No Effect of Prostacyclin on Blood Flow, Regulation of Blood Flow and Blood Coagulation Following Global Cerebral Ischemia

SUMMARY In normothermic cats under light barbiturate anesthesia, cerebral blood flow was arrested for one hour by intrathoracal occlusion of the innominate, the left subclavian, and both mammarian arteries. Recirculation of the brain after ischemia resulted in reactive hyperemia, followed by a decrease of blood flow to about 70% of control (post-ischemic hypoperfusion). During postischemic hypoperfusion, C02-reactivity was completely abolished. Intravenous infusion of prostacyclin 2 hours after ischemia (1.8 /Lig/kg/min) decreased systemic arterial blood pressure and reduced platelet aggregability but did not improve cerebral blood flow, did not restore C02-reactivity, and did not influence postischemic changes of blood coagulation. It is concluded that prostacyclin deficiency is not or not the only reason for the development of post-ischemic hypoperfusion and the associated disturbance of flow regulation. Stroke Vol 14, No 5, 1983 THROUGHOUT THE COURSE of reperfusion after a period of complete cerebro-circulatory arrest, certain physiological and metabolic phenomena develop in a regular sequence: the early reperfusion period is characterized by a shortlasting reactive hyperemia, followed by a phase of reduced blood circulation (post­ ischemic hypoperfusion). During both phases, energy- producing metabolism and blood flow are uncoupled: in reactive hyperemia, oxygen availability exceeds the oxygen requirements of the tissue, and oxygen content of cerebral venous blood increases (luxury perfusion).1 During post-ischemic hypoperfusion, the decreased oxygen availability is in misrelationship to an in­ creased metabolic demand of the tissue and therefore may result in relative cerebral hypoxia.2