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(Stroke. 1996;27:1399-1404.)
© 1996 American Heart Association, Inc.

Articles

Impaired Autoregulation in an Experimental Model of Chronic Cerebral Hypoperfusion in Rats

Katsumi Irikura, MD; Seiji Morii, MD; Yoshio Miyasaka, MD; Masaru Yamada, MD; Kaichi Tokiwa, MD Kenzoh Yada, MD

the Department of Neurosurgery, Kitasato University School of Medicine, Kanagawa, Japan.

Background and Purpose To verify the hypothesis that impaired autoregulation may contribute to cerebral swelling or hemorrhage after a sudden recovery of perfusion pressure, we studied the chronic effects of cerebral hypoperfusion on the autoregulatory responses of the pial arterioles in situ.

Methods Eight to 12 weeks after a carotid-jugular fistula was created in rats, experiments were performed under -chloralose and urethane anesthesia. Regional cerebral blood flow (rCBF) was determined by the hydrogen clearance method, and carotid pressure was measured. Using a closed cranial window, we determined the autoregulatory responses of the arterioles (30 to 50 µm) to both hypertension induced by norepinephrine and sudden fistula closure at various mean arterial pressures (MAPs).

Results rCBF on the fistula side was reduced by 27%. Carotid pressure was significantly lower than normal but was immediately increased by fistula closure. The pial arterioles showed marked elongation and enlargement. During induced hypertension, the arterioles in the fistula group started to dilate at an MAP lower than that of the control group (130 versus 180 mm Hg, respectively). The arterioles constricted when the fistula was occluded at normal MAP. However, when the fistula was occluded at an MAP higher than 130 mm Hg, the vessels dilated.

Conclusions It was demonstrated that (1) chronic hypoperfusion induced impairment of the upper limit of autoregulation and (2) sudden fistula closure under hypertensive conditions caused vasodilation of the arterioles. These findings suggest that rapid restoration of perfusion pressure is possibly followed by a pressure breakthrough phenomenon in a chronically hypoperfused cerebrovasculature.

Editorial Comment

Raymond C. Koehler, PhD, Guest Editor

Department of Anesthesiology, and Critical Care Medicine, The Johns Hopkins University, Baltimore, Md

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