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Biomedical subjects

R K Goyal

Publications and source records attributed to R K Goyal.

At least 145 records · Page 8Linked to original sources
PubMed1989

Effect of cold temperature on membrane potential responses in opossum esophageal circular muscle.

The effects of cold temperature on resting membrane potential (RMP) and membrane potential responses to depolarizing electrical current and intramural nerve stimulation were examined in opossum esophageal circular smooth muscle. Intracellular recordings were made in smooth muscle strips obtained from 7 to 8 cm (proximal site) and 1 to 2 cm (distal site) above the lower esophageal sphincter. RMP was not affected by changes in temperature between 34 and 22 degrees C. Cooling caused progressive inhibition of the amplitude and a slight increase in the duration of the spike potential produced by depolarizing current. Cooling did not modify the threshold for spike potential generation but decreased the spike amplitude from 34.0 +/- 0.5 mV at 34 degrees C to 14.1 +/- 2.2 mV at 22 degrees C (P less than 0.01). Electrical field stimulation with single electrical pulses (1.0 ms) produced tetrodotoxin-sensitive biphasic membrane responses consisting of initial hyperpolarization, or an inhibitory junction potential followed by depolarization that increased in amplitude as temperature was decreased from 34 to 26 degrees C and then decreased in amplitude as temperature was further decreased. At both proximal and distal sites cooling from 34 to 22 degrees C caused more than a twofold increase in the duration of hyperpolarization and time to peak depolarization. However, the increase in the absolute time of the duration of hyperpolarization and the time to peak depolarization was significantly greater at the distal than proximal esophageal site. Cooling to 16 degrees C decreased RMP and nearly abolished the biphasic membrane potential response.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1989

Characteristics of vagal esophageal tension-sensitive afferent fibers in the opossum.

1. Single-unit vagal afferent activity was recorded from 35 fibers that demonstrated evoked response to distension in the smooth muscle portion of the esophagus in anesthetized opossums. 2. The conduction velocities, measured in 22 fibers, varied from 1.0 to 21.33 m/s. Eight fibers (36%) had conduction velocities in the range of C-fibers (less than 2.5 m/s), whereas 14 (64%) had velocities in the range of A delta-fibers (3.16-21.33 m/s). All fibers were spontaneously active with an average discharge rate of 7.3 +/- 1.0 imp/s (mean +/- SE; range, 1.2-23 imp/s). 3. Esophageal distension produced a reproducible increase in discharge rate that adapted slowly to sustained distension. The average threshold pressure of the endings was 10 mmHg. The saturation pressure was 70 mmHg with cumulative, stepwise distension and 56 mmHg with graded, discrete distensions, respectively. 4. The discharge rate at the saturation pressure was 46 +/- 7 imp/s with cumulative, stepwise distensions and was 59 +/- 4 imp/s with graded, discrete distensions. The difference in maximum discharge between these two modes of distension was not statistically significant (P greater than 0.05). 5. Esophageal peristaltic contraction was associated with bursts of spike discharge with an average rate of 53.6 +/- 4.7 imp/s. 6. Two types of fibers were identified based on their duration of spike discharge associated with peristaltic contraction. The short-activity fibers showed a short duration of response consisting of approximately 3 s of spike bursts in response to swallows. These short-activity fibers were not activated by either stretch or contraction of the longitudinal esophageal muscle. The long-activity fibers showed a long duration of response consisting of approximately 10 s of activity in response to swallows. These long-activity fibers could be activated by longitudinal muscle stretch or contraction. 7. It is concluded that esophageal tension-sensitive mechano-receptors associated with vagal afferents are activated by physiological peristalsis and are present "in series" with either circular or longitudinal muscle layers.

Afferent Pathways↗
PubMed1989

Serum nickle estimation in acute myocardial infarction.

