Abstract
The reduction of blood flow occurring after global cerebral ischemia, designated as delayed postischemic hypoperfusion, is a consquence of various pathological processes. Employing a cardiac arrest model in cats, we evalulated the possible role of thromboxane A2 (TXA2) in reducing the cerebral blood flow (CBF) after transient global ischemia. Twenty cats were divided into two groups, a cardiac arrest group (N=13) and a sham operation group (N=7). Following thoracotomy, cardiac arrest was induced for 30 seconds. The TXA2 receptor antagonist, BAY u3405, was injected at 60 minutes after recirculation. The CBF, brain tissue PO2 (BrPO2), brain tissue pH (BrpH) and mean arterial blood pressure (MABP) were measured continuously. The CBF decreased to 89.6% at 60 minutes after the arrest, suggesting postischemic hypoperfusion. Injection of BAY u3405 significantly increased the CBF and BrPO2, whereas BrpH and MABP remained unchanged. In the sham operation group, the CBF, BrPO2, BrpH and MABP did not change significantly during 10 minutes after drug injection, although the BrPO2 was increased mildly at 10 minutes after the injection. Since the thromboxane A2 antagonist improved the CBF only after the cardiac arrest, thromboxane A2 is thought to be one of the factors causing postischemic hypoperfusion.
