Nonmuscle Arterial Constriction after Subarachnoid Hemorrhage

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Abstract
RECENT STUDIES HAVE shown that myofibroblasts cultured from spastic arteries after subarachnoid hemorrhage (SAH) can produce contractile forces and that cerebrospinal fluid obtained from SAH patients accelerates this contraction. Myofibroblast-populated collagen lattices were used to evaluate the roles of polypeptide growth factors considered to be released from intraluminal accumulated platelets. The myofibroblasts, obtained at autopsy from human cerebral arteries of victims of vasospasm, caused contractile forces by compacting collagen fibrils in the matrix. Transforming growth factor β1 (TGF-β1) and platelet-derived growth factors aa and bb (PDGFaa and PDGFbb) accelerated this contraction in a dose-dependent manner. In the presence of TGF-β1 at 1 or 10 ng/ml, PDGFaa at 10 ng/ml, or PDGFbb at 10 ng/ml, lattice areas were reduced to 69.5 ± 1.9% (mean ± standard deviation) (P < 0.001), 63.3 ± 0.4% (P < 0.001), 66.5 ± 3.0% (P < 0.01), or 74.4 ± 1.7% (P < 0.01) of the control on Day 6, respectively. The combination of subthreshold doses of TGF-β1 and PDGFaa created a stimulatory effect that appeared to act synergistically. Furthermore, myofibroblast-populated collagen lattices made with cells preincubated with TGF-β1 showed more rapid compaction with or without the presence of stimulants such as post-SAH cerebrospinal fluid. These results suggest that, in addition to other possible factors in the post-SAH cerebrospinal fluid, growth factors derived from accumulated platelets may play an important role in arterial constriction caused by nonmuscle components after SAH, by single or multiple mechanisms.

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