavy shank was eliminated and the entire shaft was made of light glass fused to a 0.2-mm. platinum wire which was connected at a plastic-insulated junction to a very light lead wire (no. 42 copper enameled) insulated by polyethylene tubing (fig. 1). A white glass bead, cemented to the shaft at the level desired, acted as a depth stop and as a marker for cinematographic studies of muscle contraction. These electrodes were made the cathodes of an electrolytic circuit measuring changes in oxygen polarographically according to

the method of Davies and Brink8 and Montgomery

and Horwitz.9 The electrodes were also used as

exploring lead-points for direct heart-body electro-cardiograms. The platinum tips in the myocardium have an electrolytic capacitance of approximately 0.5 microfarad, which makes it possible to use them for simultaneous measurement of extracellu-lar electrical activity. The reference electrode for both systems consisted of approximately two feet of 18 B&S-gauge pure silver wire immersed in a jar of physiological saline into which one of the hind limbs of the dog was also immersed. The

myocardial oxygen-reduction currents, range 10~7

to 10~9 amperes, were amplified by means of a

1268 Circulation Research. Volume IX. November 1961



special preamplifier.0 Modulation of the

oxygen-reduction current by the rayoeardial electrocardio-gram was largely eliminated by inserting a series resistor and a shunt capacitor at the input of the oxygen-reduction current preamplifier. The series resistor also allowed the electrode to follow the electrocardiogram so that the latter could be recorded separately via a capacitor and voltage preamplifier (Tectronic model 122). A circuit diagram of the apparatus is given in figure 2. The recorder was ordinarily a six-channel Brush direct-writing oscillograph with appropriate driver amplifiers. In some experiments, additional oxygen and electrocardiogram preamplifiers were added to the system.f

Color motion pictures were synchronized with the electrical activity of the heart by including in the photographic field either an epicardial

electro-cardiogram (from a nonischemic surface)1 or a

neon bulb triggered by the R wave of such a record. Special silver, silver-chloride intramyocar-dial electrodes were occasionally used with D.C. amplification to distinguish between the RS-T segment and baseline shifts which comprise the net RS-T segment displacement ordinarily

re-corded with an A.C. amplifier.11

Our myocardial explorations were largely con-fined to depths of 3 mm. or more beneath the epicardial surface. Electrodes were difficult to maintain in position when inserted less deeply, and the records obtained from them tended to be unstable. After inserting the platinum electrodes, it was necessary to await the stabilization of the

oxygen-reduction currents (initially large1) and

the electrocardiograms. R waves were at first absent; then, they might appear as notches on the ascending limbs of the monophasic ventricular complexes. After 30 to 45 minutes, the QRS configuration and net RS-T segment levels re-mained stable, the latter usually isoelectric, not infrequently somewhat elevated, occasionally very slightly depressed.

*This amplifier was originally designed for oxy-gen measurements in skin and myocardium by one of us (Mr. Peiree) under the support of USPH Grants 392(C) and 398(C4). A modification for use in blood, constructed under his supervision, was recently described by Polgar and Forster.10

tGalvanometric measurements of oxygen-reduction currents can be combined with myocardial electro-cardiograms from the same electrode, provided the input impedance is increased to the order of ] megohm. In this case, it is not necessary to shunt the galvanometer witli a filter rapacitor, because the slow speed of the instrument is sufficient to eliminate most of the electrocardiograpliic modulation.

Figure 1

Electrode for intramyocardial oxygen and electro-cardiograms. See Methods. The electrode consists of no. 32 BdtS platinum wire ivith a thin layer of soft glass fused along its entire length and a second layer fused above the bead location. The bead is attached by epoxy cement. The lead wire is no. 42 B&S-gauge copper wire soldered to the platinum wire and covered with polyethylene tub-ing (Clay Adams PE 10). The joint is covered by a short length of vinyl tubing, and the junc-tions of this with the electrode and the polyethyl-ene covered with vinyl paint (('. S. Stoneware Tygon TP-81, clear).

