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Biomedical subjects

W J Snape

Publications and source records attributed to W J Snape.

At least 91 records · Page 5Linked to original sources
PubMed1982

The role of opiate receptors and cholinergic neurons in the gastrocolonic response.

The aim of this study was to characterize the mechanism of the gastrocolonic response to eating in healthy human volunteers. A bipolar clip electrode recorded spike activity from the distal colon. A rapid increase in colonic spike activity occurred after eating a 1000-cal meal (16.1 +/- 2.8 spike potentials/10 min, p less than 0.001). The intravenous infusion of atropine inhibited the increase in postprandial colonic motility. Intragastric administration of procaine, a local anesthetic also inhibited the gastrocolonic response to eating. After sham feeding a modified 1000-cal meal, there was no increase in the gastrocolonic response. Morphine stimulated colonic spike activity (55.3 +/- 15.1 spike potentials/10 min, p less than 0.001). Naloxone (40 microgram/kg . h) completely inhibited morphine stimulation of the colon. Naloxone also inhibited the postprandial gastrocolonic response, but did not inhibit neostigmine stimulation of colonic motility. These data suggest: (1) the gastrocolonic response is mediated by afferent neural receptors in the gastroduodenal mucosa, (2) there is no cephalic phase in the gastrocolonic response to eating, and (3) efferent cholinergic neurons and opiate receptors are both necessary for the gastrocolonic response.

Adult↗
PubMed1981

Lower esophageal sphincter pressure as an index of gastroesophageal acid reflux.

The purpose of this study was to determine the relationship of lower esophageal sphincter (LES) pressure and the volume of acid placed into the stomach required to induce gastroesophageal reflux in man. LES pressure was recorded continuously and by station pull-through by three radially oriented catheters in both symptomatic and asymptomatic subjects during the graded infusions of 0.1 N HCl acid into the stomach. Symptomatic subjects had a mean LES pressure of 7.5 +/- 0.7 mm Hg and refluxed at a volume of 140.0 +/- 21.0 ml. Fifty-five percent of asymptomatic subjects refluxed at a mean volume of 380.0 +/- 24.7 ml, and had a mean LES pressure of 13.8 +/- 0.4 mm Hg. Asymptomatic nonrefluxers at a volume of 500 ml of 0.1 N HCl acid had a mean LES pressure of 18.9 +/- 1.1 mm Hg. The mean LES pressure and acid volumes showed statistical significance between the three groups (P less than 0.01). There was an excellent overall correlation between LES pressure and acid volume required to produce reflux in all subjects (r = 0.91, P less than 0.001). Following reflux, asymptomatic but not symptomatic subjects showed a significance increase in LES pressure. These studies suggest that: (1) LES pressure does provide an accurate index of the gastroesophageal antireflux mechanism, provided that acid volume is considered; and (2) asymptomatic subjects showing acid reflux have higher LES pressures, reflux at higher volumes, and develop an LES contractile response after the reflux episode.

Esophagogastric Junction↗
PubMed1981

Myoelectric properties of the cat ileocecal sphincter.

Myoelectric activity and intraluminal pressures were recorded simultaneously from the ileum, ileocecal sphincter (ICS), and proximal colon in chloralose-anesthetized cats. Slow-wave activity, seen at all areas, showed coupling of frequency in the distal ileum and ICS. ICS spike activity was both isolated and associated with ileal or colonic spike activity and correlated with phasic contractions (r = 0.86; P less than 0.01). Ileal distensions caused ICS relaxation and decreased spike activity 33.8% of the time. Colonic distensions caused contraction and increased spike activity 46.9% of the time. Migrating action-potential complexes (MAPC) induced by castor oil, ricinoleic acid, or cholecystokinin propagated to the ICS and through to the colon significantly more frequently than ileal non-MAPC (P less than 0.05). Both spike potential-dependent and spike potential-independent mechanisms were involved in ICS contraction. Bethanechol increased spike activity and phasic and tonic contractions. Phenylephrine, despite loss of spike activity in all leads, caused tonic contraction of the ICS. Isoproterenol caused loss of spike activity and decreased ICS pressure. Thus, ICS myoelectric activity appears to be important in determining sphincter function during neurohumoral and mechanical stimulation, with ICS contractions occurring through both a phasic spike-related mechanism and a tonic mechanism without spike activity.

