[Cerebral vasospasm and lipoperoxide damage--morphological localization and measurement of lipoperoxide in prolonged cerebral vasospasm].

Abstract

Prolonged vasospasm was produced in the canine basilar artery by injection of 0.75 ml/kg of fresh autologous arterial blood into the cisterna magna (subarachnoid hemorrhage, SAH group) or by subarachnoid application of oxyhemoglobin (oxyHb induced group). Lipoperoxide contents of the arterial wall was measured by thiobarbituric acid test. Prostaglandin I2 (PGI2) and thromboxane A2 (TXA2) biosynthetic activity of arterial wall was measured by radioimmunoassay as their stable metabolites, 6-keto-prostaglandin F1 alpha, thromboxane B2, respectively. Ultrastructual examination was carried out to reveal morphological localization of lipoperoxide of the spastic artery by a new method of lipoperoxide stain using thiocarbohydrazide and silver protein, the former was considered to react malondialdehyde. Lipoperoxide appeared in the electron microscope as discrete black granules. The value of lipoperoxide content of the spastic arterial wall elevated up to 7 days. Comparing with the control group, the increasing lipoperoxide contents of both day 4 SAH group and oxyHb induced group showed statistically significant difference (p less than 0.05). PGI2 biosynthetic activity in SAH group and in oxyHb induced group diminished, but statistically there was no significant difference. TXA2 biosynthetic activity did not alter. With increasing lipoperoxide value of arterial wall their PGI2 biosynthetic activity tended to diminish. Positive staining products of lipoperoxide stain were noted along the cell membrane of smooth muscle cell and endothelial cell in spastic arteries of both SAH and oxyHb induced groups. The result of this study suggests that oxyhemoglobin associated with lysis of the subarachnoid clot initiates lipid peroxidation damage of the smooth muscle cell and endothelial cell which diminishes PGI2 synthesis. This lipid peroxidation is suspected to be involved in the pathogenesis of vasospasm following SAH.