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Biomedical subjects

A van Bogaert

Publications and source records attributed to A van Bogaert.

7 recordsLinked to original sources
PubMed1979

Influence of some hypotensive drugs on the effects of hypothalamic stimulation.

Clonidine, L-alpha-methyldopa, propranolol as well as noradrenaline, when injected directly into the hypothalamic paraventricular (PV) nucleus area, enhance the activity of this center. Lidoflazine appears to be inactive. Since the electrical, chemical and pharmacological stimulation of the PV area elicits the same depressor cardiovascular reactions, a specific differentiation of this nucleus as a depressor center is proposed. The above-mentioned drugs, when introduced into the ventromedial nucleus area, enhance the pressor effects produced by stimulation of this nucleus. Thus, the hypothalamic depressor activity is not linked with an inhibition of the ventromedial pressor activity.

Animals↗
PubMed1978

Arterial and venous responses to hypothalamic stimulation in the dog.

Stimulation of the ventro-medial nucleus of the hypothalamus induces active constriction of both pre- and post-capillary vessels in the dog's hindlimb. Alpha-adrenolytic agents reduce these responses, indicating that they are mediated by the sympathetic nervous system. Stimulation of the paraventricular nucleus dilates both resistance and capacitance vessels. The present study demonstrates that hypothalamic neurones can control venomotor tone.

Animals↗
PubMed1977

New approach of the cardio-vascular depressive mechanism during lateral hypothalamic stimulation.

Paraventricular nucleus stimulation acts directly on the alpha- and beta-adrenoreceptors in heart and arterioles, eliciting arterial hypotension and cardiac chronotropism and inotropism decrease. Efferent pathways follow sympathetic nervous fibres through the medulla and the thoraco-lumbar ganglionic chain. The role of the alpha- and beta-adrenoreceptors in these depressive reactions is discussed.

Adrenergic alpha-Antagonists↗
PubMed1976

Absence of a prostaglandinic mediator in the lateral hypothalamic cardio-vascular inhibition.

The cardio-vascular inhibition elicited by electrical stimulation of the paraventricular nucleus in the lateral hypothalamus of anaesthesized and desafferentiated dogs is not linked with a mediator release like PGE. The effect of this biological agent is not registered in the isolated femoral artery of a receiver, after deviation by a cruised circulation of the arterial blood of a hypothalamic stimulated donor dog. Antipyretics, which are also prostaglandin-synthetase inhibitors, enhance the lateral hypothalamic reactions. As the thermoregulation centre is localized in the same region as the cardio-vascular inhibition centre and because lowering of temperature depends upon vasodilation and decrease in the general cellular metabolism, both functions of the paraventricular nucleus activity, a hypothesis is proposed that thermoregulation and cardio-vascular inhibition centres are a functional and anatomical unity.

Animals↗
PubMed1976

Characteristics of hypotension elicited by electrical stimulation of the lateralhypothalamusin anaesthetized dogs.

Electrical stimulation of the lateral hypothalamus near the paraventricular nucleus hypothalami, resulted in : hypotension, light bradycardia, decrease of the left ventricular systolic pressure without increase of the left ventricular end-diastolic pressure or left ventricular output, femoral vasodilatation and occasionally renal vasodilatation. The hypotensive reactions were potentiated by baroreceptor deafferentation. They were not blocked by anticholinergic, antihistaminic or antidopaminergic agents.

Animals↗
PubMed1975

Unusual mechanism of hypotensive activity exerted by erytrho-1-(1-[2-(1,4-benzodioxan-2-yl)-2-OH-ET-a1-4-piperidyl)-2-benzimidazolinone (R 28935).

In the dog, erythro-1-[2-(1,4benzodioxan-2-yl)-2-OH-ET]-4-piperidyl)-2-benzimidazolinone (R 28935) lowers the blood pressure for several hours at dosages of 80 mug/kg when injected intravenously, of 10 mug/kg when injected into the vertebral artery and of 1.25 mug/kg when injected suboccipitally. No alpha- or beta-receptor blocking activity can be elicited at these doses. The carotid occlusion reflex is markedly reduced by low doses of R 28935 (40 to 80 mug/kg i.v.), whereas the pressor response elicited by electrical stimulation of the hypothalamus remains unimpaired. The hypotensive effect of R 28935 is not antagonized by piperoxan, desmethylimipramine or nalorphine. This lowering of the blood pressure is associated with a decrease of the peripheral vascular resistance and with a slight tendency towards bradycardia. It is concluded that R 28935 is a potent blood pressure lowering drug, acting on the brain stem, presumably in the pontomedullary region--although the drug has no alpha-sympathomimetic activity.

Animals↗