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.