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Biomedical subjects

T Baum

Publications and source records attributed to T Baum.

At least 55 records · Page 3Linked to original sources
PubMed1980

Evidence for selective inhibition of sympathetic outflow by oxotremorine.

Unlike numerous centrally acting hypotensive substances which decrease blood pressure and sympathetic outflow, the muscarinic agonist oxotremorine failed to reduce heart rate in a prior study. In the present series of experiments oxotremorine decreased blood pressure and efferent renal nerve activity in anesthetized cats but, in contrast to clonidine, it did not inhibit cardiac sympathetic nerve activity or lower heart rate. Therefore, it is concluded that oxotremorine does not produce uniform sympathetic inhibition and that outflow is depressed selectively.

Animals↗
PubMed1979

Interaction of cardiopulmonary chemoreceptor (Bezold-Jarisch) and somatosympathetic reflexes.

Cardiopulmonary chemoreceptor (Bezold-Jarisch) and baroreceptor reflexes produce similar overall cardiovascular effects although central integrating mechanisms are not identical. In view of recent reports emphasizing the complexity of baroreceptor mechanisms, the influence of both reflexes on spontaneous sympathetic outflow as well as their interaction with the somatosympathetic reflex were compared in anesthetized cats. The chemoreflex and the baroreceptor reflex were activated by i.v. injection of veratrine and norepinephrine, respectively, and both inhibited spontaneous efferent sympathetic nerve traffic. Stimulation of somatic nerves produces a two-component reflex potential in sympathetic nerves. Activation of cardiopulmonary chemoreceptor and baroreceptor reflexes inhibited the amplitude of the initial (spinal) phase of this somasympathetic reflex slightly and greatly attenuated the secondary (supraspinal) component. These experiments demonstrate that the cardiopulmonary chemoreceptor and baroreceptor reflexes exert similar effects on the somatosympathetic reflex and that the former two reflexes may influence sympathetic mechanisms at spinal as well as supraspinal levels.

Animals↗
PubMed1978

Influence of a cholinergic agent, oxotremorine, on sympathetic reflexes.

Administration of cholinergic substances by various routes has been reported to produce marked cardiovascular effects. The present study examined the influence of a muscarinic agonist, oxotremorine, on aspects of sympathetic function. The compound reduced blood pressure and spontaneous sympathetic outflow in anesthetized cats after blockade of peripheral muscarinic receptors with methylatropine. Effects on potentials evoked in the splanchnic nerve by stimulation of an intercostal nerve, i.e., the somatosympathetic reflex, were also evaluated. Oxotremorine did not modify the initial or "spinal" component of the reflex but markedly reduced the amplitude and increased the latency of the secondary or "supraspinal" phase. Atropine antagonized the inhibitory response. Effects of oxotremorine differed importantly from those produced by baroreceptor and coronary chemoreceptor activation and administration of clonidine and methyldopa which also attenuated the amplitude of the supraspinal component but did not alter its latency. Consequently, oxotremorine depresses sympathetic function at loci within the brainstem and cord by mechanisms not identical with those mediating responses to these reflexes and drugs.

Animals↗
PubMed1977

Evidence for an inhibitory action of methyldopa on spinal sympathetic reflexes.

The antihypertensive activity of methyldopa is mediated primarily by effects on the central nervous system. A number of centrally acting hypotensive substances has recently been shown to depress spinal pathways and reflexes as well as inhibiting supraspinal areas. The present series of experiments evaluated the potential influence of methyldopa on spinal mechanisms. Stimulation of an intercostal nerve evoked a two-component response (early and late) in the splanchnic nerve of anesthetized cats. The "late" phase involves supraspinal neurons, whereas, the "early" component involves only spinal pathways. The i.v. administration of 100 mg/kg of methyldopa reduced systemic blood pressure and both components of the evoked potential progressively. These experiments indicate that methyldopa exerts an effect of spinal sympathetic mechanisms which may contribute to the antihypertensive response to the compound.

Animals↗
PubMed1977

Susceptibility of spontaneous sympathetic outflow and sympathetic reflexes to depression by clonidine.

