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Biomedical subjects

R K Goyal

Publications and source records attributed to R K Goyal.

At least 235 records · Page 13Linked to original sources
PubMed1975

Effect of prostaglandin E2 on esophageal motility in man.

Studies were performed to investigate the effect of prostaglandin E2 on esophageal motility in 12 healthy volunteers. PGE2 infusion caused a dose-dependent reduction in the lower esophageal sphincter pressure. The threshold dose was less than 0.05 mug-kg-1-min-1 and maximal reduction of pressure (60%) occurred with a dose of 0.4 mug-kg-1-min-1. In contrast to its effect on the lower esophageal sphincter, PGE2 did not alter the pressure in the upper esophageal sphincter. PGE2 did not influence resting esophageal pressures; the amplitude of peristaltic contractions was reduced in the lower but not in the upper part of the body of the esophagus. These studies show that in man PGE2 exerts selective inhibitory influence on the activity of the lower part of the esophagus and lower esophageal sphincter which are composed of smooth muscle fibers.

Adult↗
PubMed1975

Nature of the vagal inhibitory innervation to the lower esophageal sphincter.

The purpose of the present study was to investigate the nature of the vagal inhibitory innervation to the lower esophageal sphincter in the anesthetized opossum. Sphincter relaxation with electrical stimulation of the vagus was not antagonized by atropine, propranolol, phentolamine, or by catechloamine depletion with reserpine. A combination of atropine and propranolol was also ineffective, suggesting that the vagal inhibitory influences may be mediated by the noncholinergic, nonadrenergic neurons. To determine whether a synaptic link with nicotinic transmission was present, we investigated the effect of hexamethonium on vagal-stimulated lower esophageal sphincter relaxation. Hexamethonium in doses that completely antagonized the sphincter relaxation in response to a ganglionic stimulant, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), did not block the sphincter relaxation in response to vagal stimulation at 10 pulses per second, and optimal frequency of stimulation. A combination of hexamethonium and catecholamine depletion was also ineffective, but hexamethonium plus atropine markedly antagonized sphincter relaxation (P less than 0.001). Moreover, 4-(m-chlorophenyl carbamoyloxy)-2-butyltrimethylammonium chloride (McN-A-343), a muscarinic ganglionic stimulant, also caused relaxation of the lower esophageal sphincter. We suggest from these results that: (a) pthe vagal inhibitory pathway to the sphincter consists of preganglionic fibers which synapse with postganglionic neurons: (b) the synaptic transmission is predominantly cholinergic and utilizes nicotinic as well as muscarinic receptors on the postganglionic neuron, and; (c) postganglionic neurons exert their influence on the sphincter by an unidentified inhibitory transmitter that is neither adrenergic nor cholinergic.

Animals↗
PubMed1975

Effect of nicotine on the lower esophageal sphincter. Studies on the mechanism of action.

Intravenous administration of nicotine sulfate caused a dose-dependent reduction in the lower exophagel sphincter pressure in anesthetized opossums. The maximal reduction in pressure of 85.0 +/- 2.6% was observed with a dose of 50 mug per kg. The effect of 50 mug per kg was not antagonized by bilateral cervical vagotomy, atropine, propranolol or by catecholamine depletion with reserpine. The sphincter relaxation produced by 50 mug per kg of nicotine was antagonized during tachyphylaxis produced by a larger dose (4 mg per kg) of nicotine. Nicotine tachyphylaxis also blocked the vagal-stimulated relaxation of the sphincter. It is suggested that the main action of nicotine on the sphincter in intact animals is caused by its effect on the noncholinergic, nonadrenergic inhibitory neurons which lie in the vagal pathway to the lower esophageal sphincter.

Animals↗
PubMed1975

Blood histamine levels and eosinophil, basophil counts in urticaria.

The blood histamine levels, basophil and eosinophil counts and the percentage of vacuolated eosinophils were observed in 30 controls and 15 patients of urticaria. There was a definite rise in eosinophil and basophil count during the acute stage of the disease which decreased in the quiescent or the symptom-free stage. The behavior of blood histamine level was similar. The mechanisms involved are discussed.

