E = epinephrine
LMP
= Last menstrual periodNE = norepinephrine
NEFA = nonesterified fatty acids
SFD = small-for-date
(Received August 7; revision accepted for publication January 6, 1971.)
Supported by grants from the French National Institute of Medical Research (INSERM).
ADDRESS FOR REPRINTS: (D.E.A.) Pediatric Clinic of Athens University, “St. Sophie” Childrens Hos-pital, Goudi, Athens, Greece.
PEDIATRICS, Vol. 47, No. 6, June 1971
1000
URINARY
CATECHOLAMINE
EXCRETION
AND
PLASMA
NEFA
CONCENTRATION
IN
SMALL-FOR-DATE
INFANTS
D. E. Anagnostakis, M.D., and
R.
Lardinois, M.D.From the Centre de Recherches Biologiques N#{233}onatales, University of ParLs, France
ABSTRACT. Urinary catecholamine excretion, blood glucose, and plasma nonesterified fatty acids
(NEFA) concentration were studied in five
full-term, seven premature, and 22 small-for-date (SFD) babies (16 at term and six prematurely born) dur-ing the first 8 to 10 days of life.
Episodes of hypoglycemia (arbitrarily designed as <40 mg/100 ml for full term and <30 mg/ 100 ml for premature infants) were observed be-tween the second and fifth day of age in 12 SFD babies. During their low blood sugar period, these infants exhibited a significantly higher catechola-mine excretion (three- to fourfold for norepineph-rine and five- and sixfold for epinephrine) when compared to full term, premature, and “nonhypo-glycemic” SFD babies.
All SFD babies during the first 2 days of life showed a significantly higher plasma NEFA con-centration than the other groups of neonates; among the former, the hypoglycemic ones had a tendency to maintain for a longer period a higher NEFA concentration than the nonhypoglycemic ones.
These findings show that SFD babies are capa-ble of reacting to an hypoglycemic stress by mobilizing their fat stores and by releasing cate-cholamine; therefore, adrenal medullary unrespon-siveness cannot be considered as a cause of their transient neonatal hypoglycemia. Pediatrics, 47: 1000, 1971, URINARY CATECHOLAMINE EXCRETION, HYPOGLYCEMIA, PLASMA NEFA, NEWBORN INFANTS, SFD BABIES.
ECENTLY, much attention has been paid
to the excretion of catecholamine in
newborn infants. In the so called
small-for-date (SFD) babies, however, the reports
on this problem are scarce and even contra-dictory. Stern, et al.,1 described in five cases an inability to increase urinary
catechola-mine excretion after insulin induced
hypo-glycemia. Light, et al.,2 reported a sixfold increase in norepinephrine excretion in one case, 67 hours after birth, during a pro-found hypoglycemia. In infants born after a
pregnancy characterized by a placental
in-sufficiency syndrome, Cheek, et al., found an increased level of plasma catecholamine.
The same contradictory findings are
re-ported as far as plasma nonesterified fatty
acids (NEFA) of SFD infants are
con-cerned: Meichar, et al., and Gentz, et al.,
found a higher plasma concentration in
SFD infants than in full-term babies; such a
difference was not reported by Blum, et al.6
Considering these conflicting reports and
the possible relation between an
inade-quate medullary response and
hypoglyce-mia of SFD infants, we decided to follow
urinary catecholamine excretion as well as
plasma NEFA and glucose variations
dur-ing the first 8 to 10 days of life. MATERIAL
A total of 34 infants were studied: five
full-term
(38
to 42 weeks of gestationalage), seven prematurely born (<38
weeks), and 22 SFD whose birth weight
was below the 10th percentile on the intra-uterine growth curve of Battaglia and
Lub-chenko.7 Among the latter, 16 were born at
prema-TABLE I
DATA ON THE DIFFERENT GROUPS OF INFANTS
Number of Male! Gesta.tional Age (weeks) Birth Weight (gin)
Groups
Infants Female Mean ±1SD Mean ±1SD
Full-term 5 3/2 39.2 0.84 3,150
Premature 7 5/2 34.6 1.82 2,178 307
“Nonhypoglycemic” SFD 10 6/4 39.9 1.20 2,336 204
“Hypoglycemic” SFD 6 5/i 39.8 1.48 1,965 302
“Hypoglycemic”
premature and SFD 6 3/3 35.3 0.82 1,367 184
turely
born
(<38weeks).
