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We examined time-dependent changes in protein synthesis and in the immunoreactivities of representative contraction-related structural proteins in smooth muscle cells of canine basilar arteries after experimental subarachnoid hemorrhage (SAH). Protein synthesis was assessed by the percentage of polyribosome-forming ribosomes to total ribosomes (aggregation rate), a morphological index of the activity of protein synthesis. The aggregation rates in prostaglandin F 2α - (PGF 2α ) and 12- O-tetradecanoyl-phorbol-13-acetate (TPA)-induced contracted basilar arteries were 70.0 ± 7.0% and 71.4 ± 8.7%, respectively, quite similar to the value in normal basilar artery (73.0 ± 8.0%). In the single-SAH group with little delayed histological changes in the basilar arteries, the aggregation rate was significantly decreased to 30.5 ± 6.4% by 24 h after the SAH, and recovered to 52.3 ± 9.0% and 70.2 ± 7.6% at 7 and 14 days postSAH, respectively, when the vasospasm was moderately and completely ameliorated. In contrast, in the double-SAH group in which the basilar arteries developed delayed smooth muscle cell death and long-lasting arterial contraction, a significant decrease in the aggregation rate (25.0 ± 5.0% on day 4) persisted for 14 days. The in vitro incorporation of [ 3 H]-leucine in the basilar arterial cells was also significantly suppressed 4 and 7 days after the initial SAH (1.2 ± 0.4 and 1.4 ± 0.3 × 10 3 dpm/mg protein) in the double-SAH group, as opposed to no significant decrease in the basilar artery at 7 days postSAH in the single-SAH group (1.9 ± 0.6 × 10 3 dpm/mg protein). The immunoreactivity of α-smooth muscle actin, a contractile protein, demonstrated by immunohistochemistry and immunoblots, was not altered for up to 14 days even in the double-SAH group, but that of calponin and of h-caldesmon, contraction-inhibiting proteins, was markedly reduced 4–14 days after the initial SAH. Persistent impairment of protein synthesis and relative reduction of immunoreactivities of the contraction-inhibiting proteins were observed in arteries with severe vasospasm and loss of smooth muscle cells, as noted in the double-SAH subjects. These abnormalities may cooperate to cause cerebral arterial narrowing accompanied by degeneration of smooth muscle cells after SAH.

journal of cerebral blood flow and metabolism

Protein Synthesis and Immunoreactivities of Contraction-Related Proteins in Smooth Muscle Cells of Canine Basilar Artery after Experimental Subarachnoid Hemorrhage