Action Potentials↗
PubMed1981

Properties of the cat ileocecal sphincter muscle.

The purpose of this study was to determine the length-tension properties and the response to neurohumoral agents of the feline ileocecal sphincter (ICS) circular smooth muscle in vitro. The ICS muscle during stretch maintained a higher resting tension at lower degrees of stretch than did the adjacent ileum and colon. Sodium nitroprusside (10(-3) M) or calcium-free Krebs solution with EGTA (5.0 mM) reduced the resting tension of ICS muscle by 15.8 +/- 2.1 and 19.1 +/- 2.5%, respectively. The ICS response to KCl depolarization was lower (0.37 +/- 0.03 kg/cm2) than colonic muscle (0.55 +/- 0.06 kg/cm2) oe ileal muscle (0.51 +/- 0.04 kg/cm2) (P less than 0.05). However, in response to acetylcholine, ICS muscle tension was minimal (0.06 +/- 0.02 kg/cm2) was compared with the colon (0.49 +/- 0.05 kg/cm2) or ileum (0.53 +/- 0.05 kg/cm2) (P less than 0.01). The ICS muscle contracted in response to phenylephrine, whereas other muscles were inhibited. Secretin, gastrin, glucagon, and cholecystokinin failed to act on the ICS muscle while other muscles did respond. These studies suggest that ICS muscle differs from adjacent ileal and colonic circular muscle in that a) in response to stretch it develops a high resting tension that is relatively resistant to calcium withdrawal, and b) it also shows quantitative and qualitative differences in response to neurohumoral agents.

Acetylcholine↗
PubMed1981

Abnormal colonic motility in progressive systemic sclerosis.

Progressive systemic sclerosis alters smooth muscle function throughout the gastrointestinal tract. In 10 consecutive patients with the disease, colonic spike activity and contractile activity were measured after a 1000-kcal meal, intramuscular injection of neostigmine, or intravenous injection of metoclopramide. The 1000-kcal meal stimulated a significant increase in spike and contractile activity in normal subjects. Nine of the 10 patients had no increase in motility after eating. Neostigmine or metoclopramide stimulated colonic spike (p less than 0.01) and contractile (p less than 0.02) activity in normal subjects and stimulated colonic motility (p less than 0.01) in four of 10 patients with less severe systemic manifestations of the disease (Group 1). The drugs had no effect on patients with severe progressive systemic sclerosis (Group II). The patients with severe scleroderma had significant gastrointestinal roentgenographic abnormalities and severe cardiac, renal, or pulmonary dysfunction. Four of six Group II patients died from the disease; all four had marked smooth muscle atrophy in the colonic wall. These findings suggest that the gastrocolonic response is absent early in the disease process and that the smooth muscle atrophy occurring with progression of the disease may lead to a more severe colonic motor disturbance.

Adult↗
PubMed1981

Influence of papaverine on bethanechol or OP-CCK stimulation of feline colonic muscle.

Papaverine relaxes smooth muscle from various organ systems throughout the body. The purpose of this study was to determine the effects of papaverine on colonic smooth muscle from the transverse colon of the cat. Myoelectrical activity was recorded with monopolar glass pore electrodes. Papaverine was administered alone and simultaneously with bethanechol or the octapeptide of cholecystokinin. Higher concentrations of papaverine (10(-4) M, 10(-5) M) abolished both slow-wave activity and migrating spike bursts. Lower concentrations of papaverine (10(-6) M) had no effect on slow waves or the migrating spike burst. Bethanechol (10(-6) M) or OP-CCK (4 x 10(-9) M, 4 x 10(-10) M) stimulated spike activity (p < 0.001). Papaverine (10(-6) M had a minimal effect on the increase in spike activity that occurred after octapeptide of cholecystokinin in a concentration of 4 x 10(-10) M (p < 0.05). Papaverine had no effect on the stimulation of the colonic smooth muscle by 4 x 10(-10) M octapeptide of the colonic smooth muscle by 4 x 10(-9) M octapeptide of cholecystokinin. These studies show that (a) papaverine can inhibit smooth muscle myoelectrical activity, (b) papaverine is a potent inhibitor of cholinergic stimulation of colonic smooth muscle, but (c) papaverine has a minimal effect on octapeptide of cholecystokinin stimulation of the isolated colonic smooth muscle.

