The function of the high pressure zone appears to be two fold: to guard against the entry of air into the oesophagus and to prevent oesophageal contents entering the larynx. There is some evidence to support both these points (Winship 1983).
P r e v e n t i o n o f a i r e n t e r i n g t h e o e s o p h a g u s
Work in dogs by Levitt et al (1965) and Kawasaki et al (1964) on direct electromyographic studies on the cricopharyngeus shows that the muscle is active in inspiration and is quiescent during expiration. Goyal et al (1970) studied the influence of respiration on the intraluminal pressures in the region of the upper oesophageal sphincter in 25 patients with lower oesophageal symptoms. Inspiration was associated with a fall in pressure in the cervical oesophagus. As the catheter was withdrawn, the polarity of respiratory movements changed with the fall in pressure on inspiration in the oesophagus changing to a rise in the lower part of the upper oesophageal sphincter and then to a fall in the upper part of the upper oesophageal sphincter. In the pharynx, inspiration caused a significant drop in pressure. The inspiratory rise in pressure was most obvious at the peak pressure of the upper oesophageal sphincter which seemed to corre s p o n d to the horizontal fibres of the cricopharyngeus. A brief rise in pressure was seen in 25% of the patients in the maximal pressure region just prior to relaxation in response to
swallowing. Increased muscle activity in the sphincter, which can be demonstrated as a high pressure zone m a n o m e t r i c a l l y , prevents regurgitation of oesophageal contents into the pharynx.
Kahrilas et al (1987a), using a sleeve sensor in normal controls, found that the upper oesophageal sphincter pressure increased transiently with each respiration and was particularly noticeable during periods of rest and sleep. The upper oesophageal sphincter pressure increase was 180 degrees out of phase with the inspiratory drop of intraluminal pressure in the thoracic oesophagus. This was consistent with the hypothesis that function of the upper oesophageal sphincter is to exclude air from the oesophagus during respiration.
P r e v e n t i o n o f o e s o p h a g e a l c o n t e n t s e n t e r i n g t h e l a r y n x
Freiman et al (1981) studied in the dog the effect of bilateral vagosympathetic nerve blockade on the upper oesophageal sphincter responses to acid perfusion. Initial studies showed that the upper oesophageal sphincter in dogs has a similar asymmetry to the human sphincter w ith higher pressures anteriorly and posteriorly. Perfusion of acid at 0.5cc/min at the level of the upper oesophageal sphincter and below similarly produced an increase in pressures. This response was maximal on perfusion at the sphincter and de creased progressively with perfusion distally. Perfusion at a similar rate with saline or water failed to produce any change in sphincter pressure. Bilateral nerve block a d e by cooling produced no change in resting upper oesophageal sphincter pressure or in the response of the s p hincter to
swallowing. It produced abolition of the maximal sphincter response to acid.
Studies on normal subjects have shown that the upper oesophageal sphincter pressure rises in response to the p resence of intraoesophageal fluid especially acid perfusion. Infusions of both saline and h y d r o chloric acid increased upper oesophageal sphincter pressure above a control period when no infusion occurred, suggesting that this was a volume response. However, the pressure rise was greater with the acid infusion suggesting a response to acid stimulus. In addition, the closer to the upper oesophageal sphincter the infusion was administered the greater was the increase in pressure recorded (Gerhardt et al 1978).
Wallin et al (1978) measured upper oesophageal sphincter pressure during infusion of O.IN Hydrochloric acid (5ml/min) 5cm above the lower oesophageal sphincter in eight normal controls. There was a significant increase in the upper oesophageal sphincter pressure after one minute but this was not maintained. Stanciu and Bennett (1974) found that the upper oesophageal sphincter pressure showed no significant difference in normal controls and patients with gastro- o esophageal reflux. Within the reflux group there was no difference in upper oesophageal sphincter pressure between those with no oesophagitis and those w ith severe oesophagitis on endoscopy. There was no correlation between the severity of reflux as judged by 15 hour pH recording and the upper oesophageal sphincter pressure. Nine refluxers had 30mls of O.IN Hydrochloric acid dripped into the oesophagus 10cm below the upper oesophageal sphincter at lOmls/min.
This produced no significant change in sphincter pressure. This may be related to the distance away from the upper oesophageal sphincter that perfusion occurred. The increased threshold to acid in the lower oesophagus may explain why Stanciu and Bennett (1974) and Wallin et al (1978) failed to demonstrate a consistent rise in upper oesophageal sphincter pressure in humans when acid was perfused into the oesophagus 10cm or more below the sphincter.