The hypotensive activity of clonidine has been attributed to inhibition of sympathetic outflow. The present series of experiments examined the relative influence of clonidine on spontaneous outflow and various sympathetic reflexes in anesthetized cats. Clonidine resulted in dose-related decreases in the former. Increases in efferent sympathetic activity mediated by baroreceptors and supraspinally integrated potentials evoked in the splanchnic nerve by somatic nerve stimulation were inhibited to a lesser extent. Splanchnic potentials evoked by spinal cord stimulation in spinal animals were also diminished. In contrast, baroreceptor induced reflex decreases in sympathetic outflow were only minimally affected. These experiments indicate that clonidine can inhibit central sympathetic mechanisms at various levels including the spinal cord but that considerable differences exist in the susceptibility of sympathetic outflow and various reflexes to depression by the compound.

Action Potentials↗
PubMed1976

Studies on the centrally mediated hypotensive activity of guanabenz.

Prior studies demonstrated that guanabenz reduces systemic blood pressure by inhibiting central sympathetic outflow as well as by adrenergic neuron blockade. Potential mechanisms responsible for the reduction of efferent sympathetic activity were examined in the present series. Guanabenz failed to modify carotid sinus nerve activity in a perfused sinus preparation. It reduced sympathetic outflow, heart rate and blood pressure in debuffered cats indicating that its actions are not mediated primarily by baroreceptor mechanisms. alpha-Adrenergic blockade greatly attenuated the response suggesting that the central sympathoinhibitory effect of guanabenz results from alpha-adrenergic receptor activation. Only a high dose of the compound attenuated the increase in sympathetic nerve activity produced by stimulation of the posterior hypothalamus. These experiments lead to the overall conclusion that guanabenz acts primarily at sites which regulate the basal level of sympathetic outflow.

Adrenergic alpha-Antagonists↗
PubMed1976

Tricyclic antidepressants and cardiac conduction: changes in ventricular automaticity.

Ventricular dysrhythmias result from changes in the automaticity or the conduction properties of the specialized conduction system. Tricyclic antidepressants have been reported to cause ventricular dysrhythmias in humans and experimental animals. Consequently, it seemed to interest to determine whether these substances influence ventricular automaticity. Ventricular rhythm was produced in anesthetized dogs by blocking atrioventricular conduction. Low doses of imipramine, amitriptyline and nortriptyline resulted in small but significant increases in automaticity. Relatively high doses of these agents suppressed automaticity markedly. These changes could play a role in the development of dysrhythmias.

Amitriptyline↗
PubMed1975

Central and peripheral contribution to the antihypertensive action of indoramin.

Indoramin has been reported to reduce blood pressure in experimental animals and humans. The complex pharmacological profile of the compound suggests that it may also exert central actions. Effects on spontaneous sympathetic outflow and on sympathetic nerve and blood pressure responses to hypothalamic stimulation were examined in anesthetized cats in the present study. At a low dose (1 mg/kg) indoramin reduced blood pressure but did not significantly influence the level of efferent sympathetic nerve activity. A higher dose (5 mg/kg) lowered pressure further and inhibited activity in the splanchnic, cardiac and renal nerves indicating that reduced sympathetic outflow is a contributing factor to the hypotensive response at this dose. However, in contrast to other centrally acting antihypertensive agents, e.g., clonidine, indoramin did not inhibit the increase in sympathetic nerve activity produced by hypothalamic stimulation.

Animals↗
PubMed1975

Responses to exercise in experimental hypertension.

Exaggerated cardiovascular responses to stressful stimuli and behavioural hyperexcitability have been observed in spontaneously hypertensive rats (SHR). The present series of experiments examined blood pressure and heart rate responses of SHR and renal hypertensive rats (RHR) to a combined physical and mental stress in the form of treadmill exercise. SHRs exhibited only slight and selective hyper-responsiveness to exercise in regard to increases in heart rate, whereas, RHRs responded normally. The excessive sensitivity of "older" SHRs is related mainly to slightly lower resting heart rates.

Age Factors↗