{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T11:02:32Z","timestamp":1740135752429,"version":"3.37.3"},"reference-count":42,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2011,12,6]],"date-time":"2011-12-06T00:00:00Z","timestamp":1323129600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:p><jats:bold>BACKGROUND AND PURPOSE<\/jats:bold> Increased vascular contractility plays a fundamental role in cerebral vasospasm in subarachnoid haemorrhage (SAH). We investigated the role of thrombin and its receptor, proteinase\u2010activated receptor 1 (PAR1), and other G protein\u2010coupled receptors in the increased contractility, and examined the preventive effects of the thrombin inhibitor, argatroban, and anti\u2010oxidative agents, vitamin C and tempol.<\/jats:p><jats:p><jats:bold>EXPERIMENTAL APPROACH<\/jats:bold> A rabbit model of SAH was utilized. Contractile responses of the isolated basilar artery and the level of oxidative stress of brain tissues were evaluated.<\/jats:p><jats:p><jats:bold>KEY RESULTS<\/jats:bold> Contractile responses to thrombin and PAR1\u2010activating peptide (PAR1\u2010AP) were enhanced and prolonged after SAH. The thrombin\u2010induced contraction persisted even after terminating thrombin stimulation. When sequentially stimulated with PAR1\u2010AP, the second response was maintained in SAH, while it was substantially attenuated in the control. Only a combination of argatroban with vitamin C or tempol prevented both the enhancement and prolongation of the contractile response to PAR1\u2010AP and restored the reversibility of the thrombin\u2010induced contraction. The responses to angiotensin II, vasopressin and PGF<jats:sub>2\u03b1<\/jats:sub> were enhanced and prolonged after SAH to varying degrees, and responded differently to the treatment. The response to vasopressin exhibited a similar phenomenon to that seen with PAR1\u2010AP. Oxidative stress was increased in SAH, and normalized by the treatment with argatroban, vitamin C or their combination.<\/jats:p><jats:p><jats:bold>CONCLUSIONS AND IMPLICATIONS<\/jats:bold> Increased vascular reactivity to agonists in SAH was attributable to the enhancement and prolongation of the contractile response. A combination of argatroban and anti\u2010oxidative agents was required to prevent both the enhancement and prolongation of the contractile response.<\/jats:p><jats:p><jats:bold>LINKED ARTICLE<\/jats:bold> This article is commented on by Hollenberg, pp. 103\u2013105 of this issue. 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