Wang J, Ohta S, Sakaki S, Araki N, Matsuda S, Sakanaka M
Department of Neurological Surgery, Ehime University School of Medicine, Japan.
J Neurosurg. 1994 Feb;80(2):269-75. doi: 10.3171/jns.1994.80.2.0269.
Changes in Ca(++)-adenosine triphosphatase (ATPase) activity in the plasma membrane of smooth-muscle cells in the basilar arteries of dogs with experimental subarachnoid hemorrhage (SAH) were examined. The study methods included electron microscopic histochemistry and bioassay of the enzyme that exports cytoplasmic Ca++ to extracellular spaces. The Ca(++)-ATPase activity in the basilar artery increased significantly in response to the application of vasoconstrictive agents (prostaglandin F2 alpha and a phorbol ester), but decreased significantly 24 hours after experimental SAH, inversely with basilar artery contraction. Dogs that had undergone two arterial blood injections (double SAH) exhibited a further decrease in Ca(++)-ATPase activity as well as persistent contraction of the basilar artery for a longer period (at least 7 days) than was seen in animals with a single arterial blood injection. Bioassay of the enzyme also demonstrated a decrease in vascular Ca(++)-ATPase activity in dogs subjected to double SAH. These findings suggest that the early occurrence of and long-lasting decrease in Ca(++)-ATPase activity in dogs with experimental SAH induces a persistent disturbance of Ca++ homeostasis and indicates that damage to the plasma membrane in the cerebral arterial smooth-muscle cells proceeds to myonecrosis after SAH.
