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Biomedical subjects

R K Mittal

Publications and source records attributed to R K Mittal.

At least 73 records · Page 4Linked to original sources
PubMed1990

Electrical and mechanical inhibition of the crural diaphragm during transient relaxation of the lower esophageal sphincter.

Electrical and mechanical correlates of crural diaphragm activity during swallow-induced and transient lower esophageal sphincter relaxation were monitored in 12 healthy subjects. Simultaneous esophageal manometric, pH, and crural diaphragm electromyogram recordings were performed for 1 hour in the postprandial period. Swallow-induced lower esophageal sphincter relaxation was associated with minimal inhibition of the crural diaphragm, but transient lower esophageal sphincter relaxation was accompanied by marked inhibition of the crural diaphragm. The degree of lower esophageal sphincter relaxation appeared to correlate with the degree of crural diaphragm inhibition during transient lower esophageal sphincter relaxation. Inhibition of crural diaphragm during transient lower esophageal sphincter relaxation may play an important role in facilitating flow across the gastroesophageal junction.

Deglutition↗
PubMed1990

Modulation of feline esophageal contractions by bolus volume and outflow obstruction.

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.

Animals↗
PubMed1990

Human lower esophageal sphincter pressure response to increased intra-abdominal pressure.

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.

Abdomen↗
PubMed1990

Current concepts of the antireflux barrier.

The lower esophageal sphincter, crural diaphragm, and phrenoesophageal ligament are the anatomic structures that constitute the antireflux barrier. The intraluminal pressure at the esophagogastric junction (EGJ) reflects the strength of the antireflux barrier. The end-expiratory pressure is a result of the tonic activity of the smooth muscles of the lower esophageal sphincter. The EGJ pressure increases during inspiration owing to the effect of the crural diaphragm. There is a reflex increase in the EGJ pressure during periods of increased intra-abdominal pressure, and the crural diaphragm contributes to this reflex contraction of the EGJ. Based on the contribution of the lower esophageal sphincter and crural diaphragm to the EGJ pressure, a two sphincter hypothesis of the antireflux barrier competence is suggested.

Diaphragm↗
PubMed1989

The hypertensive lower esophageal sphincter. Manometric and clinical aspects.

Controversy exists as to whether the hypertensive lower esophageal sphincter (HLES) represents a clinical motility disorder of the esophagus or is merely the right-sided expression of a normal distribution curve. In the present study we describe 16 patients with HLES, defined as a lower esophageal sphincter (LES) pressure of greater than or equal to 40 mm Hg (mean + 3 SD of controls) with normal peristalsis. All of the patients suffered from chest pain and nine from dysphagia. Delayed bolus transit at the gastroesophageal junction was demonstrated in four patients by radiography. Manometric studies showed that during swallowing the LES residual pressures were significantly greater (9.2 +/- 5.0 mm Hg) than observed in normal controls (1.8 +/- 2.2 mmHg) (mean +/- 1 SD). However, the percent LES relaxation in patients did not differ significantly from controls. Clinical improvement was associated with pharmacological or mechanical reduction of resting LES pressure with an accompanying fall in the nadir pressure. These observations suggest that HLES may have clinical and pathophysiological significance and that evidence for the entity should be sought during manometric studies in the clinical laboratory.

Adult↗
PubMed1989

Hiccups and gastroesophageal reflux: cause and effect?

Chronic hiccups may be a problem of great significance to the affected patient. A 62-year-old man with severe heartburn and persistent hiccups despite numerous diagnostic tests and therapeutic drug trials presented to our clinic. Esophageal motility and intraluminal pH studies demonstrated decreases in intraesophageal pressure during hiccups and acid exposure during 68% of the measured time. The patient underwent Nissen fundoplication, which improved his heartburn but not his hiccups. The association between gastroesophageal reflux and hiccups is discussed. Our experience suggests that the presence of hiccups and gastroesophageal reflux in the same patient may be coincidental rather than having a cause-and-effect relationship.

Chronic Disease↗
PubMed1989

Sphincteric action of the diaphragm during a relaxed lower esophageal sphincter in humans.

