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Biomedical subjects

M Weinstock

Publications and source records attributed to M Weinstock.

155 records · Page 9Linked to original sources
PubMedDate not supplied

The influence of cardiac cholinergic activation on the induction and maintenance of ventricular fibrillation.

The influence of cardiac cholinergic activation was studied in rats and cats on the induction and maintenance of ventricular fibrillation (VF). Acetylcholine (ACH 2-25 micrograms/kg), in doses which did not cause bradycardia or hypotension, induced appearance of spontaneous VF (duration 2-60 sec.) in 9/20 rats which have a high sympathetic autoregulation and in 3/6 cats only, 20-40 secs after the latter had been given adrenaline. ACh (10-45 micrograms/kg) and methacholine (10-40 micrograms/kg) also significantly prolonged the fibrillatory period induced electrically in cats and rats with and without atrial or ventricular pacing. The induction or prolongation of VF did not occur when higher doses of ACh (50-100 micrograms/kg) were given to rats. The influence of moderate amounts of cholinergic agents on the heart may be due to localised effects resulting in asynchronous activity. Alternatively, they may produce a discharge of multiple ectopic pacemakers or a disturbance in impulse conduction. Higher doses of ACh depress the S-A and ventricular ectopic activity node thereby decreasing the probability of inducing VF. It is concluded that under conditions of raised cardiac adrenergic activity, a moderate increase in cholinergic influence can both induce and prolong VF. The relevance of these findings to the "sudden infant death" syndrome is discussed.

Acetylcholine↗
PubMedDate not supplied

Antagonism by propranolol of the ganglion stimulant action of 5-hydroxytryptamine.

The effects of racemic propranolol and its constituent isomers were studied on ganglionic stimulation produced in situ by close arterial injection of 5-HT and DMPP to the superior cervical ganglion. Ganglion stimulation was recorded in terms of the resultant contraction of the nictitating membrane. d,l-Propranolol caused a biphasic antagonism of the ganglion stimulant effect of 5-HT. At low doses, 0.5-10 mug, the antagonism was surmountable by increasing the amount of 5-HT. The l-isomer (0.2-4 mug) but not d-propranolol also caused antagonism. At higher doses, 0.1-5 mg, both d,l- and d-propranolol caused a second type of blockade of 5-HT which was not surmountable and resembled that seen with procaine. The ganglion stimulant effects of DMPP and acetylcholine were only antagonised by the higher doses of d- and d,l-propranolol. d,l-Propranolol did not reduce the direct stimulation by 5-HT on the muscle of the nictitating membrane.

Acetylcholine↗
PubMedDate not supplied

Gender differences in sympathoadrenal activity in rats at rest and in response to footshock stress.

A comparison was made of the dynamics of sympathoadrenal activity in 11 age-matched male and female rats, under basal conditions and after exposure to footshock. Rats were prepared with indwelling catheters in the tail artery 24 h before the experiment. Measurements were made of plasma corticosterone (COR), norepinephrine (NE), epinephrine (EPI), dihydroxyphenylalanine (DOPA), dihydroxyphenylglycol (DHPG) and dihydroxyphenylacetic acid (DOPAC) under resting conditions, after transfer to the shock box (novelty) and at various times after footshock. Under basal conditions, males have significantly higher blood pressure and plasma DHPG/NE ratios but lower plasma levels of COR, NE and DOPAC than females. Three min after exposure to the shock chamber (novelty stress) there were significant increases in COR, EPI, NE and DHPG in both sexes, while DOPA increased only in females and DOPAC remained unchanged in both sexes. Footshock produced a further increase in EPI, NE and DOPAC within 2 min, which lasted about 15 min. There were significant sex differences in the extent and duration of the response of COR, EPI and DHPG. The data show that the female sympathoadrenal system is more reactive than that of the male to the stresses of a novel environment and footshock. The smaller DHPG/NE ratios in females at rest and after stress suggest that neuronal uptake of NE is lower in females than in males. The finding that stress produces larger increments of plasma DOPA and DOPAC in female rats indicates that tyrosine hydroxylase in the sympathetic nerve terminals and adrenal medulla may also be higher than in males.