Inaddition,
in
low blood sugar(arbitrarily
designed
asthe SFD group, six infants
born
at term and <40mg/100
ml and <30 mg/ 100 ml forallsix prematurely
born
exhibited,
between
the full term and the premature babiesre-the second and fifth day of life, a period of spectively). For this reason, the SFD
in-TABLE II
INDIVIDUAL CLINICAL DATA ON SFD INFANTS
Lowest Treatment
Case Gestational Birth Maternal blood
Number Sex Age (weeks) Toxemia Sugar D.W. D.W. ACTH Remarks
(mg/lOOml) 15% 10%
13 d’ 42 2,600
14 9 41 2,500
15 9 39 2,000 +
16 d’ 40 2,550 +
17 9 39 2,150 “nonhypoglycemic” SFD
18 9 38 2,120 +
19 d’ 40 2,460
20 d’ 41 2,250
21 d’ 40 2,450
22 d’ 39 2,280 +
23 d’ 39 1,900 + 15 +
24 d’ 39 1,760 + 15 +
25 d’ 42 2,500 10 + “hypoglycemic” SFD
26 o 41 1,860 + 18 +
27 d’ 38 1,660 10 +
28 9 40 2,110 <10 + +
29 a” 34 1,290 <10 +
30 a” 35 1,310 + 10 + + +
31 a” 35 1,400 <10 + + + “hypoglycemic”
pre-32 9 36 1,400 15 + mature and SFD
33 9 36 1,680 18 +
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fants were subdivided in two groups: a
“nonhypoglycemic”
and an “hypoglycemic” one (Table I).Gestational age was calculated from the
first day of the last menstrual period
(
LMP). Only infants whose mothers werecertain about their LMP were included in
the study. Data pertaining to the different
groups of infants are shown in Table I.
All infants were delivered vaginally, had
an
Apgar score > 7 at 5 minutes, andal-most all were fed in the same way: glucose in water feedings were started at 6 hours
of age; then, from the twelfth hour, breast milk was given at a rate of 50 mi/kg for the first day, and increased progressively to 150
mi/kg by the seventh to eighth day.
Feed-ings were given every 4 hours to all
fuli-term babies and every 2 or 3 hours to
pre-maturely born and SFD infants. All babies
(
except full-term infants) were kept inincubators equipped with a servo control sys-tern, at environmental temperatures
appro-priate for their weight and maturity.8
In-fants with rectal temperature < 36#{176}Cat the
admission to the hospital were discarded
from the study. The neonatal period of all
infants was uncomplicated except for the
episodes of low blood sugar mentioned
above. Clinical manifestation of hypogly-cemia was detected in 4 of our 12
“hypogly-cemic”
infants(
Cases 28, 29, 31, and 34Table II).
The only drugs given to the babies were
vitamins. Furthermore, the “hypoglycemic”
group received glucose infusion
(
ninein-fants were infused with 10% glucose in
wa-ter at a rate of 60 to 90 ml/kg and the
re-maining three were perfused for 12 hours
with 15% and then with 10%; infusion was
started in all (but two) “hypoglycemic”
in-fants the second day of life and was contin-ued until the sixth to seventh day). In
addi-tion, two SFD babies received ACTH (5
units/kg/day for 4 days). Among the
pre-mature babies, a set of twins born at 32
weeks of gestation received also a 10% glu-cose infusion for 3 days.
Table II summarizes some clinical data
on the SFD babies.