Serum nickle was estimated by atomic absorption spectrometer in 20 healthy controls and in 25 cases of acute myocardial infarction at 12 hourly intervals upto 48 hours, after the onset of chest pain. The mean serum nickel was 0.27 micrograms/dl in healthy controls and 0.40,050,049 and 0.30 micrograms/dl in patients of acute myocardial infarction. The serum nickel values were significantly (P less than 0.001) raised upto 36 hours in acute myocardial infarction when compared with controls.

Adult↗
PubMed1988

Inhibitory effect of calcitonin gene-related peptide and calcitonin on opossum esophageal smooth muscle.

Calcitonin gene-related peptide (CGRP) is widely distributed in the gastrointestinal nerves, including those of the esophagus. The present investigation was undertaken to examine the effect and the mechanism of action of CGRP on the lower esophageal sphincter and esophageal contractions. This peptide caused dose-dependent relaxation of the lower esophageal sphincter. The D50 for inhibitory effect of intraarterial CGRP on the sphincter was 5.0 X 10(-13) mol/kg. Calcitonin gene-related peptide is 3000 times more potent than calcitonin. The effect of CGRP on the lower esophageal sphincter was partially antagonized by tetrodotoxin or black widow spider venom. The inhibitory effect of CGRP on the sphincter appears to be exerted at two levels: (a) at the sphincteric smooth muscle, and (b) at the noncholinergic, nonadrenergic inhibitory neurons. Calcitonin gene-related peptide also exerts a potent inhibitory effect on the peristaltic contraction of the esophageal body in response to swallowing and vagal efferent stimulation. Using immunohistochemical studies we also showed the presence of CGRP-immunoreactive neurons within the myenteric ganglia of the esophagus. These studies suggest that CGRP may play an important role as an inhibitory neurotransmitter in the esophagus.

Animals↗
PubMed1988

Identification, localization and classification of muscarinic receptor subtypes in the gut.

Muscarinic receptors in the gastrointestinal tract are present on enteric neurons, presynaptic and prejunctional axonal endings, intramural endocrine cells as well as directly on effector cells such as smooth muscle and glandular and epithelial cells. Neural M1 stimulatory receptors are present on myenteric and submucous neurons, while neural M2 inhibitory receptors are present on their axonal endings. Muscle M2 and glandular M2 receptors are stimulatory. Functional and ligand binding studies show that there is heterogeneity among different muscarinic receptors in the gastrointestinal tract. The neural M1 muscle M2 and glandular M2 receptors are distinct from each other, but presynaptic and prejunctional M2 receptors appear to be similar to muscle M2 receptors. The relationship of the gut muscarinic receptors to the structurally-defined muscarinic receptors in the brain is unclear. However, they appear to be different from cardiac M2 and brain M2 receptors.

Animals↗
PubMed1988

Localization of galanin immunoreactivity in the opossum esophagus.

Galanin-like immunoreactivity was studied at 7 levels of the opossum esophagus, lower esophageal sphincter (LES) and adjacent portion of the stomach by indirect immunofluorescence; it was restricted to nervous structures. The majority of myenteric and submucous neurons were galanin-positive and received positive axo-somatic terminations. They also sent out axons staining positively. Galanin-positive fibers and a few atypically located neurons formed a mucous plexus at the bases of mucous glands. Varicose galanin fibers innervated the muscularis mucosae, circular and longitudinal muscle layers, while thick fascicles traversed the muscularis mucosae and circular muscle, possibly interconnecting the myenteric, submucous and mucous plexuses. Galanin-positive fibers did not supply blood vessels. There was no obvious gradient of innervation density along the esophagus, but the sphincter appeared to be more densely innervated than the esophageal body. There was no galanin-positive input to striated muscle. In view of its widespread distribution, this neuropeptide may serve multiple functions in the esophagus.

Animals↗
PubMed1988

Esophageal responses to transient and sustained esophageal distension.

