| pubmed-article:6362092 | pubmed:abstractText | 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 mammary 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, CO2-reactivity was completely abolished. Intravenous infusion of prostacyclin 2 hours after ischemia (1.8 micrograms/kg/min) decreased systemic arterial blood pressure and reduced platelet aggregability but did not improve cerebral blood flow, did not restore CO2-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. | lld:pubmed |
