SUMMARY Thirty-one cats were divided by age into 3 groups, young (Y), middle (M) and old (O). Continuous recordings of local cerebral blood volume (CBV) and frequent measurements of mean transit time of blood (I) were made from the Sylvian opercula after ischemia was produced by transorbital clipping of the middle cerebral artery at its origin (MCA occlusion). Control recordings were made simultaneously from the corresponding area of the contralateral cerebral hemisphere.MCA occlusion temporarily stopped cerebral blood flow (CBF) in the area supplied by the ipsilateral MCA, as indicated by a rapidly decreasing CBV and complete disappearance of hemodilution curves. Within 30 sec, CBF resumed with a dilatation of the vascular bed and reappearance of hemodilution curves through newly developed collateral channels. Despite a low CBF, below half the control, CBV recovered, overshooting the control level. The appearance of hyperemia In the iscbemic area was statistically significant. Such "low perfusion hyperemia" was slower in appearance and of more diverse magnitude in group O than in group Y. This suggested that aging may lead to a decrease in rapidity of the vascular response to ischemia and impair the integrity of collateral vessels.

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SUMMARY The steal phenomenon due to a vasodilator was investigated in 6 cats in which cerebral ischemia had been produced by left middle cerebral artery (MCA) occlusion. The photoelectric method was employed for continuous recording of the cerebral blood volume together with frequent determinations of the cerebral blood flow (CBF) through the ischemic cerebral tissue at the following four stages: 1) before MCA occlusion, 2) 2 hours after MCA occlusion before the injection of papaverine, 3) after the injection of papaverine, and 4) when the systemic arterial blood pressure (SABP) was adjusted non-pharmacologically to the control level using a "vasculator". The administration of the vasodilator produced conflicting results for the CBF changes in the ischemic area with a decrease in SABP as reported previously in the literature. However, when the SABP was corrected to the control level, the CBF in the ischemic region became increased in all 6 cases to above the control ischemic flow values.It is concluded that the decreased CBF in the ischemic tissue after vasodilator administration was not due to the steal phenomenon, but simply to a fall in SABP. Stroke Vol 16, No I, 1985 CEREBRAL VASODILATING AGENTS have not been recommended for use in the therapy of patients with acute stroke.'" 3 However, the pioneer opinion proposed by Browne and Poskanzer in 1969 that cerebral vasodilators were of no value or even harmful to the patient with acute stroke, was based on observations of the steal phenomenon.5 - 6 The decrease in cerebral blood flow (CBF) to the ischemic tissue by CO 2 inhalation was studied extensively in laboratory animals, 7 " 10 but the issue still remained controversial. Since it has been observed that the pharmacological sites of CO 2 and vasodilating agents in the cerebral arteries are different," the findings for the former cannot be extended to the effect of the latter. In the literature, the reported changes in CBF due to vasodilators, e.g., papaverine, in ischemic regions of patients with acute stroke and of animals with acute cerebral arterial occlusion, have been diverse and inconclusive.12 " 18Even when CBF was demonstrated to decrease with papaverine, as in the cases reported by Olesen and Paulson 19 and Regli et al, 20 the decrease could not necessarily be attributed to the intracerebral steal phenomenon. It might be simply due to the influence of a concomitant decrease in SABP.This paper attempts to re-evaluate the effect of vasodilators on the CBF of an ischemic area produced acutely by middle cerebral artery (MCA) occlusion in cats, under conditions where any decrease in SABP, after papaverine administration, was adjusted to the control level. Methods Six cats of both sexes weighing 2.5-4.2 kg were used. All cats were anesthetized with 50 mg/kg body weight of alpha-chloralose and 500 mg/kg body weight of urethane and immobilized with alcuronium chloride. Tracheal intubation was performed and respiration was controlled with a Harvard respirator. The left femoral artery and femoral vein were ...

We examined the effect of aspirin on the enhanced erythrocyte aggregability in 19 patients with cerebral infarction during the chronic phase. Aspirin (81 mg/day) was administered for 8 weeks. The rate of erythrocyte aggregation (aggregability) was measured using the whole-blood erythrocyte aggregometer developed by us (Am. J. Physiol. 251, H1205-H1210, 1986) before, and at 4 and 8 weeks after initiation of the aspirin administration. Concomitant measurements were made of certain blood factors such as the hematocrit, albumin-globulin (A/G) ratio and fibrinogen concentration. The erythrocyte aggregation rates before, and at 4 and 8 weeks were 0.154 +/- 0.019/s, 0.144 +/- 0.020/s, and 0.143 +/- 0.020/s, respectively. The erythrocyte aggregation rates at 4 and 8 weeks were significantly (P < 0.05, Bonferroni's modified t-test) lower than that before aspirin administration. Although the hematocrit value and A/G ratio were not changed at 4 and 8 weeks after the initiation of aspirin, the concentration of fibrinogen were significantly (P < 0.05) reduced at 4 weeks. The above results suggest that aspirin can improve the enhanced erythrocyte aggregability in patients with cerebral infarction during the chronic phase.

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