Adrenal Glands↗
PubMedDate not supplied

The effects of the acetylcholinesterase inhibitor ENA713 and the M1 agonist AF150(S) on apolipoprotein E deficient mice.

Apolipoprotein E (apoE)-deficient and control mice were treated chronically with either the acetylcholinesterase (AChE) inhibitor ENA713, or the M1 muscarinic agonist AF150(S). Both treatments reversed the spatial working memory impairment of apoE-deficient mice but they differed in their effects on the levels of brain AChE activity. AF150(S) enhanced the brain AChE activity of apoE-deficient mice and rendered it similar to that of the untreated controls, whereas ENA713 reduced the brain AChE activity of control mice but had no effect on that of apoE-deficient mice. These findings suggest that AChE inhibition and M1 muscarinic activation have similar beneficial cognitive effects on apoE-deficient mice, but that the cellular and molecular mechanisms underlying these effects differ.

Animals↗
PubMedDate not supplied

An analysis of the respiratory stimulant effect of physostigmine and neostigmine in the conscious rabbit.

1. The effects of physostigmine and neostigmine, given by continuous intravenous infusion, were studied on respiration in conscious rabbits. 2. Physostigmine (5 mg/kg per min) significantly increased respiration rate, decreased arterial PaCO2 from 25.4 +/- 0.9 to 19.8 +/- 1.5 mmHg, increased PaO2 from 100.3 +/- 1.9 to 108 +/- 3.0 and pH from 7.42 +/- 0.01 to 7.46 +/- 0.01 within 30 min of its infusion. 3. Neostigmine (2.5 mg/kg per min) also decreased PaCO2 and increased PaO2 significantly, but caused a concomitant lactic acidosis, which was associated with the increased muscular activity and fasciculations. 4. The respiratory stimulant effect of neostigmine, but not that of physostigmine, was abolished by hexamethonium 2 X (1.5 mg/kg). Atropine methyl nitrate (1 mg/kg) failed to influence the respiratory stimulant effect of physostigmine, but hyoscine (10 mg/kg) blocked it completely. 5. It is suggested that augmentation of respiratory activity by neostigmine is mediated via peripheral nicotinic receptors in the carotid and aortic bodies. This may occur either through the accumulation of acetylcholine or H+ ions from raised blood lactic acid. 6. It is further suggested that physostigmine stimulates respiration by raising the concentration of acetylcholine in the central nervous system which, in turn, activates muscarinic receptors.

Animals↗
PubMedDate not supplied

Relative contributions of vagal and cardiac sympathetic nerves to the reflex bradycardia induced by a pressor stimulus in the conscious rabbit: comparison of 'steady state' and 'ramp' methods.

The bradycardic response to a pressor stimulus, phenylephrine, was studied simultaneously in conscious rabbits by two different methods. The 'steady state' method, in which bradycardia was measured at the peak of each pressor stimulus, demonstrated the existence of two groups of animals, in which the maximal heart periods were 867 (s.e.m. = 49) and 563 (s.e.m. = 34) ms and the slopes of the MAP-HP relationship were 24.6 (s.e.m. = 1.6) and 8.1 (s.e.m. = 0.7) ms/mmHg, respectively. The difference in baroreflex sensitivity in the two groups was abolished by sympathetic nerve blockade with guanethidine (10 mg/kg) but not by vagal blockade. The 'ramp method' which measures bradycardia during the rapid phase of MAP rise after phenylephrine did not detect any difference in response of the two groups of rabbits. Guanethidine did not alter the slope of the MAP-HP relationship in either group of rabbits when this was assessed by the 'ramp' method. These findings demonstrate that the 'steady state' method can detect changes in both vagal and sympathetic activity, while the 'ramp' method measures only vagally induced bradycardia. It is concluded that some rabbits may have a genetic ability to activate baroreflex pathways mediating cardiac sympathetic inhibition in addition to vagal stimulation in response to a pressor stimulus.

Animals↗