Cerebral blood vessels of the dog have been shown to receive vasodilator and constrictor nerves. In isolated ring arterial preparations, neurogenic vasodilation was blocked while neurogenic vasoconstriction was potentiated by hemolysates isolated from hemolyzed erythrocytes. These results suggest that an overall increase in cerebral neurogenic vasoconstriction may occur in vivo following subarachnoid hemorrhage. The significance of this finding in the pathogenesis of cerebral vasospasm is discussed.
CheungSTMcIlhanyMPLimRMullanS, (1980) Preliminary characterization of vasocontractile activities in erythrocytes. J Neurosurg53:37–43
2.
D'AlecyLG, (1977) Adrenergic and cholinergic influence on CBF as determined with the venous outflow method. In: Neurogenic Control of the Brain Circulation (OwmanCEdvinssonL, eds). Oxford, Pergamon Press, pp 327–330
3.
EchlinFA, (1971) Experimental vasospasm, acute and chronic, due to blood in the subarachnoid space. J Neurosurg35:646–656
LeeTJ-F, (1982) Morphopharmacological studies of cerebral vasodilator and constrictor nerves. In: Cerebral Blood Flow: Effects of Nerves and Neurotransmitters (HeistadDDMarcusML, eds). Amsterdam, Elsevier, pp 431–439
6.
LeeTJ-FChiuehCCAdamsM, (1980) Synaptic transmission of vasoconstrictor nerves in rabbit basilar artery. Eur J Pharmacol61:55–70
7.
McIlhanyMPJohnsLMLeipzigTPatronasNJBrownFDMullanSF, (1983) In vivo characterization of vasocontractile activities in erythrocytes. J Neurosurg58:356–361
8.
OsakaK, (1977) Prolonged vasospasm produced by the breakdown products of erythrocytes. J Neurosurg47:403–411