Adult↗
PubMed1974

Neural control of the lower esophageal sphincter: influence of the vagus nerves.

We performed studies in the opossum to define the influence of the vagi in the control of lower esophageal sphincter (LES) function. Bilateral vagotomy caused transient sphincter hypertension which was prevented by phentolamine and by atropine. Stimulation of the peripheral end of vagus, after bilateral cervical vagotomy, caused relaxation of the LES over a wide range of frequency and intensity of electrical stimulation. The relaxation was less marked at the lower frequencies of stimulation, and atropine treatment did not enhance this relaxation. In other experiments, atropine treatment reversed the rise in gastric (fundic) pressure with the vagal stimulation, but atropine did not enhance the degree of LES relaxation. Stimulation of the central end of the vagus caused an increase in LES pressure due to a centrally mediated reflex; the efferents for this motor response were not present in the vagi, as the reflex contraction persisted after bilateral vagotomy. The LES contraction with the stimulation of the vagal afferents was antagonized by phentolamine as well as by atropine. These studies suggest that: (a) the vagi do not mediate any cholinergic excitatory influences to the LES and the vagal influence of the sphincter is entirely inhibitory; (b) the vagi carry afferent fibres for a centrally mediated neural reflex which contracts the LES, but the efferent path of this reflex arc does not lie in the vagi.

Animals↗
PubMed1973

Mechanism of the lower esophageal sphincter relaxation. Action of prostaglandin E 1 and theophylline.

The intravenous injection of prostaglandin E(1) (PGE(1)) causes a dose-dependent relaxation of the lower esophageal sphincter (LES) in the intact, lightly anesthetized opossum. The action of PGE(1) is not inhibited by the drugs that produce muscarinic or nicotinic cholinergic antagonism or alpha and beta adrenergic antagonism in the doses that inhibited the action of respective agonists. Moreover, this action is not affected by exogenous gastrin pentapeptide. The action of PGE(1) on the LES is mimicked by isoproterenol, theophylline ethylenediamine, and dibutyryl cyclic AMP. Both theophylline, a phosphodiesterase inhibitor, and isoproterenol, an adenyl cyclase stimulator, added to the action of PGE(1). On the other hand, adenyl cyclase inhibitor nicotinic acid, as well as phosphodiesterase stimulator, imidazole inhibited its action. Further, both nicotinic acid and imidazole inhibited the degree of LES relaxation produced by esophageal distension. These studies suggest that intracellular cyclic AMP may act as the "second messenger" in the regulation of the lower esophageal sphincter relaxation.

Animals↗
PubMed1973

Mechanics of sphincter action. Studies on the lower esophageal sphincter.

The purpose of this study was to evaluate the mechanical factors involved in the genesis of lower esophageal sphincter pressure. We determined the relationship between intraluminal pressure and inside diameter, estimated the ratio between the wall thickness to inside radius, and calculated the tension in the wall of the lower esophageal sphincter as a function of the inside diameter. Various degrees of circumferential stretch were applied by introducing probes of different diameters in the rat lower esophageal sphincter in vivo. The intraluminal pressure produced by the lower esophageal sphincter around each probe was measured and pressure-diameter curves were constructed during (a) resting state, (b) contraction produced by electrical stimulation, and (c) relaxation produced by esophageal distension. The intraluminal pressure at an inside diameter of 0.5 mm was similar to that at inside diameter of 3.2 mm. This was true for the sphincter at rest as well as upon electrical stimulation. The pressure diameter curve, however, was sigmoid in shape; at first it showed a decline and then an increase followed by decline in pressure again with increasing diameters. The ratio of wall thickness to inside radius or the magnification factor varied with inside diameters as expected and this ratio increased steeply at small inside diameters. The tension diameter curves of the sphincter muscle showed that optimal tension development occurred not near sphincter closure but at a much wider diameter of 3.2 mm and that this muscle developed tension even at small luminal diameters. This behavior of the sphincter muscle ensures effective intraluminal pressure over a wide range of luminal diameters.

Animals↗