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At least 271 records · Page 15Linked to original sources
PubMed1964

PARTICIPATION OF AN UNUSUAL GANGLIONIC PATHWAY IN THE MEDIATION OF THE PRESSOR EFFECT OF PHYSOSTIGMINE IN THE RAT.

In spinal rats physostigmine failed to produce a pressor response even after treatment of the animals with hexamethonium, whereas noradrenaline, McN-A-343 (4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride) and AHR602 (3-acetoxy-1-benzyl-1-methylpyrrolidinium bromide) all produced large pressor effects. In rats anaesthetized with urethane, hexamethonium completely abolished the pressor effect of dimethylphenylpiperazinium but only partially blocked the pressor response to physostigmine; pressor effects of noradrenaline, McN-A-343 and AHR602 were potentiated. Combined treatment with hexamethonium and atropine and with hexamethonium and cocaine, however, completely abolished the pressor effect of physostigmine; simultaneously the pressor effects of McN-A-343 and AHR602 as well as of dimethylphenylpiperazinium were also blocked. P-286 (N-diethylaminoethyl-N-isopentyl-N'N'-di-isopropylurea) produced an early and a late block of the pressor effect of physostigmine; the initial block was due to an adrenergic blocking action while the late block was probably due to a dual action of the drug in abolishing the effects of both the nicotinic and non-nicotinic ganglion stimulants. Pressor responses to physostigmine, McN-A-343, AHR602 and dimethylphenylpiperazinium were abolished immediately after ganglion-blocking doses of nicotine. It is suggested that an unusual ganglionic pathway participates in the mediation of the pressor response to physostigmine in the rat, especially when the established ganglionic pathways are blocked.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1964

THERMOREGULATORY AND ADAPTIVE BEHAVIOR OF BROWN ADIPOSE TISSUE.

Brown adipose tissue has been shown to be a strongly thermogenic effector organ in homeothermic animals exposed to cold and in hibernators during cold-induced arousal from deep hibernation. Because of the anatomical distribution of brown fat and the utilization of vascular countercurrent heat exchange, this cold-induced thermogenic response protects the animal by contributing heat to the vital organs of the thorax, the cervical and thoracic segments of the spinal cord, and the sympathetic chain. Evidence indicates that control of thermogenic activity of brown fat is mediated by the sympathetic nervous system.

Acclimatization↗