Experimental Procedures

Once stable control configurations for myoear-dial electrocardiograms and levels of oxygen-reduc-tion currents had developed, reversible localized or generalized alterations of myocardial function were produced, using techniques described pre-viously, '• u-w We discarded information from electrodes which did not return to control con-figurations between procedures. Localized changes

consisted of maximal ischemia1 with

release-re-covery (occlusion of a medium-sized branch of the left anterior descending coronary artery for two to five minutes), and alteration of superficial myocardial layer behavior by local wanning or cooling, and by topical procaine HC1 (25 to 50 per cent) or KC1 (5 per cent) solutions. Blood-pressure and heart-rate changes were negligible with these procedures. In four animals, two or three simultaneous records of myocardial oxygen and electrocardiograms were followed to permit comparison of the borders of ischemic areas with the centers. Generalized changes included the effects of inhalation of 100 per cent oxygen, hypoxia (10 per cent oxygen for 10 to 15 minutes), asphyxia (respirator turned off), and intravenous levarterenol. In four animals, D.C.-amplifier myocardial eleetrocardiographic studies of localized changes and of levarterenol effects were carried out. Insulation was used only in these animals. Most of the animals had been studied Circulation Research, Volume IX. November 1901





Figure 2

Circuit for simultaneous recording of polarographic oxygen-reduction current and intramyocardial electrocardiogram from same electrode. See Methods and Discussion. In operation, the grounding of the dog and the connection to the dog via the silver reference electrode is completed before turning on the apparatus. (SW-5) is closed, and one minute later (SW-1) is closed and the polarising voltage set by adjustment of the (4K) potentiometer. With (SW-6) open and (SW-4) set to desired sensitivity, the (20K zero adj.) potentiometer is so set that closure of zero test (SW-2) or (SW-3) produces minimum deflection of the (0-10V) output meter. Full-scale sensi-tivity is equal to 10V -r- feedback resistance selected by (SW-4). This circuit has tvorked satisfactorily vith feedback resistance as high as 10" ohms.

before we were aware of the desirability of insulat-ing the ventricles from the body as completely as possible.12 However, the surface of all locally altered ventricular muscle, as well as a wide perimeter of unaltered muscle, was exposed to the air in every instance.

Results Control Records

An Rs, RS, or rS complex was present in niyocardial electrocardiograms whenever the lead-point lay in the outer 9 mm. of the left-ventricular wall (estimated to be about two-thirds of its thickness in our dogs). There was a wide variability of RS-wave

configura-tions (fig. 3), but Q waves preceding R waves were very rare and small. At greater depths than 10 to 12 mm., QS patterns were almost invariably found. Absolute values for the amplified and recorded oxygen-reduction cur-rents ranged from 0.01 to 0.1 microamperes. They were unrelated to the depths of elec-trode insertion, and were similar to what we previously described for galvanometric de-terminations.1 Muscle temperatures in ex-posed hearts gradually fell 1 to 2 C. below left-ventricular blood temperature.14 The T wave became negative in the outer layers of the wall, and of small amplitude in the inner Circulation Research, Volume IX. November 1061


ISCHEMIC LEFT VENTRICLE 1271 layers. Muscle-contraction variations

re-sembled those previously described.1' 2

Regional Ischemia

Central Zones

Within a few seconds of coronary occlusion, net RS-T segment elevation appeared in the myoeardial electrocardiogram, and S-wave amplitude diminished (fig. 4). It-wave am-plitude then increased, but a slight decrease usually preceded this. The first measurable changes in electrical activity were sometimes seen as early as the onset of muscle-contrac-tion failure (late systolic bulge) and, not in-frequently, preceded any fall of local oxygen. The rapidity and severity of myoeardial elec-trocardiographic and oxygen changes were independent of the depth of electrode inser-tion, except that electrodes in the deeper lay-ers showed little or no measurable abnormal-ity of the R wave, if one were present. Decreased S-wave amplitude occurred at all depths. When occlusions were maintained, small Q waves not infrequent]3r developed within 60 seconds, but since they were some-times delayed as much as 30 to 60 minutes, they were not useful indices of early isehemic change. The order of appearance of the first measurable myoeardial electroeardiographic and oxygen abnormalities after 25 seconds of coronary occlusion is shown in figure 5 (up-per portion). After release of brief (2 to 5 minutes) occlusions, myoeardial electrocardio-grams and oxygen began to return toward normal in two to ten seconds (fig. 5, lower portion). The electrocardiograms regained control configurations within 10 to 30 sec-onds: concurrently with epicardial records, if these were abnormal.