We studied the effects of involuntary and voluntary contraction of the diaphragm on esophagogastric junction (EGJ) pressure during esophageal distension in healthy human volunteers. The EGJ pressure was monitored using a Dent sleeve device. Along with the pressure we concurrently monitored diaphragm electromyogram (EMG) using intra-esophageal bipolar electrodes that were placed on the nonpressure sensing surface of the sleeve device. Graded esophageal distensions were performed by graded inflations of a 2-cm-diameter balloon that was positioned 7 cm above the EGJ. The graded esophageal distensions caused a graded increase in the amplitude of lower esophageal sphincter (LES) relaxation (end-expiratory EGJ pressure). In a majority of the subjects, esophageal distension had no effect on spontaneous inspiratory EGJ pressure increase and diaphragm EMG. During sustained LES relaxation of greater than 70% induced by sustained esophageal distention, graded voluntary contractions of the diaphragm induced proportional increases in the EGJ pressure and diaphragm EMG. The EGJ pressure and diaphragm EMG were similar during diaphragmatic contraction both before and during esophageal distension. During a maximal and sustained diaphragm contraction, esophageal distension had no effect on the EGJ pressure. We conclude that there are two distinct sphincteric mechanisms at the EGJ, the LES and crural diaphragm, and they respond differently to distension of the distal esophagus.

Adult↗
PubMed1989

Segmental high amplitude peristaltic contractions in the distal esophagus.

High amplitude peristaltic contractions in the distal esophagus ("nutcracker esophagus") is the most common manometric disorder seen in patients with noncardiac chest pain. Although this abnormality is found in the distal esophagus, the definition regarding its precise level in the esophagus is unclear. A careful analysis of 99 consecutive manometric tracings performed during a 1-yr period revealed that in patients with noncardiac chest pain and/or dysphagia, the location of the abnormal esophageal contractions varied: 1) in 11 patients the esophageal contractions were abnormal at 2 cm, as well as 7 cm, above the lower esophageal sphincter (LES); 2) the abnormality was limited to the 2-cm location above the LES in six patients; and 3) was confined to the 7-cm location above the LES in five patients. If the conventional criteria of averaging the distal esophageal contraction amplitudes at 2 and 7 cm above the LES were adopted, six of the 11 patients with segmental esophageal contraction abnormality would not have been identified. We suggest that, by inspection of each location of the distal esophagus separately, localized high amplitude contractions can be identified, and the distal 2 cm segment of the esophagus should be routinely included in the manometric evaluation.

Adult↗
PubMed1988

Characteristics and frequency of transient relaxations of the lower esophageal sphincter in patients with reflux esophagitis.

Electromyogram of the submental muscles, esophageal manometry, and pH studies were simultaneously performed in an unselected group of 12 patients with subjective and objective evidence of gastroesophageal reflux (GER) disease to determine the frequency of transient relaxation of the lower esophageal sphincter (LES) and mechanisms of GER. Findings from these patients were compared with data from 10 asymptomatic healthy volunteers. Recordings were obtained for 1 h in the fasting state and 3 h after a standard 850-kcal meal. Transient relaxation of the LES was the only mechanism of acid reflux in normal subjects and accounted for 73.0% of the episodes of acid reflux in patients with GER disease. In both normal subjects and patients with GER, a large number of transient relaxations were associated at their onset with an attenuated submental EMG complex, a small pharyngeal contraction, and an esophageal contraction. The incidences of these associated events were similar in the two study populations. The frequency of transient relaxation of the LES in patients with GER was identical to that of controls. The frequency did not differ even in 9 patients with GER disease who had endoscopic esophagitis. Thirty-six percent of transient relaxations in the normal subjects were accompanied by pH evidence of reflux, but in the GER patients with endoscopic esophagitis 65% of the transient LES relaxations resulted in a reflux event. Acid reflux at the moment of deep inspiration was the second most common mechanism of GER in our patients. Four patients who demonstrated this mechanism had hiatal hernias and more severe esophagitis than the rest of the group. Our findings confirm that transient relaxation of the LES is the major mechanism of GER in patients with reflux esophagitis. However, the similar frequency of this relaxation in GER patients and in healthy asymptomatic subjects suggests that factors other than transient LES relaxation play an important role in the pathogenesis of GER disease.

Adult↗
PubMed1988

Electrical and mechanical activity in the human lower esophageal sphincter during diaphragmatic contraction.

