| Research Abstract |
Vasospasm was produced in the canine basilar artery by a two-hemorrhage method, whereas vasocontraction by a topical application of KCl or serotonin, and the experimental results with regard to calpain are as follows.
1. Immunoblot analysis of mu-calpain in the basilar artery using antibodies against pre- and post-autolysis forms showed a continuous activation of mu- calpain in vasospasm and in contrast, a transient activation of mu-calpain only in the early stage of vasocontraction. Activities of calpastatin (endogenous inhibitor of calpain) was not changed in vasocontractin but significantly decreased in vasospasm, suggesting a proportional increase in calpain activities. 2. A topical treatment with calpeptin (selective inhibitor of calpain) was in-effective for vasocontraction but induced a dose-dependent dilation of the basilar artery in vasospasm.
3. Immunoblot analysis of alpha-smooth muscle actin, myosin, desmin, filamin, talin, vinculin and alpha-actinin in the basilar artery demonstrated a severe progressive degradation of all proteins in vasospasm and only a slight degradation of myosin, filamin, talin and alpha-actinin in vasocontraction.
In conclusion, it would be suggested that all intracellular devices responsible for the vascular smooth muscle contraction are degraded severely by calpain in vasospasm to induce resistance to therapy.
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