Epicardial electroeardiographic disturb-ance was variable. Usually there was no change for at least 10 to 30 seconds. Large dogs (>20 Kg.) were likely to show the least abnormality; not infrequently, they showed none. When epicardial electroeardio-graphic changes did occur, they were limited to the center of the ischemic areas, never ex-tending beyond the limits of surface cyano-sis when this could be discerned.

Circulation Research, Volume IX, November 1061

V . • •

. • * ' ' I :

"• * I

Figure 3

R wave in per cent of total RS amplitude related to depth of electrode insertion—21 dogs and 167 electrode insertions. Q waves preceding R leaves were not present in these animals. While there is a tendency to larger amplitude with the more super-ficially placed electrodes, the variation is great at any particular depth. The height of all R leaves would have been significantly greater had these hearts been maximally insulated.11

Border Zones

Simultaneous, continuous records from more than one area during occlusion showed that altered myoeardial electrical activity was the only unequivocal abnormality at the peri-phery of ischemic zones. Polarographie oxy-gen fell early, but stabilized at comparatively high levels. Muscle-contraction abnormalities were complex, as described previously.1'3 While abnormal electrical activity demar-cated the outermost limits of measurable dys-function, distinction of the borders of ischemic areas from the centers required simultaneous comparison of relative myoeardial oxygen levels, since myocardial electrocardiograms changed early, consistently, and in a quali-tatively similar fashion at centers and



-. -. -.


. I

^ ^ — - — - ^

Figure 4

Polarogrojihic oxygen, and electrocardiogram from the same electrode during coronary occlusion and release. The fall in o.rygen (upward on the record) begins almost at once and is fastest between 5 and 20 seconds. Myocardial electrocardiographic changes (net RS-'f segment elevation, diminished S-icave amplitude, and slightly lessened B-ivave amplitude) are present within 10 seconds. Return toward a normal electrocardiographic pattern is well advanced when o.rygen overshoots control values, and is largely complete by 100 seconds (oxygen beginning to return toward control).

ders. Profound falls of oxygen occasionally occurred at electrodes considered to be well outside ischemic areas, but the electrocardio-grams recorded from such electrodes pro-vided decisive evidence of artifact. Net RS-T elevation due to local trauma appeared much sooner than the earliest ischemic changes, the electrical abnormality diminished instead of increasing with the passage of time, and the low oxygen levels did not rise following re-lease of the coronary occlusion.

Localized Alterations of Ventricular Electrical Behavior Without Change of Myocardial Oxygen

Localized cooling (>0.5 C.) immediately increased the negativity of T waves in the outer third of the left-ventricular wall, with-out otherwise changing the electrocardiogram. Local warming decreased the negativity of myoeardial T waves or made them positive. The changes were limited to the outer myo-eardial layers immediately beneath the heated or cooled area of heart surface and to the local epicardial electrocardiogram, which

re-Circulation Research, Volume IX, November 39G1


ISCHBMIC LEFT VENTEICLE 1273 fleeted them best. Myocardial oxygen and

contractility were not measurably altered. Electrocardiograms from lead-points 3 to 5 mm. beneath the surface did not change when potassium chloride solutions (1 to 5 per cent) or proeaine HC1 solutions (25 to 50 per cent) were applied to overlying portions of the exposed ventricular epicardium. As usual, there were striking reversible changes (net RS-T elevation and shallower S waves) in the local epicardial electrocardiogram.12 Both agents caused transient failure of local muscle contraction, but did not alter myocardial oxygen. Direct heart-body leads from the rest of the heart were unchanged by localized temperature or drug effects.