To determine the effect of contraction of the diaphragm on the lower esophageal sphincter (LES) pressure, we studied eight healthy volunteers during spontaneous breathing, maximal inspiration, and graded inspiratory efforts against a closed airway (Muller's maneuver). Electrical activity of the crural diaphragm (DEMG) was recorded from bipolar esophageal electrodes, transdiaphragmatic pressure (Pdi) was calculated as the difference between gastric and esophageal pressures, and LES pressure was recorded using a sleeve device. During spontaneous breathing, phasic inspiratory DEMG was accompanied by phasic increases in Pdi and LES pressure. With maximal inspiration, DEMG increased 15-20-fold compared with spontaneous inspiration, and LES pressure rose from an end-expiratory pressure of 21 to 90 mmHg. Similar values were obtained during maximal Muller's maneuvers. LES pressure fell promptly when the diaphragm relaxed. Graded Muller's maneuver resulted in proportional increases in the Pdi, LES pressure, and DEMG. The LES pressure was always greater than Pdi and correlated with it in a linear fashion (P less than 0.001). We conclude that the contraction of the diaphragm exerts a sphincteric action at the LES, and that this effect is an important component of the antireflux barrier.

Atmospheric Pressure↗
PubMed1987

Do bile acids reflux into the esophagus? A study in normal subjects and patients with gastroesophageal reflux disease.

To determine if bile acids reflux into the esophagus in patients with gastroesophageal reflux disease and in normal subjects during physiological gastroesophageal reflux episodes, esophageal aspiration and pH monitoring were performed simultaneously in 16 patients with gastroesophageal reflux disease and 8 normal subjects. Esophageal samples were collected for 30 min in the fasting state and for 3 h (as hourly samples) after the ingestion of a test meal (egg salad sandwich, peaches, and milk). Bile acids were assayed by a standard enzymatic assay and also by a sensitive and specific assay, liquid secondary ion mass spectrometry. Bile acids were not detected by enzymatic assay in any of the fasting samples. In 6 of the 8 normal subjects and 15 of the 16 patients with gastroesophageal reflux disease, bile acid-like reactivity was detected by the enzymatic assay in postprandial samples. However, bile acid-like reactivity was also found by enzymatic assay in aliquots of the homogenized test meal in concentration similar to the highest concentrations detected in esophageal aspirates. Bile acids were not detected by the liquid secondary ion mass spectrometry method in any of the fasting or postprandial esophageal aspirates (limit of detection greater than 2 microM). However, this assay accurately identified samples to which exogenous bile acids were added as controls. Our results suggest that bile acids did not reflux into the esophagus of patients with gastroesophageal reflux disease whom we studied and caution must be exercised in the use of enzymatic assay for bile acids in postprandial gastrointestinal fluids, as the commonly used hydroxysteroid dehydrogenase assay is not specific for bile acids alone.

Adult↗
PubMed1987

Identification and mechanism of delayed esophageal acid clearance in subjects with hiatus hernia.

To determine if hiatus hernia (HH) contributes to the delayed clearance of acid from the esophagus in patients with gastroesophageal reflux (GER), we performed simultaneous esophageal pH recordings and radionuclide studies in three study populations: 12 GER patients with HH, 5 GER patients with no HH, and 8 subjects with HH but no GER symptoms. Acid clearance was measured at 5 cm. above the manometrically located lower esophageal sphincter (LES) after injecting a 15-ml. bolus of 0.1 N HCl at 15 cm. above the LES. The acid was labeled with 200 mu Ci of 99mTc-sulfur colloid. Acid clearance was also measured at 10 cm. above the LES after injection of a 15-ml. bolus of 0.1 N HCl at 20 cm. above the LES. Acid clearance at 5 cm. above the LES was faster in GER patients with no HH compared to GER patients with HH and asymptomatic HH subjects. Acid clearance was faster at 10 cm. than 5 cm. above the LES in all HH and non-HH subjects studied. In non-HH subjects, each swallow resulted in an increase in pH (a monophasic pH response) at 5 and 10 cm. above the LES. In symptomatic as well as asymptomatic HH subjects, swallows resulted in an initial fall followed by a rise in pH at 5 cm. above the LES (a biphasic pH response). Radionuclide studies showed reflux of the isotope-labeled acid into the esophagus followed by clearance (a biphasic response) accompanying swallows in 15 of the 20 HH subjects. Swallow-induced reflux was not detected by radionuclide scanning in non-HH subjects. Based on these observations, we conclude that during acid clearance a small amount of acid is trapped in the HH sac and refluxes into the esophagus during subsequent swallows when there is relaxation of the LES, and these repeated episodes of acid reflux from the HH account for the delayed acid clearance observed in GER patients with HH.

