{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T09:41:50Z","timestamp":1773308510993,"version":"3.50.1"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Stroke"],"published-print":{"date-parts":[[1996,10]]},"abstract":"<jats:p><jats:italic>Background and Purpose<\/jats:italic>The role of extracellular Ca<jats:sup>2+<\/jats:sup>in the maintenance of chronic vasospasm after subarachnoid hemorrhage (SAH) is largely unknown. Indeed, studies thus far have been limited to demonstrations that L-type Ca<jats:sup>2+<\/jats:sup>\u2212channel antagonists were unable to reverse the spasm. This study tested whether SAH-induced vasospasm is maintained, at least in part, through the influx of extracellular Ca<jats:sup>2+<\/jats:sup>and whether the influx of extracellular Ca<jats:sup>2+<\/jats:sup>occurs through L-type Ca<jats:sup>2+<\/jats:sup>channels and possibly, in addition, through store operated channels (SOCs). Furthermore, as there is considerable evidence in the literature to suggest that the spasm is mediated through endothelin-1 (ET-1) release, we tested whether the Ca<jats:sup>2+<\/jats:sup>dependency of the spasm was consistent with the mediation of the spasm by ET-1.<\/jats:p><jats:p><jats:italic>Methods<\/jats:italic>Chronic spasm of the basilar artery was induced in a double SAH rabbit model. Relaxation of SAH-, ET-1\u2212, serotonin-, and KCl-constricted basilar artery in response to Ca<jats:sup>2+<\/jats:sup>-free solution, verapamil, and Ni<jats:sup>2+<\/jats:sup>was measured in situ with the use of a cranial window.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>SAH induced 23% constriction of the basilar artery. Ca<jats:sup>2+<\/jats:sup>-free solution and 1 \u03bcmol\/L verapamil reversed the constriction of SAH vessels by 60% and 17%, respectively. In contrast, control vessels challenged with 40 to 50 mmol\/L KCl, which induced 34% constriction, relaxed in response to Ca<jats:sup>2+<\/jats:sup>-free solution and verapamil by 98% and 89%, respectively. In SAH vessels, verapamil followed by 0.1 mmol\/L Ni<jats:sup>2+<\/jats:sup>, which is known to block SOCs, induced a combined relaxation of 67%. Control vessels challenged with 3 nmol\/L ET-1, which induced a magnitude of constriction similar to that of SAH (29%), relaxed in response to Ca<jats:sup>2+<\/jats:sup>-free solution, verapamil, and verapamil plus Ni<jats:sup>2+<\/jats:sup>by 69%, 20%, and 50%, respectively (<jats:italic>P<\/jats:italic>&gt;.05 versus respective values in SAH vessels). In contrast, control vessels challenged with 2 to 8 \u03bcmol\/L serotonin, which induced a magnitude of constriction similar to those of SAH and ET-1 (22%), completely relaxed in response to Ca<jats:sup>2+<\/jats:sup>-free solution and verapamil.<\/jats:p><jats:p><jats:italic>Conclusions<\/jats:italic>These results demonstrate that the maintenance of chronic spasm in the two-hemorrhage rabbit model after SAH is due to smooth muscle cell contractile mechanisms partly dependent on the influx of extracellular Ca<jats:sup>2+<\/jats:sup>. The influx of extracellular Ca<jats:sup>2+<\/jats:sup>results from the opening of L-type Ca<jats:sup>2+<\/jats:sup>channels and an additional channel or channels. We speculate that the L-type Ca<jats:sup>2+<\/jats:sup>channel\u2212independent influx of extracellular Ca<jats:sup>2+<\/jats:sup>results from the opening of SOCs. The Ca<jats:sup>2+<\/jats:sup>-dependent characteristics of the spasm likely reflect the mediation of the spasm by ET-1.<\/jats:p>","DOI":"10.1161\/01.str.27.10.1896","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T20:08:03Z","timestamp":1308341283000},"page":"1896-1902","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":37,"title":["Role of Extracellular Ca<sup>2+<\/sup>in Subarachnoid Hemorrhage\u2212Induced Spasm of the Rabbit Basilar Artery"],"prefix":"10.1161","volume":"27","author":[{"given":"Mario","family":"Zuccarello","sequence":"first","affiliation":[{"name":"the Departments of Neurosurgery (M.Z., R.B.) and Pharmacology &amp; Cell Biophysics (R.B., M.T., R.M.R.), University of Cincinnati College of Medicine, and Veterans Affairs Medical Center, Cincinnati, Ohio."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Riccardo","family":"Boccaletti","sequence":"additional","affiliation":[{"name":"the Departments of Neurosurgery (M.Z., R.B.) and Pharmacology &amp; Cell Biophysics (R.B., M.T., R.M.R.), University of Cincinnati College of Medicine, and Veterans Affairs Medical Center, Cincinnati, Ohio."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Metiner","family":"Tosun","sequence":"additional","affiliation":[{"name":"the Departments of Neurosurgery (M.Z., R.B.) and Pharmacology &amp; Cell Biophysics (R.B., M.T., R.M.R.), University of Cincinnati College of Medicine, and Veterans Affairs Medical Center, Cincinnati, Ohio."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert M.","family":"Rapoport","sequence":"additional","affiliation":[{"name":"the Departments of Neurosurgery (M.Z., R.B.) and Pharmacology &amp; Cell Biophysics (R.B., M.T., R.M.R.), University of Cincinnati College of Medicine, and Veterans Affairs Medical Center, Cincinnati, Ohio."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"H230","volume":"269","year":"1995","unstructured":"Bian K, Bukoski RD. 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