Cerebral vasospasm: contractile activity of hemoglobin in isolated canine basilar arteries

Abstract

Recent studies suggest the possible role of the red blood cell (RBC) in causing chronic cerebral vasospasm. The basic action of Hb, the major component of the RBC, on cerebral arteries is unknown. The contractile effects of human Hb (purified by ion-exchange chromatography) on canine arteries in vitro are studied. The contractile activity of lysed RBC was shown to be derived from Hb. HbO2 caused a maximum contraction equal to .apprx. 70% of that induced by serotonin in the basilar artery. Ferrous Hb (HbO2 and HbCO2) produced much greater contraction than feric Hb (methemoglobin and cyanmethemoglobin), suggesting that superoxide radicals, an active species of O2, may be related to the contractile activity of Hb. Neither methysergide, phentolamine, mepyramine nor aspirin inhibited the vasoconstrictive activity of HbO2. The activation of serotonergic, .alpha.-adrenergic or histaminergic H1 receptors, or prostaglandin synthesis may not be involved in the mechanism of action of HbO2. The constituents of Hb caused little or no contraction as compared with Hb as a whole. The basilar artery was more highly sensitive to Hb than arteries from other anatomical locations. cAMP caused a very slight decrease in the Hb-induced contraction. HbO2 apparently can contract cerebral arteries in vitro. These results, coupled with recent reports on the participation of the RBC in producing chronic vasospasm, strongly suggest that HbO2 released from RBC plays an important role in the pathogenesis of chronic cerebral vasospasm.