Adult↗
PubMed1987

Effect of the diaphragmatic contraction on lower oesophageal sphincter pressure in man.

The effect of diaphragmatic contraction and relaxation on the lower oesophageal sphincter (LOS) pressure was studied in 10 healthy volunteers. Pressures in the oesophagus, LOS, and stomach were measured in three phases. Phase I, end tidal expiration; phase II, subjects inspired to total lung capacity (TLC) and kept the airway open (sustained diaphragmatic contraction); and phase III, at TLC subjects relaxed against a closed glottis (diaphragm relaxed). The LOS pressure in phase II was significantly higher than in phase I, while in phase III it was significantly lower compared with phase I. There was a net increase in LOS pressure of 32 mmHg in phase II as compared to phase I. After phase II, as subjects moved into phase III, there was a sudden drop in the LOS pressure. The LOS pressure in phase II correlated with the transdiaphragmatic pressure in a linear fashion. These observations suggest that diaphragmatic contraction in man enhances the LOS pressure and this augmentation of sphincter tone may be a vital component of the antireflux mechanism.

Adult↗
PubMed1987

Characteristics of transient lower esophageal sphincter relaxation in humans.

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)

Adult↗
PubMed1986

Effects of morphine and naloxone on esophageal motility and gastric emptying in man.

We studied the effect of morphine and naloxone on lower esophageal sphincter pressure, esophageal contraction amplitude, and gastric emptying of solids and liquids in ten normal healthy subjects. Morphine sulfate in a dose of 8 mg intravenous bolus significantly decreased sphincter pressure with a maximum fall of 22.8% of the basal tone. Naloxone, 5 mg intravenous bolus, resulted in a 20% increase in the baseline pressure. There was no change in the esophageal contraction amplitude, duration, or frequency of peristalsis with either morphine or naloxone. Gastric emptying was measured using a dual-isotope technique to simultaneously assess the emptying rates of both solid and liquid meal components. Morphine, 8 mg intravenous bolus, led to a significant inhibition (P less than 0.05) of the gastric emptying of both solids (99mTc sulfur colloid-labeled chicken liver) and liquids (111In DTPA-labeled water). Naloxone, 5 mg intravenous bolus, accelerated the gastric emptying of both solid and liquid components, but this did not achieve statistical significance. These observations suggest that: morphine's inhibitory effect on gastric emptying and lower esophageal sphincter pressure may contribute to its potent emetic properties; the human lower esophageal sphincter and stomach may have opiate receptors and further investigations should be addressed to determining if endogenous opiates play a role in the modulation of sphincter pressure and gastric emptying in humans.

Adult↗
PubMed1986

Dysphagia aortica. Clinical, radiological, and manometric findings.

Three patients with dysphagia caused by compression of the distal esophagus by a tortuous nonaneurysmal atherosclerotic aorta are described. All three patients were elderly women; systemic hypertension and cardiomegaly were present in two patients. Barium studies of the esophagus showed displacement and compression of the distal esophagus by the thoracic aorta. Debilitating dysphagia was treated surgically in one patient. The other two patients had milder symptoms and were managed conservatively. Esophageal manometry in these three patients showed superimposed pulsations and elevated intraluminal pressure just proximal to the lower esophageal sphincter. To evaluate the significance of these manometric findings and their correlation with clinical symptoms, we reviewed manometric tracings in 47 normal subjects. Ten of these subjects had an elevation of baseline intraluminal esophageal pressure as a result of superimposed vascular pulsations. We conclude that compression of the distal esophagus by a tortuous atherosclerotic aorta in the appropriate setting can lead to clinically significant dysphagia and a manometric finding of vascular compression of the esophagus does not necessarily correlate symptomatic dysphagia.

Adult↗