Animals↗
PubMed1981

Effect of bethanechol or vagal nerve stimulation on ileocecal sphincter pressure in the cat.

Ileocecal sphincter pressure was studied in the cat, using an open-tipped perfused catheter system. Ileocecal sphincter pressure was measured under basal conditions and in response to bethanechol or direct vagal nerve electrical stimulation. The pressure was 26.1 +/- 5.0 mmHg basally, and was unaltered by section of either or both cervical vagi (p less than 0.05). Peripheral cervical vagal stimulation gave a 9.1 +/- 1.1 mmHg increase in ileocecal sphincter pressure (p less than 0.05) but central stimulation had no effect on ileocecal sphincter pressure. The ileocecal sphincter response to peripheral vagal nerve stimulation was antagonized completely by propranolol or phentolamine. Bethanechol gave a dose-response increase in ileocecal sphincter pressure with a maximal response of 18.0 +/- 2.9 mmHg at 50.0 microgram/kg (p less than 0.01). The ileocecal sphincter relaxed with ileal distension and contracted with colonic distension. These studies indicate that (a) the ileocecal sphincter shows an excitatory response to vagal stimulation and cholinergic agonists; (b) basal ileocecal sphincter pressure is independent of the vagi; (c) ileocecal sphincter inhibition can be initiated by ileal distension but not by vagal stimulation.

Animals↗
PubMed1981

Provocation of esophageal pain by ergonovine or edrophonium.

Ten patients with anginal symptoms and ergonovine-induced chest pain without coronary artery spasm had esophageal manometry with provocative pharmacologic testing. Increased amplitude of esophageal contractions on baseline manometry (68.2 +/- 10.3 mmHg) was the only characteristic discriminating these patients from normals (40.9 +/- 6.3 mmHg) and from patients with esophageal motility disorders (39.6 +/- 7.5 mmHg). The administration of ergonovine or edrophonium provoked typical chest pain in association with high amplitude, long duration, and repetitive esophageal contractions in all 10 patients. Patients with esophageal motor disorders showed a similar, but less marked esophageal response with pain infrequently produced. Normals showed no response to ergonovine, and a minimal response to edrophonium, but without chest pain. Clinical features of patients with ergonovine-induced chest pain could not distinguish them from patients with coronary artery disease; esophageal symptoms were infrequent and mild. These studies suggest that certain patients with chest pain of esophageal origin may be identified only by provocative testing during esophageal manometry. However, these provocative drugs may also induce coronary artery spasm and should not be used during routine clinical manometry.

Adult↗
PubMed1980

Inhibition of postprandial colonic motility after ingestion of an amino acid mixture.

Previous studies suggested that the ingestion of a mixture of amino acids inhibited the fat-stimulated increase in colonic motility. This study determine the effect of the ingestion of an amino acid mixture on the postprandial distal colonic spike potential (SP) response to a standard 1000-calorie meal in normal subjects and in patients with the irritable bowel syndrome. The distal colonic response was measured following a standard meal with and without the preadministration of a protein hydrolysate solution. After the meal, normal subjects had their maximum response within the first 30-min postprandial period (41.0 +/- 6.3 SP/30 min). Spike activity returned to fasting activity by 60 min. Most patients with irritable bowel syndrome did not have a significant early postprandial distal colonic spike response (P > 0.05), but all patients had a large late increase in spike activity occurring 60-90 min postprandially (50.0 +/- 5.0 SP/30 min) (P < 0.001). Ingestion of the protein hydrolysate solution prior to the meal resulted in suppression of the early colonic spike response in normal subjects (P < 0.01) and the late colonic spike response in the irritable bowel patients (P < 0.01). This study suggests that amino acids can modulate postprandial colonic motility and that dietary alteration may be beneficial in the irritable bowel syndrome.

Amino Acids↗
PubMed1980

Abnormal gastrocolonic response in patients with ulcerative colitis.