Gerhardt et al (1980) found that the m ean peak upper oesophageal sphincter pressure in controls and patients with heartburn was significantly greater than in patients with o esophago-pharyngeal regurgitation. These patients all had an awareness of spontaneous movement of fluid from the oesophagus into the pharynx, most frequently at night. Nine controls responded to intraoesophageal perfusion with saline or acid with an increase in upper oesophageal sphincter pressure but the group with o e s o p h a g o -pharyngeal regurgitation showed no change in pressure. They concluded that in these patients there was a breakdown of the normal mechanisms that serve as barriers to o e s o p hago-pharyngeal regurgitation. Sondheimer (1983) found similar resting upper oesophageal sphincter pressures in infants with gastro- oesophageal reflux and controls. Oesophageal a c idification produced a significant increase in mean upper oesophageal sphincter pressure in controls and refluxers.
Spontaneous episodes of gastro-oesophageal reflux did not produce any alteration in the upper oesophageal sphincter pressure which is at variance with experimental work. A p ossible explanation may be that in the experimental work
the duration and degree of acid exposure is much greater (Kahrilas et al 1987b).
Gerhardt et al (1978) suggest that the upper oesophageal sphincter functions as a dynamic barrier preventing oesophago-pharyngeal reflux and possible subsequent a s p i r a t i o n .
Kahrilas et al (1987b) used the sleeve sensor for prolonged o v ernight recording in normal subjects and found that with deep sleep the mean upper oesophageal sphincter pressure fell from roughly 40mmHg to about 10mm Hg. The swallow rate was also significantly less during sleep than awake periods. These findings may have significance as the fall in upper oesophageal sphincter pressure with sleep diminishes the barrier to nocturnal regurgitation and potential aspiration. Basal upper oesophageal sphincter pressure in awake subjects is sufficient to serve as an adequate barrier to prevent r e gurgitation because intraluminal oesophageal pressure resulting from gastro-oesophageal reflux rarely exceeds 1OmmHg (Dent et al 1989).
Freiman et al (1981) also studied in the dog the effect of bilateral vagosympathetic nerve blockade on the upper oesophageal sphincter responses to intraoesophageal distension. Balloon distension at levels up to 20cm below the upper oesophageal sphincter produced a large increase in the sphincter pressure. The threshold for this response increased and the maximum response decreased as distension was performed more distally in the oesophagus. Bilateral nerve blockade by cooling produced a partial r e duction in maximal upper oesophageal sphincter response to distension.
Similar results have been obtained in humans. Creamer et al (1956), using a nonperfused catheter, showed that the upper o esophageal sphincter pressure increased immediately after b alloon inflation especially if the stimulus was in the upper two thirds of the oesophagus and was m a i n t a i n e d for the period of distension. This was associated w ith a decrease in the lower oesophageal sphincter pressure. The oesophagus above the balloon contracted v i g orously and repetitively but below the balloon there were very few contractions. Rapid distension of the upper o e s ophagus with SOmls of water also produced an increase in pressure in the upper oesophageal sphincter. Enzmann et al (1977) also found an increased pressure in the upper oesophageal sphincter in response to intraluminal balloon distension with resultant initiation of secondary peristalsis above the d i stension site which they felt comprised a highly integrated pressure barrier to regurgitation. Kahrilas et al (1987a), using the sleeve sensor, studied balloon d i s tension in normal controls. Balloon distension in the oesophageal body caused a significant increase in upper oesophageal sphincter pressure. The increase was directly related to the balloon diam e t e r and proximity to the sphincter. The maximal augmentation of upper oesophageal sphincter pressure, 214% above basal pressure, occurred with the balloon 5cm below the upper oesophageal sphincter, inflated to a d i a m e t e r of 2.5cm. Using a similar technique, Kahrilas et al (1986) studied the effect on the upper oesophageal sphincter of belch i n g in normal volunteers. Belching was p r e c e d e d by complete upper oesophageal sphincter relaxation. Abrupt
oesophageal distension with air 8 cm below the sleeve p roduced upper oesophageal sphincter r e l axation and secondary peristalsis and mimicked the effect of a belch. Increasing the volume of injected air significantly p r olonged the duration of complete upper oesophageal sphincter relaxation. Saline injected at 3ml/second caused either no change in upper oesophageal sphincter pres s u r e or an augmentation of upper oesophageal sphincter pressure. Mucosal anaesthesia did not change the response of the upper o esophageal sphincter to either rapid air d i s t e n s i o n or saline infusion. The use of a cylindrical balloon 15cm long to distend abruptly the proximal 75% of the oesophagus p recipitated either partial or complete upper oesophageal sphincter relaxation in the small number of subjects tested. These findings suggest that the rapidity and spatial pattern of distension, rather than discrimination of the type of material causing the distension, determines w h e ther or not upper oesophageal sphincter relaxation occurs.
1.3.6: HYPERTENSIVE UPPER OESOPHAGEAL SPHINCTER PRESSURE