Literature DB >> 1251740

Sympathetic control of cerebral blood flow in acute arterial hypertension.

A Bill, J Linder.   

Abstract

The cervical sympathetic chain on one side was stimulated electrically at 10-20 Hz and an acute rise in arterial blood pressure was produced by: intravenous injection of angiotensin, ligation of the thoracic aorta, or ligation of the aorta combined with injection of metaraminol. The blood flow through the cerebrum and the cerebellum was determined by using labelled microspheres. At high blood pressures there was multifocal breakdown of the blood-brain barrier in the cerebrum as indicated by leakage of Evans blue. The breakdown was restricted to the control side or much more marked on that side than on the stimulated side. Sympathetic stimulation prevented also breakdown of the blood-aqueous barrier. The blood flow through the cerebrum on the control side was higher than that on the stimulated side in all experiments. Regions with breakdown of the blood-brain barrier had flow rates which were about 10 times normal values. Cerebellar blood flow was less affected by the hypertension and did not react significantly to sympathetic stimulation. The results indicate that stimulation of the sympathetic nerves to the brain tends to prevent forced dilatation of the arterioles with a resulting regional overperfusion with blood and breakdown of the blood-brain barrier. It is concluded that one role of the sympathetic nerves supplying the brain is to extend the pressure region with autoregulation in its upper part under conditions of a general increase in sympathetic vasomotor activity.

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Year:  1976        PMID: 1251740     DOI: 10.1111/j.1748-1716.1976.tb10176.x

Source DB:  PubMed          Journal:  Acta Physiol Scand        ISSN: 0001-6772


  36 in total

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3.  The pathophysiology of the blood-brain barrier dysfunction induced by severe hypercapnia and by epileptic brain activity.

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Review 8.  The adaptation of the cerebral circulation to pregnancy: mechanisms and consequences.

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9.  Effect of an anion transport inhibitor on blood-brain barrier lesions during acute hypertension. Possible prevention of transendothelial vesicular transport.

Authors:  J E Hardebo; B B Johansson
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