Changes of Myocardial Oxygen Without Electro-cardiographs Change

Changes of the level of myocardial oxygen-reduction current associated with spontaneous heart rate (fig. 6, left half), and blood-pres-sure changes1 induced by inhalation of pure oxygen (fig. 6, right half) had little or no effect on the myocardial electrocardiogram recorded from the same electrode. This was also true of hypoxia (15 to 50 per cent fall of myocardial oxygen1) and asphyxia (prior to the development of arrhythmias). Large increases or decreases of the oxygen-reduction currents recorded from nonischemic hearts were often associated with no electrocardio-graphic change at all. When changes did occur, their amplitude rarely exceeded 10 per cent of the total QRS complex.

D.C.-Amplifier Analysis of Myocardial Electro-cardiograph^ Changes

The net RS-T elevation immediately con-sequent on insertion of an intramyocardial electrode was found to be the result of a large, downward, baseline shift and a smaller, upward, RS-T segment shift. The first ischemic rnyocardial electrocardiographic change was baseline depression at centers and borders. With short occlusions, this was often the only change, except for QRS-amplitude alteration (fig. 7). The degree of the base-line depression exceeded any subsequent RS-T elevation for the first 60 to 180 seconds


j a a o a aa

o oo o o o

Oxygen Eitratytfoie

Tint fc secorafe

Figure 5

Firnt measurable abnormalities following coronary occlusion, and first changes toward normal after release. Continuously followed myocardial elec-trodes in 13 animals and 25 occlusions. lielease-recovery was studied in 7 animals and 10 episodes. See test for description.

of ischemia (fig. 8). The net RS-T segment changes produced by levarterenol in non-ischemic, non-ischemic, or hypoxic heart muscle were found to consist of a negative RS-T segment shift frequently combined with ele-vation of the baseline. These changes were much better seen in epicardial heart-body leads11' i:t than in myocardial leads. We sometimes recorded such changes in the outer layers of the wall, but have failed to find them in the deeper layers.


No other combined study of myocardial contractility, electrical activity, and oxygena-tion is known to us. For myocardial elec-trocardiograms in nonischemic dog hearts, Prinzmetal et al. reported in 1953ir' that R waves were present for not more than a few millimeters beneath the ventricular surface. In subsequent reports,16-17 the data of this group differ less from the findings of others,18"21 as has been summarized else-where.22' -3 There is general agreement that Circulation Research, Volume IX, November 1901


1274 SAYEX, PEIRCE, KATCHER, SHELDON Fbtrcxyuphc Oxygen and Smjtaneous MyorartW Etedrocardogjams:

Effect of Spontaneous Rate Changes and of Oxygen AoYnnstncrtion

E X P T . 113


-IUCTMIK « • • • 1 •

-l • • t > » W II

Figure 6

Continuously recorded myocardial oxygen and electrocardiograms from the same elec-trodes. (Left half of figure)—effects of rate on recorded polavographic oxygen (upper channel) and myocardial electrocardiogram from the same electrode site (lower channel). The polarity of the oxygen record is such that downward motion from the baseline indicates a rise of current. Rhythmic rises and falls are synchronous with slowing and speeding of the ventricular rate due to sinus arrhythmia. Similar relationships are shown at two other electrodes at different times in the run. (Jiight half of figure)— continuous record of a shift from air inhalation to oxygen. Intermittent readings from each electrode in an array before and after, with continuous record from one electrode during the period of rapid change.

significant Q waves are not found in the outer third to half of the normal canine left ven-tricular wall, and that R waves are absent in the inner third. We have found greater variability of R-wave amplitude at different sites and levels of electrode insertion than lias been generally reported, irrespective of the variability that is introduced by the na-ture of the contact between the heart and the body.12 For studies concerned only with changes in myocardial function, the wide variability of control behavior at different sites causes no difficulty. As in previous work, we have not attempted to interpret absolute values.

