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At least 253 records · Page 14Linked to original sources
PubMed1976

An assessment of the cardiovascular sympathectomy induced by guanethidine.

Guanethidine treatment of rate (30 mg kg(-1), i.p. daily for 6 weeks) produced a profound reduction in the catecholamine present (as indicated by fluorescence histochemistry and catecholamine determinations) in tissues taken from the cardiovascular system, but there was evidence of the return of catecholamines within 8 weeks. While these changes are consistent with a sympathectomy, the unaltered pressor responses to physostigmine (100 mug kg(-1), i.v.) and to carotid occlusion indicate an unimpaired functional capacity of noradrenergic nerves supplying the cardiovascular system. Although part of the response may be attributed to the unaffected adrenal medulla enhanced by the presence of considerable supersensitivity as shown to exogenous noradrenaline, there would appear to be a dissociation between the results obtained from physical and functional tests of the sympathectomy induced by guanethidine.

Animals↗
PubMed1976

A comparison of the effects of morphine and pethidine upon body temperature and the reversal of reserpine's effects upon body temperature in the mouse.

The effects of morphine and pethidine upon body temperature and upon the reversal of reserpine hypothermia in the mouse were investigated. Both morphine and pethidine produced a dose-dependent fall in body temperature, that of morphine being totally antagonized by nalorphine and partially by naloxone, while that of pethidine was antagonised by naloxone and enhanced by nalorphine. Both drugs reversed reserpine-induced hypothermia. The reversal by morphine, but not by pethidine, was partially antagonized by naloxone. Adrenalectomy prevented the reversal of reserpine hypothermia by pethidine but morphine produced a partial reversal. Ganglion blockade and alpha-and beta-blockade all prevented reversal of reserpine hypothermia by both drugs. The results are discussed with regard to differences between pethidine and morphine and possible involvement of opiate receptors.

Adrenalectomy↗
PubMed1985

The interaction of cimetidine with various antihypertensive agents in the spontaneously hypertensive rat.

The H2-receptor antagonist cimetidine (250 micrograms) administered intracerebroventricularly (i.c.v.) 15 and 30 min before clonidine (25 micrograms kg-1 i.v.), significantly antagonized clonidine-induced hypotension in anaesthetized spontaneously hypertensive rats. The hypertensive response of cimetidine was correlated with the inhibition of clonidine-induced hypotension. In addition, cimetidine (250 micrograms i.c.v.) counteracted the hypotensive effects of pentolinium (5.0 mg kg-1 i.v.), guanethidine (5.0 mg kg-1 i.v.) and minoxidil (1.0 mg kg-1 i.v.) These data do not support previous suggestions that the hypotensive action of clonidine is caused by stimulation of the H2-receptor, but suggest that central administration of cimetidine causes peripheral vasoconstriction and this may offer resistance to the hypotensive action of different antihypertensive agents.

Animals↗
PubMed1966

The inhibitory innervation of the taenia of the guinea-pig caecum.

1. The inhibitory innervation of the taenia of the guinea-pig caecum has been studied, after blocking the responses to stimulation of excitatory cholinergic nerves with atropine.2. Stimulation of the perivascular nerves supplying the taenia caused relaxations. These nerves had properties which were typical of sympathetic post-ganglionic adrenergic nerves. The relaxations caused by stimulation were maximal at frequencies of stimulation above 30 pulses/sec and they were abolished by bretylium, guanethidine and 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP).3. The taenia is also innervated by intramural inhibitory nerves with their cell bodies in Auerbach's plexus. These nerves can be excited by electrical stimulation of the taenia or by the application of ganglion-stimulating drugs.4. The intramural inhibitory nerves have different properties from sympathetic adrenergic nerves. Relaxations in response to stimulation were maximal with frequencies of stimulation of about 5 pulses/sec and they were not blocked by bretylium, guanethidine or DMPP.5. Preganglionic cholinergic fibres in the caecal wall make synaptic connexions with the intramural inhibitory neurones.6. The role of the intramural inhibitory neurones in intestinal activity and their possible connexions with the central nervous system have been discussed.

Anesthetics, Local↗
PubMed1972

Some properties of the presynaptic nerve terminals in a mammalian sympathetic ganglion.

1. Superior cervical ganglia of adult rats were excised and maintained in vitro in stable conditions. Potentials were recorded with external electrodes. After transmission was blocked by mecamylamine, a small potential change was recorded from the rostral area of the ganglion in response to preganglionic stimulation.2. This electrical response was identified as the presynaptic action potential recorded from the nerve terminals by a number of criteria based on histological and physiological considerations including the disappearance of the spike in a glucose free solution. As shown by Nicolescu, Dolivo, Rouiller & Foroglou-Kerameus (1966) on the same preparation this condition causes an irreversible and selective lesion of the presynaptic nerve endings.3. A suitable concentration of mecamylamine permitted the presynaptic response and the excitatory post-synaptic potential (EPSP) to be recorded simultaneously. As the stimulus was increased, the EPSP increased linearly with the amplitude of the presynaptic response.4. After replacement of potassium ions in the bathing solution by caesium and during the early phase of post-tetanic facilitation there was an increase in the presynaptic response accompanied by a disproportionate increase in the EPSP.5. No changes in the presynaptic response were found in the presence of the following drugs, all of which depressed the EPSP: acetylcholine, hemicholinium, curare, further doses of ganglion-blocking agents, and high Mg(2+) and low Ca(2+) concentrations.6. Ouabain (4.5 x 10(-4)M) reversibly decreased the amplitude of the presynaptic response and increased the spontaneous release of transmitter. The EPSP was at first enhanced and then depressed.

Acetylcholine↗
PubMed1974

Drinking and antidiuresis elicited by isoprenaline in the dog.

1. Isoprenaline hydrochloride injected subcutaneously or infused intravenously caused drinking and simultaneous antidiuresis in the dog. The minimal effective dose was between 20 and 50 mug per dog.2. Isoprenaline-induced drinking was prevented by the beta-adrenergic antagonist propranolol and enhanced by the alpha-antagonist phentolamine.3. Ganglionic blockade with pentolinium or with hexamethonium did not interfere with the response.4. A delay of 1 hr after injection of 100 mug isoprenaline, before drinking was permitted, did not significantly reduce the amount of water subsequently drunk. A preload of water approximately equal to the volume of water normally drunk caused a greater reduction in water intake in some dogs.5. Isoprenaline caused an increase in heart rate and pulse pressure which lasted for between 1 and 3 hr according to dose. Central venous pressure fell, but mean arterial pressure was little altered. Haemodynamic changes preceded drinking by about 5 min.6. Infusion of isoprenaline caused drinking in the bilaterally nephrectomized dog.7. We conclude that isoprenaline is a potent stimulus to drinking in the dog and that the effect is not exclusively mediated by the renin-angiotensin system.

Animals↗
PubMed1983

Cyclic changes of plasma pancreatic polypeptide and pancreatic secretion in fasting dogs.

Fasting conscious dogs, each with a gastric fistula, Heidenhain pouch and Thomas duodenal fistula, were used. Basal pancreatic secretion showed periodic increases in phase with the periodic contraction of the stomach and duodenum. Periodic increases of plasma pancreatic polypeptide (PP), but not of gastrin, were observed in phase with the periodic contraction and secretion of the gut. Ganglion blockade abolished the cyclical activity, both secretory and motor, of the gut and of plasma PP. Intraduodenal infusion of lidocaine suppressed the spontaneous increase of pancreatic secretion and plasma PP. It is concluded both that the cyclical release of PP and the increase in pancreatic secretion are under the control of the intrinsic nerves of the duodenum.

Animals↗