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Biomedical subjects

R M Quock

Publications and source records attributed to R M Quock.

97 records · Page 6Linked to original sources
PubMed1974

Apomorphine: modification of its hyperthermic effect in rabbits by p-chlorophenylalanine.

The hyperthermic response of rabbits to apomorphine, a dopaminergic agonist, is abolished by prior treatment with p-chlorophenylalanine. If such 5-hydroxytryptamine (5-HT)-depleted animals are administered a peripherally acting decarboxylase inhibitor plus 5-hydroxytryptophan, central stores of 5-HT are regenerated and the hyperthermic response to apomorphine is restored in part. The effects of apomorphine in rabbits with elevated concentrations of 5-HT are not different from those in control animals. The behavioral effects of apomnorphine appear to be constant in all groups of animals tested. It is suggested that the hyperthermic effects of apomorphine in rabbits require the presence of 5-HT.

Animals↗
PubMedDate not supplied

Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides.

Previously it was demonstrated that nitrous oxide antinociception in the mouse abdominal constriction test is mediated by kappa-opioid receptors. Since nitrous oxide is thought to cause the neuronal release of endogenous opioid peptide to stimulate opioid receptors, this study was designed to identify the opioid peptides involved, especially in the spinal cord, by determining whether nitrous oxide antinociception can be differentially inhibited by intrathecally (i. t.) administered antisera to different opioid peptides. Male NIH Swiss mice were pretreated i.t. with rabbit antisera to opioid peptides then exposed 24 h later to one of three different concentrations of nitrous oxide in oxygen. Dose-response curves constructed from the data indicated that the antinociceptive effect of nitrous oxide was significantly antagonized by antisera to various dynorphins (DYNs) and methionine-enkephalin (ME), but not by antiserum to beta-endorphin (beta-EP). The AD(50) values for nitrous oxide antinociception were significantly elevated by antisera to DYNs and ME but not beta-EP. These findings of this study support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test involves the neuronal release of DYN and ME in the spinal cord.

Analgesics, Non-Narcotic↗
PubMedDate not supplied

Effect of subtype-selective opioid receptor blockers on nitrous oxide antinociception in rats.

Nitrous oxide antinociception in rats was evaluated by the warm water tail withdrawal test following central pretreatment with blockers of various opioid receptor subtypes. The analgesic dose, 50% (AD50) value for nitrous oxide antinociception was significantly elevated by MR-2266 (which is relatively selective for kappa-opioid receptors) and increased to a lesser degree by ICI-174,864 (which is selective for delta-opioid receptors). However, pretreatment with beta-funaltrexamine (which is selective for mu-opioid receptors), even at extremely high doses, was ineffective in altering the AD50 for nitrous oxide antinociception. According to these findings, nitrous oxide antinociception, as evaluated in this paradigm, appears to be mediated by kappa- and possibly delta- but not mu-opioid receptors.

Animals↗
PubMedDate not supplied

Modification of nitrous oxide analgesia by benzodiazepine receptors.

The interaction with nitrous oxide analgesia of drugs that act at the benzodiazepine receptor was evaluated in the rat tail flick model. Nitrous oxide produced dose-related analgesia, which was potentiated by diazepam, a benzodiazepine agonist, antagonized by noreleagnine, a benzodiazepine inverse agonist. Pretreatment with the benzodiazepine antagonist Ro 15-1788 blocked the effects of both diazepam and noreleagnine on nitrous oxide analgesia. Subanesthetic doses of sodium pentobarbital and chloral hydrate produced nonsignificant trends to reduce the analgesic action of nitrous oxide. These data provide evidence for the presence of specific benzodiazepine receptors capable of modulating the analgesic effect of nitrous oxide.

Animals↗
PubMedDate not supplied

Cardiovascular influences of nitrous oxide in spontaneously hypertensive rats.

Cardiovascularly compromised outpatients undergoing minor elective oral surgical or dental care have not frequently received the anxiolytic and analgesic benefits of nitrous oxide ostensibly because of the reported likelihood of sympathetic nervous stimulation and possible exacerbation of hypertension or cardiac complication. Recent studies, though, have shown that the hemodynamic effects of nitrous oxide are negligible and possibly even beneficial. The present study was conducted to determine the cardiovascular effects of nitrous oxide and nitrogen (as control gas) in the spontaneously hypertensive rat (SHR) and its normotensive Wistar-Kyoto counterpart (WKY). SHRs exposed to nitrogen did not exhibit any significant change in SBP or HR, but SHRs exposed to nitrous oxide exhibited a generally concentration-related reduction in both SBP and HR. WKYs, however, displayed reductions in SBP and HR when exposed to either nitrous oxide or nitrogen. These findings indicate a difference in the hemodynamic responses of SHRs and WKYs to nitrous oxide and nitrogen. The specificity and mechanism of the nitrous oxide effects in hypertension were not determined in this study, however, these findings do indicate that nitrous oxide does not exacerbate hypertension in normal or hypertensive rats.

Animals↗
PubMedDate not supplied

Combination effects of chloral hydrate and nitrous oxide/oxygen in the mouse staircase test.

The effects of chloral hydrate and/or nitrous oxide were assessed in the mouse staircase test. In this paradigm, the number of steps ascended is thought to reflect locomotor activity, whereas the number of rears is an index of anxiety. Chloral hydrate alone produced a dose-dependent decrease in the number of rears but no change in the number of steps ascended except at the highest dose. Nitrous oxide alone produced a concentration-related increase in the number of steps ascended but no change in rearing. When the two drugs were combined, nitrous oxide appeared to potentiate the rearing suppressant activity of chloral hydrate. Analysis of our experimental findings suggests that chloral hydrate exerts a specific anxiolytic drug effect that can be potentiated by concurrent treatment with nitrous oxide.

Animals↗