PROCEDURE AND ANALYTICAL
METHODS
At 8.00 A.M., 4.00 it., and 11.30 i.t.,
al-ways after a 90-minute fast, 0.2 ml blood
sample was collected by heel puncture in
tubes containing sodium fluoride, kept in
refrigerator and analyzed for glucose, the
same day, by a glucose oxidase niethod.#{176} An
additional 0.5 ml blood sample was drawn
at 8.00 A.M., in heparinized tubes for NEFA
duplicate analysis by a colorimctric micro-10 Catecholamine determinations
were performed on urines of 24 hours,
col-lected
with a pediatric urine collector bag connected through a plastic tube to a flask containing 3 to 5 ml of 2 N HC1. Diuresiswas exactly measured and specimens were
tested only when no loss of urine was
noted; thus, from a total of 34 babies and for a period of 8 to 10 days, 160 urine speci-mens were studied. Urines were stored at
4#{176}C;free norepinephrine (NE) and
epi-nephrine (E) were determined by a
fluori-metric method.’1
Blood Glucose
RESU LTS
According to the criteria of low blood
glucose concentration mentioned above, all
five full-term, all seven premature, and 10
of 22 SFD babies did not present low blood
sugar episodes during the whole period of
the study. Individual blood glucose values of these infants showed a rather wide range and the mean values did not differ
signifi-cantly
between
the groups (Table III).In the “hypoglycemic” SFD infants’
blood glucose values were very scattered
from infant to infant and from time to time in the same baby
(
very low concentrationduring the hypoglycemic attacks and high
concentration following intravenous
infu-sion (Table IV).
In all but two cases, hypoglycemia
be-came evident after 36 hours of age and,
al-most in all cases, lasted for 3 days in spite
of the therapy. After treatment, glucose
TABLE V
CATEcIIoIA1INE URINARY EXCRETION (a/KG/24 iiouas)
First l)ay Second Day Third Day Fourth Day Fifth Day Sixth Day Seventh Day
Groups Cau NE. E. NE. E. NE. E. NE. E. NE. E. NE. E. NE. E. NE. E. Number
I - - 0.614 0.139 - - 0.776 0.192 0.800 0.100 0.798 0.103 - 0.789 0.190
I 0.608 0.138 - - 0.647 0.165 - - - - 0.680 0.172 0.695 0.176 0.864 0.210
S .- - 0.656 0.186 - - 0.703 0.190 - - - - 0.795 0.210 0.808 0.263 4 0.641 0.146 --- 0.690 0.180 - - 0.781 0.200 -
-Full-term
5 0.670 0.160 0.690 0.161 0.683 0.175 0.700 0.168 - - 0.763 0.178 - - 0.787 0.186
Mean 0.639 0.148 0.656 0.161 0.665 0.170 0.726 0.183 0.745 0.190 0.747 0.183 0.756 0.195 0.812 0.212
±1 SD 0.031 0.011 0.033 0.017 0.025 0.007 0.043 0.013 0.078 0.014 0.060 0.016 0.033 0.017 0.036 0.035
NE/E
ratio 4.33 4.15 3.91 3.97 3.92 4.05 3.88 3.89
6 - - 0.265 0.115 - - - - 0.386 0.153 - - - - 0.678 0.231
7 0.236 0.069 - - 0.406 0.112 0.470 0.165 - - 0.540 0.188 0.610 0.188 -
-I 8 0.360 0.054 0.580 0.064 - - 0.670 0.216 - - - - 0.860 0.220 -
-Premature 9 0.625 0.106 0.675 0.145 0.732 0.151 0.785 0.151 0.811 0.121 0.837 0.143 - - -
-10 0.617 0.197 0.709 0.200 0.771 0.190 0.913 0.214 0.887 0.238 0.984 0.280 - - 1.000 0.260 11 0.666 0.230 - - 0.687 0.197 - - 0.800 0.189 - - 0.851 0.193 -
-12 - - - - 0.300 - 0.540 0.100 0.560 0.125 0.661 0.132 - - 0.785 0.170