Studies of ischemic hearts by other groups have been limited almost completely to large, ischemic areas. Kennamer et al.16 reported that coronary occlusion produced less net

RS-T elevation in the inner than in the outer layers of the left ventricle. Conrad et al.21 found that R waves frequently disappeared in the deeper layers of the wall, and attrib-uted this to a change of electrical activity of ischemic origin. We have not been able to confirm these two sets of observations for small or medium-sized ischemic areas. The myocardial electrocardiographs studies of Rakita et al.,17 in general agreement with ours,1 have been discussed elsewhere.11 Diir-rer's group24'23 studied ischemic areas mas-sive enough to show early, extenmas-sive, epi-cardial electrocardiographic abnormality and found net RS-T segment elevation greatest in the outer myocardial layers soon after coronary occlusion, but later greatest in the subendocardial layers. They recorded RS-T segment depression in the ventricular cavity

Circulation Research, Volume IX, November 1961



Siffoce mop 00QfT7


O M C * Occkaon S * » myocana •ectrode

depth 5.5mm. *•


23 tea

f W % ^

A v

365 IO«a 2 8 M O

v^rv-T^t^h--K - H r H " T-T-'T'

Figure 7

Simultaneous, direct-coupled amplifier myocardial and epicardiai electrocardiographs responses to coronary occlusion and release. Standardizations 1 cm. = 20 mv. The epicardiai record from the surface above the myocardial electrode shows no changes except T-wave alterations of no significance. There is no RS-T segment change in the myocardial record, but baseline depression was measurable at 10 seconds and is easily seen at 23 seconds, together with slight diminution of both R- and S-xoave amplitudes. Return to normal is complete within 38 seconds of release. Much of it occurs within the first 10 seconds.

opposite the endocardial surface of the is-chemic area, but not at the borders of such areas. The extent of exposure of the heart was not specified. The form of the ischemia QRS disturbances in direct heart-body leads from ventricular surface or wall, resembled those we have described, but the much greater size of the ischemic areas studied makes diffi-cult a comparison of these studies with ours. So far, we have found no discrepant electro-eardiographic reports that cannot be explain-ed by differences in size of area studiexplain-ed, or by variations in the nature of the heart-body contact areas for open-chest preparations. No other group has reported D.C.-amplifier intramyocardial electrocardiographic data. This study shows them to be useful as an intermittent analytic procedure; but, so far, myocardial D.C. electrocardiograms have pro-vided no information that epicardiai D.C.-amplifier records, in retrospect, could not have provided.

Circulation Research. Volume IX, November 1961

Husni and Simeon20 reported that follow-ing coronary occlusion, myocardial tempera-ture fell contemporaneously with an early profound fall of myoeardial oxygen. They used small-caliber oxygen electrodes and an undescribed amplification system. The tem-perature findings are not discrepant with our own observation14 that no fall occurs for 15 to 30 seconds in medium-sized ischemic areas, since in exposed hearts, cooling would be faster for larger areas. Myocardial p l l de-clined, as others have noted.2" Reynolds et al.,28 after coronary ligation in semiclosed-chest dogs, noted (as we had14) that the direction of ischemic T-wave abnormality was opposite to what could be accounted for by the unchanged or lower local temperatures. They demonstrated accelerated recovery of excitability (shortened effective refractory period) soon after ligation. This could ac-count for local T-wave positivity.

In any study of oxygen-reduction currents,



^ -3

OO 125 150 TIME IN SECONDS Figure 8

Comparison of liS-T segment and baseline devia-tion in myocardial electrocardiograms following coronary occlusion: i dogs and 8 ischemia episodes. Control baseline and RS-T segment levels are tifken at zero for all electrodes. See text and com-pare with epicardial electrocardiographic D.C. response, illustrated elsewhere.'1 Dog no. 177 showed electrical alternans of the RS-T segment during the third minute of one ischemia period.

it is necessary to bear in mind that some interaction of polarographic information and myocardial electrocardiographic information is unavoidable, owing to the high capacitance of the platinum cathode, which introduces modulation currents into the oxygen-redue-tion-current record as a result of alternating potentials in the surrounding tissues. "When a recorder with a fast response is used, the electrocardiographic modulation may be larger than the oxygen-reduction current and may obscure it so that nothing is seen in the "oxygen" record but a distorted electro-cardiogram.* In addition to modulation of

*.Iust after insertion of an electrode, when a wide nionophasic electrocardiogram is produced, it is pos-sible to misinterpret distorted records of this sort .-is reflecting myocardial contraction.

