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A De Wilde

Publications and source records attributed to A De Wilde.

10 recordsLinked to original sources
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

Vascular and noradrenalic reactions in the musculocutaneous bed during hypothalamic stimulation.

When electrical stimulation is applied to the ventromedial hypothalamic zone one observes an increase in systemic blood pressure. There also occur blood pressure variations in the isolated femoral circuit: two distinct phenomena were observed. The early event, being either an increase or a decrease in peripheral resistance, is directly related to the amount of noradrenaline produced locally. The late event is due to catecholamines arriving from the general circulation. Inhibition of local catecholamine release through the baroreceptor reflex and inhibition of ganglionic transmission by a large and sudden increase in adrenaline blood levels do influence the response in the isolated femoral circuit. Moreover the peripheral vasomotor tonus seems to be influenced by yet another mechanism, independent of local catecholamine release. This delicate mechanism depends on the balance between the degree of excitation of hypothalamic pressor (medial) and depressor (lateral) zones.

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↗