Mean 0.500 0.146 0.557 0.131 0.579 0.162 0.675 0.169 0.728 0.165 0.755 0.186 0.773 0.200 0.821 0.220
±1 SD 0.191 0.081 0.202 0.056 0.212 0.039 0.180 0.048 0.146 0.049 0.195 0.067 0.141 0.017 0.164 0.045
NE/E
ratio 4.40 4.88 4.00 4.10 4.59 4.31 3.8.5 3.80
13 - - 0.695 0.164 - - - - 0.758 0.185 - - 0.800 0.200 -
-14 0.661 0.154 - - - - 0.674 0.151 0.680 0.158
15 0.030 0.130 0.675 0.138 - - 0.725 0.200 0.800 0.208 0.738 0.162 - - 0.880 0.239
“Nonhypo- 16 - - 0.585 0.158 0.700 0.186 0.723 0.184 0.760 0.205
glycemk” 17 0.600 0.160 0.660 0.142 - - 0.780 0.180 - - 0.760 0.180 - - -
-SFD 18 - - - - 0.606 0.124 0.770 0.163 0.814 0.187 0.807 0.208 0.872 0.230 -
-19 0.740 0.170 - - 0.770 0.189 - - 0.960 0.218 20 0.6900.172 0.8900.215
21 - - 0.7300.200 - - - 0.8500.240 - - -
-22 - - 0.600 0.135 0.780 0.184 - - 0.780 0.190 - - - - 0.885 0.189
Mean 0.645 0.154 0.657 0.159 0.695 0.164 0.737 0.173 0.787 0.190 0.785 0.195 0.798 0.204 0.871 0.212
± SD 0.038 0.017 0.055 0.022 0.087 0.033 0.042 0.018 0.069 0.020 0.044 0.030 0.074 0.020 0.082 0.021
NE/F
ratio 4.22 4.16 4.30 4.29 4.13 4.05 3.90 4.12
23 - - - - 2.050 0.550 2.440 0.822 - - - - 0.683 0.19.5 -
-24 0.650 0.140 - - 1.700 0.510 1.800 0.600 - - 0.684 0.198 - - -
-“Hypogly- 23 0.510 0.123 0.694 0.152 1.266 0.629 2.100 0.700 1.360 0.585 0.672 0.235 0.669 0.137 0.800 0.220
cemic’ 26 0.680 0.128 0.740 0.200 1.594 0.970 - - 1.187 0.659 0.900 0.240 0.705 0.226 0.920 0.225
SF1) 27 0.633 0.111 0.639 0.137 - - 1.336 0.642 1.356 0.576 0.892 0.240 - - 0.910 0.225
28 0.610 0.135 0.630 0.164 - - 2.850 0.916 2.346 0.841 0.880 0.214 - - 0.750 0.188
Mean 0.617 0.127 0.675 0.163 1.652 0.664 2.145 0.736 1.562 0.665 0.805 0.225 0.685 0.192 0.845 0.214 ± SD 0.065 0.011 0.031 0.027 0.323 0.209 0.518 0.130 0.328 0.123 0.116 0.019 0.018 0.034 0.083 0.018
NE/F
‘I’ABLE V (Continued)
CATECHOLAMINE URINARY EXCRETION (zG/Ka/24 IIOURS)
“llypogly-cemic”
premature
and
SFD
1005
First Day Second Day Third Day Fourth Day Fifth Day Sixth Day Seventh Diiy
Group Case NE. E. NE. E. NE. E. NE. E. NE. E. Nil. E. NE. E. NE. E Number
29 0.483 0.00 0.651 0.281 0.945 0.370 0.968 0.403 -- - 0.50 0.19-t 0.500 0.183 -
-SO 0.660 0.170 0.702 0.580 - - 2.155 0.685 - - 0.716 0.08 - - 0.900 0.240 31 - - 0.673 0.187 1.315 0.530 4.160 1.275 2.331 0.700 1t02 0.369 1.008 0.33 -
-32 0.680 0.180 - - 1.400 0.467 1.440 0.492 - - - - 0.635 0.136 0.657 0.170
33 0.610 0.113 0.697 0.130 2.546 0.876 2.883 0.923 2.546 0.876 - - - - 0.890 0.215
34 - - - - 1.125 0.375 1.32 0.447 - - 0.785 0.142 0.714 0.139 0.800 0.200
Mean 0.608 0.140 0.680 0.194 1.466 0.523 2.140 0.704 2.438 0.788 0.813 0.228 0.714 0.202 0.811 0.206
± SD 0.088 0.040 0.023 0.063 0.628 0.208 1.212 0.339 0.152 0.124 0.277 0.098 0.214 0.101 0.112 0.029
NE/F
Ratio 4.70 3.79 2.79 2.94 3.12 3.77 3.83 3.94
Catecholamine Excretion (Table V)
In each group of neonates, there is a
ten-dency for both catecholamines excretion to
increase with age. Nevertheless, there is no statistically significant difference in the
mean NE excretion between the first and
the eighth to tenth day in any group of
in-fants, whereas a statistically significant dif-ference
(
