Effect on body temperature in dogs of perfusion of cerebral ventricles with artificial CSF deficient in calcium or containing excess of sodium or calcium

Dhumal, V R; Gulati, O. D.

doi:10.1111/j.1476-5381.1973.tb08547.x

Cited by 7 publications

(1 citation statement)

References 6 publications

(11 reference statements)

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“…Intraventricular perfusion with calcium-free solution and sodium edetate (which chelates calcium) was associated with marked hypothermia. This result is apparently, contrary to what is reported by Myers & Veale (1971) and Myers & Yaksh (1971) for cats and monkeys and is the subject of another report (Dhumal & Gulati, 1973). During perfusion with calcium-free solution, the spontaneous release of noradrenaline was not affected, but GABA failed to release noradrenaline or have any effect on temperature.…”

Section: A Naesthetized Dogscontrasting

confidence: 86%

Analysis of the Effects on Body Temperature of Intracerebroventricular Injection in Anaesthetized Dogs of Gamma‐aminobutyric Acid

Dhumal

Gulati

Raghunath

et al. 1974

British J Pharmacology

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1 The cerebral ventricles of dogs under intravenous pentobarbitone sodium anaesthesia, were perfused with artificial cerebro-spinal fluid (CSF) at a rate of 0.4-0.5 ml/min from the ventricular to the aqueductal cannulae. The effluent was collected from the aqueductal cannula in 20 min samples. The animals' temperatures were recorded from the rectum.2 y-Aminobutyric acid (GABA) 0.1-5 mg when injected into the ventricles produced variable temperature effects. Doses of 0.1 and 0.5 mg always produced hyperthermia and 1 and 5 mg doses sometimes produced hyperthermia and sometimes hypothermia. 3 Intraventricular perfusion with 2-bromolysergic acid diethylamide (BOL) and hyoscine did not block hyperthermia. Tests on the rat isolated stomach strip or the guinea-pig isolated superfused ileum for the possible release, respectively, of 5-hydroxytryptamine or acetylcholine by GABA were negative. 4 When tested for the presence of prostaglandin E(PGE)-like substances on the isolated rat stomach strip, both the control effluent and the GABA effluent showed activity, the latter being much more potent. There was a temporal correlation between this effect and hyperthermia. Intraventricularly administered sodium salicylate converted the GABA-induced hyperthermia to hypothermia and blocked the release of PGE-like substances. 5Hypothermia induced by GABA alone or in the presence of sodium salicylate was associated with the release of noradrenaline into the effluent. 6 Intraventricular administration of GABA in reserpinized dogs produced hyperthermia and not hypothermia. Similar results were obtained with phentolamine perfusion in normal dogs. 7 Perfusion with calcium-free solution blocked both the noradrenaline-releasing and hypothermic actions of GABA. 8 It is concluded that hyperthermia associated with intraventricular injections of GABA is due to the release of PGE-like substance and hypothermia is due to the release of noradrenaline.

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Section: A Naesthetized Dogscontrasting

confidence: 86%