the oxygen record by the electrocardiogram, the measurement of the oxygen-reduction cur-rent necessarily involves shunting of the electrode, producing a reduced electrocardio-graphic time constant. The circuit values used are a compromise between conflicting requirements. The speed of response of the oxygen preamplifier with filter (time constant about 0.35 second) is sufficiently slow to re-move most of the electrocardiographic modu-lation, while still permitting the rapid changes in myocardial oxygen with coronary occlusion or release to be followed satisfac-torily. Very rapid changes in the myocardial oxygen-reduction currents, such as differ-ences during a cardiac cycle, cannot be fol-lowed because of the electrical activity of the myocardium and the limited frequency response of the amplification system which is necessitated by this activity. Possibly, if a reference electrode could be so located rela-tive to the exploring electrode that both would be subject to the same potential vari-ations, phasic changes of oxygen could be followed. The 1.2-megohm resistor at the input of the oxygen-reduction current pre-amplifier reduces shunting of the electrode capacitance sufficiently to permit simulta-neous electrocardiographic recording at a time constant of about 0.6 second via a separate preamplifier coupled by a capacitor to the same electrode, but at the same time, it holds the mean potential of the electrode close to 0.6 volt, with respect to the reference electrode. An increase in the decoupling resistor would have increased the electro-cardiographic time constant, but permitted too great a change in electrode polarization voltage with changes in oxygen-reduction cur-rents.

Each of the three basic indices of local myocardial function—myocardial electrocar-diogram, polarographic oxygen, and cine-matographic muscle-motion records—provides unique information, can show changes when the others do not, and may be essential for interpreting the changes they do show. No single index suffices for studying the conse-quences of coronary occlusions, even under

Circulation Research, Volume IX, November 19G1


TSCHEMIC LEFT VENTRTCLE 1277 stable systemic circulatory conditions.

Myo-eardial electrocardiograms are indispensable for demarcating the extent of ischemic areas, for determining the earliest changes of elec-trical activity, and for excluding changes outside the ischemic zone. Continuous oxy-gen-reduction current records prevent con-fusion of local traumatic artifacts with early myocardial isehemic changes in the electro-cardiogram. The initial rate of fall and the relative level of the oxygen-current plateau are reflections of residual or collateral circu-lation.1 Motion-picture records of ischemic situations provide visual estimates of con-tractility and vein color changes, as well as material for more precise analysis from any segment of the experimental field.1 Muscle contraction is the last abnormality of func-tion to be restored to normal with release of occlusion, and the manner in which it re-covers from ischemia differs strikingly from its response to levarterenol under both is-chemic and nonisis-chemic conditions.1-13

These studies reveal certain limitations of epicardial electrocardiograms for the study of exposed hearts. The absence of epicardial heart-body lead changes is no guarantee that profound disorders of tissue electrical activ-ity, oxygenation, or contractility are absent in the heart wall beneath. Only with massive localized ischemia can one expect the epi-cardial electrocardiogram to reflect the sever-ity of physiological disturbance. Even then, its use as an isolated index may lead to underestimation of the extent of any ischemic area. Epicardial heart-body leads, however, must be retained as one of the essential in-dices of experimental ischemic dysfunction for at least two reasons. Provided that the occluded coronary vessel is of moderate size, the "sweep" technique11 permits comparison of baseline and RS-T segment levels in ischemic and control muscle over long periods of observation. This cannot be done with silver intramyocardial electrodes because of electrode drift. The myoeardial effects of small doses of levarterenol and other physio-logical eatechol amines are best seen in epi-eardial heart-body leads,13 although

super-Circulation Research, Volume IX, November 1901

ficially placed myocardial lead-points can provide similar information.


