We studied the effects of increased intra-abdominal pressure on the lower esophageal sphincter (LES) pressure in 15 healthy subjects. The role of the diaphragm in the genesis of LES pressure during increased intra-abdominal pressure was determined by measuring diaphragm electromyogram (EMG). The latter was recorded using bipolar intraesophageal platinum electrodes that were placed on the nonpressure sensing surface of the sleeve device. We also measured the LES pressure response to increased intra-abdominal pressure during inhibition of the smooth muscles of the LES by intravenous atropine (12 micrograms/kg). Straight-leg raising and abdominal compression were used to increase intra-abdominal pressure. Our results show that the increase in LES pressure during straight-leg raising is greater than the increase in gastric pressure. During abdominal compression, the rate of LES pressure increase is faster than that of the gastric pressure, suggesting an active contraction at the esophagogastric junction. The increase in LES pressure during periods of increased intra-abdominal pressure is associated with a tonic contraction of the crural diaphragm as demonstrated by EMG recording. Atropine inhibited the resting LES pressure by 50-70% in each subject but had no effect either on the peak LES pressure attained during increased intra-abdominal pressure or tonic crural diaphragm EMG. We conclude that 1) there is an active contraction at the esophagogastric junction during periods of increased intra-abdominal pressure and 2) tonic contraction of the crural diaphragm is a mechanism for this LES pressure response.
We studied the effect of bolus volume and esophageal obstruction on esophageal peristalsis by using synchronized video-fluoroscopic and manometric techniques in cats. A specially designed pressure cuff was surgically implanted around the distal esophagus to control the degrees of outflow obstruction. Secondary esophageal peristalsis was evoked by injecting bolus volumes of 3, 6, and 9 ml at cuff pressures of 0, 20, 40, and 60 mmHg. Increases in outflow obstruction reduced the velocity of peristalsis. The amplitude of esophageal contraction increased with increasing outflow obstruction at low bolus volumes but decreased with larger bolus volumes and larger outflow obstruction. In the absence of outflow obstruction, each esophageal contraction traversed the entire esophagus distal to its site of origin, but in the presence of outflow obstruction contractions only traversed part of the esophagus. The incidence and site of failure of propagation was directly related to cuff pressure and bolus volume. The relationship between the onset of manometric pressure complex at a given site in the esophagus to the passage of the bolus from that esophageal site was markedly affected by outflow obstruction. We conclude that esophageal peristalsis can be modulated by the bolus volume and outflow obstruction.
Transient lower esophageal sphincter relaxations (TLESR) were studied in 10 normal healthy subjects. Electrical activity of mylohyoid muscle measured by an electromyogram (MEMG), pressures from pharynx, three esophageal sites, lower esophageal sphincter, and stomach were simultaneously recorded for 1 h, while fasting and 3 h after an 850 kcal meal. Reflux of acid into esophagus and/or occurrence of belching accompanying a TLESR was also monitored. TLESRs occurred with an equal frequency in fasting and postprandial state (6.2 vs. 6.4 h). However, frequency of an acid reflux during a TLESR was much greater postprandially than after fasting (44.8 vs. 9.6%). Belching coincided with 8% of TLESRs. A small MEMG complex and a small pharyngeal complex were present at onset of TLESR in 41.6 and 26.9% of instances, respectively. TLESRs were then categorized as either postswallow, if it occurred within 10 s of a preceding swallow-induced LES relaxation, or isolated, if its onset to previous swallow was greater than 10 s. Esophageal contractions were noticed at onset of 84% of isolated TLESRs. When present at two distal sites, this contraction was always of a simultaneous nature. Esophageal contractions at onset of postswallow TLESR were less frequent (33.3%) but when present were usually observed at the proximal esophageal site. At completion of a TLESR, the LES never recovered without an associated esophageal contraction, the latter was either swallow mediated or a spontaneous simultaneous esophageal contraction. Our data indicate that 1) MEMG and pharyngeal motor events may accompany TLESRs; and 2) esophageal contraction frequently heralds the onset, and it always occurs at completion of a TLESR.(ABSTRACT TRUNCATED AT 250 WORDS)
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