The purpose of these studies is to determine the colonic myoelectrical and contractile response after eating a 1000 calorie meal in patients with active ulcerative colitis. During fasting, slow waves are identifiable significantly more in patients with ulcerative colitis than in normal subjects (p < 0 . 01). The predominant slow wave frequency is 6 . 1 +/- 0 . 2 cycles/min, which is similar to the normal subjects. The slow waves are not altered by eating in either group. Minimal spike or contractile activity occurs during the fasting period both in patients with ulcerative colitis and in normal subjects. In patients with ulcerative colitis, spike activity increases rapidly after eating the 1000 calorie meal (P < 0 . 01), but the maximal response is decreased and shorter in duration than in normal subjects. There is no simultaneous increase in colonic contractility above fasting levels after the meal in patients with ulcerative colitis. This is strikingly different from the simultaneous increase in contractile and spike activity (P < 0 . 01) that occurs after eating in normal subjects. These studies suggest that in ulcerative colitis (1) the colonic smooth muscle slow wave activity is intact; and (2) a disturbance in the normal colonic contractile response to eating is present despite an adequate spike response. This lack of colonic contractility may contribute to the increase in diarrhoea that occurs in these patients after eating.

Adult↗
PubMed1980

Effect of deoxycholic acid on colonic motility in the rabbit.

The purpose of the study was to determine the effect of the bile salt, deoxycholic acid, on colonic myoelectrical and contractile activity recorded from a loop of proximal colon in the anesthetized rabbit. Myoelectrical activity was recorded from bipolar electrodes attached to the serosal surface of the proximal colon. Contractile activity of the circular smooth muscle was measured with a strain gauge attached in the circular direction on the serosal surface of the colonic loop. The colonic slow wave frequency was 12.5 +/- 1.1 cycles/min. The slow wave frequency throughout the loop was homogeneous with a low coefficient of variation of the slow wave frequency (5.8 +/- 0.3). There were spike potentials superimposed on 78.1 +/- 3.4% of the slow waves. The addition of 8 or 16 mM deoxycholic acid did not change the slow wave or spike activity. However, deoxycholic acid stimulated a dose-dependent increase in migrating action potential complexes. These complexes were associated with a forceful contraction of the circular smooth muscle that propelled luminal contents in the direction of the burst. Deoxycholic acid also stimulated an increase in luminal fluid content.

Action Potentials↗
PubMed1980

Abnormal gastrocolic response in patients with intestinal pseudo-obstruction.

Gastrointestinal motility disturbances after endogenous stimuli have been demonstrated only in the esophagus and small intestine in patients with chronic idiopathic pseudo-obstruction. The 1,000-calorie meal stimulated a significant increase in spike and contractile activity in normal subjects. No increase in colonic spike or contractile activity occurred in patients with chronic idiopathic pseudo-obstruction even though colonic motility increased normally following the administration of neostigmine methylsulfate. These findings suggest that the normal response to eating is absent in patients with chronic idiopathic intestinal pseudo-obstruction even though their smooth muscle has been shown to be responsive to cholinergic stimulation. This loss of a gastrocolic response is further evidence for a disorder of the neurohumoral control mechanisms in patients with chronic idiopathic intestinal pseudo-obstruction.

Adult↗
PubMed1980

Colonic dysfunction in diabetes mellitus.

Colonic myoelectrical and motor activity were measured in 12 patients with diabetes mellitus. Diabetic patients with severe constipation were compared to diabetics with mild or no constipation. Gastric emptying and peripheral nerve conduction studies were performed in all patients. Normal subjects had a rapid increase in colonic spike and motor activity (P < 0.001) within the first 30-min postprandial period. Diabetic patients with mild constipation had a postprandial increase in colonic motility; however, the response was delayed to 60-90 min after eating. Diabetic patients with severe constipation had no postprandial increase in colonic motility. There was no correlation between colinic motility and gastric emptying of a liquid meal (r = 0.23) (P > 0.05) or peripheral nerve conduction (r = 0.36) (P > 0.05). Neostigmine (0.5 mg, intramuscularly) or metoclopramide (20 mg, intravenously) increased colonic spike (P < 0.005) and motor (P < 0.005) activity in all diabetic subjects regardless of their symptoms. These studies suggest that patients with diabetes mellitus and severe constipation may have an autonomic neuropathy which leads to an absent postprandial gastrocolonic response.

Action Potentials↗