With the use of intraluminal manometry in alpha-chloralose-anesthetized opossums, distal esophageal and lower esophageal sphincter responses to prolonged midesophageal balloon distension were compared with those evoked by single transient distensions, vagal efferent stimulation, and swallowing. Balloon inflation caused sphincteric relaxation that recovered during small volume but persisted during large volume-prolonged distension. The esophageal body was either quiescent or exhibited nonperistaltic contractions during prolonged distension. Balloon deflation induced non-peristaltic esophageal and sphincteric contractions as well as further sphincter relaxation. Responses to prolonged large and small volume balloon distension resembled those evoked by high- and low-frequency vagal efferent stimulation, respectively. However, vagal-stimulated "on" contractions were not seen with balloon distension, and atropine did not modify excitatory responses occurring during or after prolonged distension. Although transient distension induced peristaltic esophageal contractions, the peristaltic velocity was faster than swallow-induced peristalsis. With transient distension, atropine prolonged the latency to contraction in the mid but not the distal smooth muscle segment and thus increased peristaltic velocity. These studies demonstrate that 1) esophageal distension evokes a wide spectrum of lower esophageal sphincter and esophageal body response, and 2) cholinergic neurons play a minimal role in distension-induced responses of the distal esophageal circular muscle below the distending balloon.

Animals↗
PubMed1988

BCG vaccination.

Explore the source record for details and available documents.

Adolescent↗
PubMed1987

Effect of galanin on the opossum lower esophageal sphincter.

The objective of this investigation was to examine the effect of galanin on the resting tone and neurally mediated relaxation of the lower esophageal sphincter (LES) in anesthetized opossums. Galanin caused a dose-dependent rise in the sphincter pressure when given either intra-arterially or intravenously. The D50 of intra-arterial galanin was 1.OX10(-11) mols/kg. The rise in the sphincter pressure caused by galanin was not modified by atropine, phentolamine, methysergide, pyrilamine or indomethacin. Furthermore, the contractile response of galanin on the LES was also not affected by tetrodotoxin. The fall in the sphincter pressure in response to vagal efferent stimulation, intramural stimulation or esophageal distension was antagonized by galanin. The results of these studies suggest that, 1) galanin causes sphincter contraction by its direct action on the smooth muscle, and 2) galanin suppresses LES relaxation. These studies suggest that galanin may be an important neuropeptide for the modulation of resting tone and LES relaxation.

Animals↗
PubMed1987

Atypical localization of myenteric neurons in the opossum lower esophageal sphincter.

This study investigated sphincter-body differences in neuronal density and morphometry between the esophageal sphincter and body with a view to determining whether previously reported differences are authentic. The anatomical limits of the opossum lower esophageal sphincter were correlated with its physiological behavior by manometric demarcation. Following this, peeled whole mounts and paraffin and cryosections were used to study the morphology and morphometry of the esophageal myenteric plexus. Thirty animals were used and seven quantitated. The plexus of the esophageal body was located as usual in a plane between the longitudinal and circular muscle, which coincided with the plane of cleavage when these muscle layers were peeled apart for studying the plexus in whole mounts. In contrast, the plexus was located in several planes in the lower esophageal sphincter, which had no cleavage plane. Therefore, peeling the sphincter removes neurons and yields falsely low counts, making peel preparations of this region unsuitable for neuronal quantitation. In paraffin sections, the neuron density in the esophageal body 7 cm above the sphincter was 6,353 +/- 850/cm2, but decreased significantly to 2,254 +/- 353/cm2 at the 1-cm segment. In the lower esophageal sphincter, the neuronal count increased again to 8,530 +/- 1,606/cm2. Flash-frozen cryosections, which produced neuronal morphology similar to the in vivo condition, showed that there was no difference in neuronal size between esophageal body and sphincter. These studies show that atypical myenteric plexus localization causes spuriously low neuronal counts reported in the lower esophageal sphincter and that reported neuronal size differences are technique-dependent.

