Effect of subarachnoid hemorrhage on the extracellular microenvironment.
Local experimental subarachnoid hemorrhage (SAH) was produced over the cerebral cortex in 15 cats. The cellular response was monitored using ion-specific electrodes for extracellular potassium (K+) and calcium (Ca++) activity, DC cortical potential, and electrocorticogram. The response was characterized by a profound cellular depolarization and extracellular calcium (Ca++) depletion which accompanied extracellular potassium (K+) accumulation. The prehemorrhage baseline calcium levels measured 1.14 +/- 0.11 mM, and were lowered to 0.4 to 0.7 mM/liter in different experiments. The K+ accumulation reached levels between 16 and 31 mM from a baseline of 3.17 +/- 0.52 mM and were cleared to normal or nearly normal within 5 minutes. The Ca++ levels also returned to normal within 5 minutes, but remained depressed for the duration of the experiment in two animals. These results confirm that blood extravasated into the subarachnoid space had a direct effect on parenchymal elements. The combination of transient K+ elevations and calcium depression may play an important role in the development of vascular spasm by inducing or facilitating a contraction in the muscular layer in the wall of major intracranial vessels.
D000818:Animals; D002118:Calcium / Q000502:physiology; D002415:Cats; D002540:Cerebral Cortex / Q000503:physiopathology; D005110:Extracellular Space / Q000502:physiology*; D006706:Homeostasis; D008839:Microelectrodes; D011188:Potassium / Q000502:physiology; D012965:Sodium Chloride / Q000494:pharmacology; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D013346:Subarachnoid Space / Q000187:drug effects
D012965:Sodium Chloride; D011188:Potassium; D002118:Calcium