A new technique for simultaneous ampli-fication and recording of intramyocardial oxygen-reduction currents and electrocardio-graphic voltages from the tips of platinum oxygen electrodes was combined with cine-matographic muscle contraction records from exposed dog hearts. The picture of localized is-chemia produced by occlusion of medium-sized coronary arterial branches was compared, under stable systemic circulatory conditions, with the changes of myocardial oxygena-tion, electrical activity, and contractility, separately or together. Myoeardial electro-cardiographic abnormality appeared as early as disturbances of local oxygen and contrac-tion at the centers of ischemic areas; at the borders, only the myocardial electrocardio-gram was unequivocally abnormal. The epi-cardial electrocardiogram could be normal despite severe, acute disturbance of electrical activity in the underlying myocardium, and was not useful for the study of small isehemic areas, the onset of ischemia, or the borders of any isehemic area. No single index of myo-cardial function was dependable for follow-ing the course and estimatfollow-ing the extent of regional ischemic dysfunction, or for dis-tinguishing it from traumatic or nonischemic myocardial disturbances. The most complete description of the sequence of ischemic events was derived from the analysis of changes in local myocardial electrical activity. For this, however, it was necessary to interpret and compare direct heart-body electrocardiograms from myocardial and epicardial sites inside and outside an ischemic area, with attention to simultaneous records of myoeardial oxygen and local contraction. Such a combination of indices is considered essential for adequate description and differentiation of any local-ized myoeardial change in a working, blood-perfused heart.


The help of Dr. P. T. Kuo with the experimental procedures for many of the earlier animals in this series is gratefully acknowledged.



1. SAYEN, J . .T., SHELDON, W. F., PEIECE, G., AND Kuo, P . T.: Polarographic oxygen, the epi-eardial electrocardiogram and muscle contrac-tion in experimental acute regional ischemia of the left ventricle. Circulation Research 6: 779. 1958.

2. SAYEN, J. J., SHELDON, W. F., PEIRCE, G., AND Kuo, P . T.: Motion picture studies of ven-tricular muscle dynamics in experimental local-ized ischemia, correlated with myocardial oxy-gen tension and electrocardiograms (abstr., Proc. Amer. Soc. Clin. Tnvcst.). J. Clin. Invest. 33: 962, 1954.

3. SAYEN, .T. J., SHELDON, W. F., PEIRCE, G., AND Kuo, P . T.: Intramyocardial and epicardial electrocardiograms in acute localized ventricu-lar ischemia: Correlated with oxygen tension determinations and with muscle dynamics (abstr.). Proc. Am. Fed. Clin. Res. 3: 38, 1955. 4. SAYEN, J . J., KATCHER, A. H., PEIRCE, G., SHELDON, AV. F., AND CHKISTMAN, B. H.: Myo-cardial ECGs in localized ischemia (abstr.). Fed. Proe. 19: 113, 1960.

5. KATCHER, A. H., SAYEN, .T. J., SHELDON, AV. F., AND PEIRCE, G.: Cardiac contraction as meas-ured by a cinematographic method: Disturb-ances produced by regional ischemia (abstr., Proc. Physiol. Soe. Phila.). Am. J. M. Sc. 237: 130, 1959.

6. SAYEN, J. J., SHELDON, AV. F., AND AVOLFERTH, C. C.: Heart muscle and electrocardiogram in coronary disease: TIT. Xew classification of ventricular myocardial damage derived from clinieopathologic findings in 100 patients. (Parts 1 and 2). Circulation 12: 321, and 531, 1955.

7. SAYEN, J. J., SHKI.DON, AV. F., HORWITZ, O., KUO, P. T., PEIRCE, G., ZINSSER, IT. F., AND MEAD, J., J R . : Studies of coronary disease in experi-mental animal: I I . Polarographic determina-tions of local oxygen availability in the dog's left ventricle during coronary occlusion and pure oxygen breathing. J. Clin. Invest. 30: 932, 1951.

8. DAVIES, P . AV., AND BRINK, F., J R . : Micro-electrodes for measuring oxygen tension in animal tissues. Rev. Scient. Instr. 13: 524, 1942.

9. MONTGOMERY, H., AND HORWITZ, O.: Oxygen tension of tissues by polarographic method: I. Introduction: Oxygen tension and blood flow of skin of human extremities. J . Clin. Invest. 29: 1120, 1950.

10. POLGAK, G., AND FORSTER, R. E.: Measurement of oxygen tension in unstirred blood with a platinum electrode. J. Appl. Physiol. 15: 703, I960.