p < 0.05) was noticed for E excre-tion in all groups.The mean values of NE and E excretion
did not differ signfficantly among the differ-ent groups of infants at any day of age, with
the exception of the hypoglycemic period
(
third to fifth day) in SFD infants. During this hypoglycemic period, a five- to sixfoldincrease of E and a three- to fourfold
in-crease of NE excretion was noticed.
The NE:E ratio is almost constant regard-less of the age; it did not differ signfficantly between the different groups of neonates,
with the exception of the hypoglycemic
period of SFD babies: here, a marked
de-crease of this ratio was observed, reflecting the relatively higher E over NE excretion.
NEFA
(Fig. 1)In each group of infants, the highest
plasma NEFA concentration is on the
sec-ond day of life.
During the first 4 to 5 days of age SFD
babies showed a higher NEFA
concentra-tion than full-term or premature infants
(
the difference being statistically highly sig-nificant (p < 0.01),
the first 2 days ). Sucha difference was not noted between
full-term and premature infants at any age of
life.
During the first 2 days, the plasma NEFA concentration showed no difference
be-tween “hypoglycemic” and
“nonhypogly-cemic” SFD babies; afterwards and until
the fifth day, the former maintained a
higher NEFA concentration than the
“non-hypoglycemic” SFD babies. This difference is statistically highly significant (p < 0.01)
and significant (p < 0.05) at the third and fourth day respectively.
By 8 to 10 days of age, plasma NEFA
mean values did not differ significantly be-tween the groups.
Glycemia
COMMENTS
Transient hypoglycemia which has been
recognized as a clinical entity in SFD
in-fants12” was found in 12 of our 22 SFD
babies. Our different criteria for identifying
“hypoglycemic” infants from those
gener-ally used,’4’15 the systematic repetition of
glucose determination (which might detect
unrec-I!
201 a
I
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4w N
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I 2 3 4 5 6 7 80
DAYS
F’iu. I. ‘[he mean
(
± 1 S.!).) plasma NEFA concentra-tioii (Iurmg the 1ieoiiattl period in: five full-terni(A A) seven premature
(D --L1)
six “hypo-gly(-elIli(- premature and SF1) (O-O) 10 “non htypoglyceink-” SF1)()
atid six“hypogly-Ct”nJC Fl) infants (
ognized), and the fact that all six babies
who were at the same time SFD and
pre-mature showed a low blood sugar
concen-tration, may explain the relatively high mci-dence of hypoglycemia in this study.
Hypoglycemia became evident in all our
cases
(
but two) after 36 hours of life: therelative early feeding of the babies
in-cluded in this study could have resulted in
a later onset of the hypoglycemia than pre-viously reported.’3’16’17
Catecholamine
The present data confirm the observation of earlier workers that all newborn infants, even the premature babies,3’18 from the first
few days of life are capable of excreting
catecholamine. When expressed in terms of
body weight, we found no difference in cat-echolamine excretion between the different
groups (except for the hypoglycemic
pe-nod of SFD babies
)
during the wholepe-nod of this study.
