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KMID : 0390119940340020215
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Journal of Pusan Medical College
1994 Volume.34 No. 2 p.215 ~ p.228
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A Study on the Impairement of Cerebral Autoregulation following Experimental Subarachnoid Hemorrhage in the Rat
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Abstract
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As a homeostatic mechanism, cerebral arterial system autoregulates effectively via vasodilation during acute hypotension and via vasoconstriction during transient hypertension.
In the present study, it was aimed to investigate the alterations in cerebral autoregulatory response in the rats subjected to the experimental subarachnoid hemorrhage (SAH) by intracisternal injectio of autologous whole blood. Changes in pial
arterial
diameters were monitored by using a system of stereoscope-CCD camera-width analyzer-analog output through the cranial window installed on the parietal bone.
1. Mean arterial blood pressure was 104.5±5.5mmHg in the contrl and 96.3±8.2 and 98.4±4.3 mmHg in the 2-day and 4-day groups of SAH rats, respectively.
2. The autoregulatory vasodilation and vasoconstriction phases of the rat pial arteries in response to hypotension (during bleeding) and its reverse (during infusion) were normally observed in the control and SAH( 2-day) rats. However, they were
ablished in the SAH (4-day) rats.
3. Upon suffusion of the mock cerebrospinal fluid containing capsaicin (3×10-7M) on the cerebral surface, the pial arteries of SAH(4-day) rats showed only a transient vasoconstriction, whereas those of control rats exerted a large vasodilation.
4. The basal pial arterial diameter was slightly increased in response to acetlycholine (10-10-7M) in the control rats, but it was enhaned up to 40-50% by 10-9-10-7 M) of acetylcholine in the SAH (4-day) group.
5. The vasodilator responses to calcitonin gene-related peptide (CGRP: 10-10-10-7 M) of the pial artery which was normally observed in the control rats were abolished in the SAH(4-day) group.
6. The weak vasodialtor responses to substance P(10-10-10-7 M) of the pial arteries were markedly enhanced in the SAH(4-day) group.
Based on these results. it is suggested that the impairement of cerebral autoregulatory responses of the pail arteries in the SAH group is, in part, related with the decreased release of CGRP and uncoupling of signal transduction in the
vasodilation
mechanism of CGRP.
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