11. KATCHER, A. H., PEIRCE, G., AND SAYEN, J . J . : Effects of experimental regional ischemia and levarterenol on RS-T segment and baseline of ventricular surface electrocardiograms ob-tained by direct-coupled amplification. Circu-lation Research 8: 29, 1960.


Electroeardiographic effects of changing the nature of the contact between exposed heart and body. Circulation Research 9: 497, 1961. 13. SAYEN, J. J., KATCHER, A. H., SHELDON, AV. F., AND GILBERT, C. M.: Effect of levarterenol on polarographic myocardial oxygen, epicardial electrocardiogram and contraction in non-ischemic dog hearts and experimental acute regional ischemia. Circulation Research 8: 109, 1960.

14. SAYEN, J. J., SHELDON, AV. F., AND PEIRCE, G.: Studies of experimental localized myoeardial ischemia with special reference to its epicardial electroeardiographic reflection and intramyo-cardial temperature changes (abstr., Proe. Physiol. Soe. Phila.). Am. J. M. Sc. 231: 362, 1956.

15. PRINZMETAL, M., KKNNAMER, B., SHAW, C. M., KlMURA, N . , LlNDGREEN, I . , AND GOLDMAN, A . : Intramural depolarization potentials in myo-cardial infarction: A preliminary report. Circulation 7: 607, 1953.

16. KENNAMER, R., BERNSTEIN, J., MAXWELL, M., PRINZMETAL, M., AND SHAW, C. M.: Studies on mechanism of ventricular activity: A7. Intra-mural depolarization potentials in the normal heart with a consideration of currents of injury in coronary artery disease. Am. Heart J. 46: 379, 1953.

17. RAKITA, L., BORDUAS, J. L., ROTHMAN, S., AND PRINZMETAL, M.: Studies on mechanism of ventricular activity: X I I . Early changes in RS-T segment on QRS complex following acute coronary artery occlusion: Experimental study and clinical applications. Am. Heart J. 48: 351, 1954.

I S . Dl'RRER, D . , AT

AN DER TWEEL, LI. H . , AND B L I C K -MAN, J. R.: Spread of activation in left ven-tricular wall of the dog: I I I . Transmural and intramural analysis. Am. Heart J . 48: 13, 1954.

19. SCHER, A. M., YOUNG, A. C, MALMOREN, A. L., AND PATON, R. R.: Spread of electrical activity through wall of the ventricle. Circulation Research 1: 539, 1953.

20. SODI-PALLARES, D., BISTENI, A., MEDRANO, G. A., AND CINEROS, F . : Activation of the free left ventricular wall in the dog's heart: In normal conditions and left bundle-branch block. Am. Heart J. 49: 587, 1955.

Circulation Research, Volume IX, Sovcmbcr l i l



21. CONRAD, L. L., CUDDY, T. E., A N D BAYLEY, E. H.: Activation of ischemie ventricle and acute peri-infarction block in experimental coronary occlu-sion. Circulation Kesearch 7: 555, 1959.

22. HECHT, H. H., Ed.: Eleetrophysiology of the

heart. Ann. New York Acad. Sc. 65: 768-817, 1957.

23. KOSSHANN, C. E.: Advances in

Eleetrocardiog-raphy. New York, Grune & Stratton, 1958, p. 113.

24. FOEMIJNE, P., AND DUEEEB, D.: Acute effects

of coronary artery ligation on intramural excitation pattern. In Proceedings I I I World Congress on Cardiology, Brussels, September, 1958, p. 40.



F. L.: Electrocardiogram in normal and some abnormal conditions: In revived human fetal heart and acute and chronic coronary occlusion. Am. Heart J. 61: 303, 1961.

26. HUSNI, E. A., AND SIMEON, F. A.: Observations

on myocardiiil collateral circulation. Surg. Forum 9: J99, 1959.


experi-mental coronary occlusion: Chemical and ana-tomical changes in myocardium after coronary ligation. Am. Heart J. 12: 168, 1936.


JOHNSTON, F. D.: Effect of acute myoeardial infarction on electrical recovery and trans-mural temperature gradient in left ventricular wall of dogs. Circulation Research 8: 730, I960.

Circulation Research, Volume IX, November 1061


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