In each group, between the first and the
tenth day of age, there is a statistically sig-nificant increase for E, but not for NE; since urinary NE excretion in newborn
largely represents secretion from
extramed-ullary ehromaffin tissue, which is rich in
NE,19 whereas urinary E is a better
reflee-tion of adrenal medullary secretion, this
finding may suggest an initiation of an
adult type metabolism in the adrenal gland
the content of which is largely E in the
adult human.b0
During the hypoglycemic period, SFD
infants increased the excretion of catechola-mine; all 12 “hypoglycemic” babies showed a five- to sixfold increase of E and a
three-to fourfold increase of NE in comparison to
their “nonhypoglycemic” counterpart or
even to their own “nonhypoglycemic”
pe-nod. Although “hypoglycemic” SFD infants
were under intravenous glucose infusion,
we believe that the 15 to 40% increase in
urinary output is not the cause for the high
catecholamine excretion since it has been
demonstratedhl that there is no correlation
between catecholamine excretion and
un-nary volume; on the other hand,
catechola-mine excretion diminished as soon as
hypoglycemia disappeared, in spite of a
prolonged infusion.
Our findings are consistent with the
ob-servation of Light, et al.,2 who reported an
increase of catecholamine
(
E and NE)
inone SFD infant, 67 hours after birth, during a profound hypoglycemia.
Among seven newborn infants with
pla-cental insufficiency studied between 10 and
36 hours of age by Cheek, et a!.,’ two were
SFD; one of the latter exhibited an
in-creased plasma E and NE concentration;
the higher plasma catecholamine level was
attributed to a chronic overproduction of catecholamine due to a prolonged hypoxia;
but glucose determinations were not
per-formed in this study. Since hypoxia has not
been proven to increase catecholamine
ex-cretion in newborn infants,22 other factors
1007
E and NE concentration in Cheek’s cases.
Stern, et al,’ provoked, between 15 and 60 days of age, an insulin-induced
hypogly-cemia in five SFD infants who had been
profoundly hypoglycemic during the first
week of life. No increase of urinary
cate-cholamine excretion was noticed. These
in-vestigators suggested that SFD babies may
present an adrenal medullary exhaustion
consecutive to a long standing
(
intra-uter-me
)
hypoglycemia.Our experiments were made before,
dur-ing, and just after the “hypoglycemic”
pe-nod; they show that SFD babies were able
to increase urinary catecholamine excretion during the low blood sugar period. As far as
catecholamine release is concerned, one
might speculate that SFD infants might
ex-hibit a different response to the “endoge-nous” and “insulin-induced” hypoglycemia.
Such a difference, however, was not
re-ported for full-term babies who react
gen-erally to hypoglycemia by increasing
cate-cholamine excretion”23 In any case, the
prompt adrenal medullary response of our
SFD babies to the “endogenous”
hypogly-cemia suggests that these infants do not
present any exhaustion of their adrenal me-dulla, at least during the first few days of life, and consequently the transient
neona-tal hypoglycemia in SFD babies cannot be
explained by such a mechanism. The same
is probably true for full-term infants. Kaye,
et al.,24 studied the total urinary
catechola-mine excretion
(
including compoundsde-nived from E
)
in asymptomatichypogly-cemic and normoglycemic full-term babies.
These investigators used urinary samples
collected for periods less than 24 hours and therefore their results are difficult to be
in-terpreted; nonetheless, their data seem to
indicate that deficient E release cannot be
invoked as a contributory factor in neonatal
hypoglycemia in full-term babies.
Although “hypoglycemic” infants react
by increasing E rather than NE, three- to
fourfold increase of NE does occur in both
prematurely born and full-term SFD
ba-bies. This finding is in good agreement with that of Goldfein, et al.,25 who demonstrated
a significant increase in plasma NE after in-sulin stimulation.