Animals↗
PubMed1987

Effects of ranitidine on the enzyme cholinesterase and the rat anococcygeus muscle.

Ranitidine in lower doses, (100 ng and 1 microgram) accelerated the rate of reaction of the enzyme acetylcholinesterase with the substrate acetylthiocholine. However, in higher doses (10 micrograms and 100 micrograms) it inhibited the enzyme activity. In rat anococcygeus muscle preparation, the responses to acetylcholine were significantly inhibited in lower doses whereas in higher doses there was a dose-dependent potentiation of the responses to acetylcholine by ranitidine. The responses to carbachol were however, not affected by ranitidine in the same preparation. Our data suggest cholinomimetic as well as cholinolytic activity of ranitidine.

Acetylcholine↗
PubMed1987

Intracellular studies of electrical membrane properties of opossum esophageal circular smooth muscle.

It has been suggested that regional differences in membrane properties of circular esophageal smooth muscle play an important role in the mechanism of esophageal peristalsis. The purpose of this study was to examine both the passive and active membrane properties of circular smooth muscle at proximal and distal esophageal sites so as to delineate the role of myogenic properties in the intramural mechanism of peristalsis. Intracellular recordings were made in circular muscle strips taken from proximal (8 cm above the gastroesophageal junction) and distal (2 cm above the gastroesophageal junction) sites in 10 opossums using the partition method of Abe and Tomita. At both esophageal sites, determinations were made of resting membrane potentials, time constants, space constants, thresholds for action potentials, action potential amplitudes, rates of rise of action potentials, and action potential durations at half-amplitude. The values for these parameters at the proximal and distal sites, respectively, were as follows: mean resting membrane potential, 49.7 +/- 0.24 and 49.5 +/- 0.3 mV; length constant, 4.0 +/- 0.4 and 3.8 +/- 0.4 mm; time constant, 513 +/- 49 and 456 +/- 53 ms; threshold for action potentials, 9.3 +/- 0.4 and 8.8 +/- 0.3 mV; amplitude of action potentials, 36.0 +/- 5.2 and 35.3 +/- 1.7 mV; rate of rise of action potentials, 2.3 +/- 0.3 and 2.6 +/- 0.4 mV/ms; duration of action potentials at half-amplitude, 5.0 +/- 1.2 and 4.1 +/- 0.4 ms; and the conduction velocity for evoked potentials, 3.9 +/- 0.3 and 3.8 +/- 0.4 cm/s. Our studies show that there are no differences between proximal and distal esophageal sites in any of these determinations. These studies also show that regional differences in the electrical membrane properties of circular smooth muscle do not account for esophageal peristalsis.

Action Potentials↗
PubMed1987

Effect of tri-iodothyronine on cardiac responses to adrenergic-agonists in STZ-induced diabetic rats.

Diabetes can produce a state of hypothyroidism which is known to alter adrenoceptor activity in rat hearts. We studied the effect of six-week STZ-induced diabetes on responsiveness to adrenergic agonists and also determined if tri-iodothyronine (T3) treatment for 6 weeks could modify these responses. T3 treatment produced a marked tachycardia and a slight but significant decrease in serum glucose and serum lipids in diabetic rat. Methoxamine produced positive inotropic and positive chronotropic effects in untreated control left and right atria, respectively. These effects were significantly increased in untreated diabetic preparations. T3 treatment for 6 weeks in diabetic rats prevented this effect. Isoproterenol also produced a dose-dependent positive inotropic and positive chronotropic effect in untreated control left and right atria, respectively. These responses were attenuated in untreated diabetic preparations. T3 treatment by itself decreased the responsiveness to isoproterenol in control left atria and further decreased the responses to isoproterenol in diabetic left atria. Similarly, in diabetic right atria T3 treatment did not produce any alteration in the responses to isoproterenol. The results indicate that only some of the diabetes-induced alterations in adrenoceptor activity can be associated with hypothyroidism.

Animals↗