NEFA
It is generally accepted that the major
factor influencing the plasma NEFA
con-centration appears to be fatty acids release from adipose tissue rather than uptake and
utilizationlc,27 Although in the adult the mechanisms controlling lipid mobilization
are influenced by nutritional,’
neuro-genie,’#{176} and hormonal factors,28,lOhl in new-born infants this process is still obscure.
In all our cases, the peak values of NEFA
concentration were on the second day of
life; this is in good agreement with data re-ported by other authors.’32
During the first 2 days of life, SFD
ba-bies showed a higher NEFA concentration
than full-term or premature infants. This
finding, which is consistent with previous observations,” is difficult to be explained.
As blood glucose concentration and
cate-cholamine release did not differ between
SFD and the other groups of infants during the first 2 days, these factors do not
contrib-ute to the higher NEFA concentration in
our SFD babies during this period. This
finding cannot be explained as a result of
reactions to cold and/or hypoxia, since all
infants have been studied after rigid
selec-tion criteria, excluding the interference of
these factors. One of the factors promoting lipolysis, human growth hormone, which
has been found to be increased in SFD
ba-bies,3’ may be related to their higher
plasma NEFA concentration. Other
hor-mones such as insulin and placental
lacto-gen hormone may also play an important
role.
If it is difficult to explain the elevated
plasma NEFA concentration in SFD babies
during the 2 first days of life, in contrast, this finding observed afterwards (between the third and fifth day of life) in
“hypogly-cemic” SFD infants could be related to the
low blood sugar concentration and the
in-creased catecholamine release of these
ba-bies. The fact that during this period the
1008
SFD infants did not rise above the level
reached at the second day of life, in spite of
a threefold increase of NE, may be due to
the glucose infusion resulting in a mild sup-pression of NEFA release’ and to a relative exhaustion of lipid stores during this time.
SPECULATIONS
Although one might suggest that, as a re-sult of different states of intra-utenine un-dernutrition and/or different degrees of fe-tal distress, SFD infants do not constitute
an
homogeneous population among theneonates, our findings suggest that under
hypoglycemic stress SFD babies exhibit a
marked catecholamine release and a high
degree of lipid mobilization; nevertheless, in spite of these reactions and of a high ca-brie intake, blood glucose concentration
re-mains low during several days. Thus
hypo-glycemia in this group of infants cannot be interpreted as a result of adrenal medullary inresponsiveness. This points out the inter-est of further studies on liver carbohydrates stores, activity of glycogenolytic pathway,
neoglycogenic capacity, and efficiency of
catecholamines in SFD babies in the
neona-tal period.
Our finding, on the other hand, that all
“hypoglycemic” SFD infants reacted by
in-creasing urinary E as well as NE excretion, suggests that the classical view that NE
ex-cretion is unaffected by hypoglycemia
could be reevaluated. SUMMARY
Studies on urinary catecholamine
excre-lion and plasma NEFA concentration were
carried out during the 8 to 10 first days of life in five full-term, seven prematurely
born, and 22 SFD infants. Twelve of the
latter presented a low blood sugar
concen-tration between the second and fifth day of
age.
These infants showed during this
hypo-glycemic period and only during this
pe-riod, a higher excretion of catecholamine and especially of epinephrine as compared to nonhypoglycemic newborns.
All SFD babies exhibited during the 4 to
5 first days a higher NEFA concentration than full-term or prematurely born infants.
Among the former, the “hypoglycemic”
SFD babies had a tendency to maintain a
higher NEFA concentration for a longer
pe-riod than the nonhypoglycemic ones.
It is concluded that SFD babies react to
an hypoglycemic stress by mobilizing their
fat stores and by increasing catecholamine
excretion; therefore, adrenal medullary
ex-haustion cannot be invoked as a cause of
hypoglycemia in these infants.
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