{"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":1773308510955,"version":"3.50.1"},"reference-count":35,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2007,1,1]],"date-time":"2007-01-01T00:00:00Z","timestamp":1167609600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2007,1]]},"abstract":"<jats:p> The pathogenesis of cerebral ischaemia after subarachnoid haemorrhage (SAH) still remains elusive. The purpose of the present study was to examine whether specific protein kinas C (PKC) inhibition in rats could alter the transcriptional SAH induced Endothelin (ET) type B and 5-hydroxytryptamine type 1B (5-HT<jats:sub>1B<\/jats:sub>) receptor upregulation and prevent the associated cerebral blood flow (CBF) reduction. The PKC inhibitor RO-31-7549 or vehicle was injected intracisternally after the induced SAH in rats ( n = 3 to 10 in each groups for each method). The involvement of the PKC isoforms was investigated with Western blot; only PKC\u03b4 and PKC\u03b1 subtypes were increased after SAH RO-31-7549 treatment abolished this. At 2 days after the SAH basilar and middle cerebral arteries were harvested and the contractile response to endothelin-1 (ET-1; ET<jats:sub>A<\/jats:sub> and ET<jats:sub>B<\/jats:sub> receptor agonist) and 5-carboxamidotryptamine (5-CT; 5-HT1 receptor agonist) were investigated with a myograph. The contractile responses to ET-1 and 5-CT were increased ( P &lt; 0.05) after SAH compared with sham operated rats. In parallel, the ET<jats:sub>B<\/jats:sub> and 5-HT<jats:sub>1B<\/jats:sub> receptor mRNA and protein expression were significantly elevated after SAH, as analysed by quantitative real-time polymerase chain reaction and immunohistochemistry, respectively. Administration of RO-31-7549 prevented the upregulated contraction elicited by application of ET-1 and 5-CT in cerebral arteries and kept the ETB and 5-HT<jats:sub>1B<\/jats:sub> receptor mRNA and protein levels at pre-SAH levels. Regional and global CBF evaluated by an autoradiographic technique were reduced by 60%\u00b14% after SAH ( P &lt; 0.05) and prevented by treatment with rO-31-7549. Our study suggests that PKC plays an important role in the pathogenesis of cerebral ischaemia after SAH. <\/jats:p>","DOI":"10.1038\/sj.jcbfm.9600313","type":"journal-article","created":{"date-parts":[[2006,5,31]],"date-time":"2006-05-31T16:01:16Z","timestamp":1149091276000},"page":"21-32","source":"Crossref","is-referenced-by-count":35,"title":["Protein Kinase C Inhibition Prevents Upregulation of Vascular ET<sub>B<\/sub> and 5-HT<sub>1B<\/sub> Receptors and Reverses Cerebral Blood Flow Reduction after Subarachnoid Haemorrhage in Rats"],"prefix":"10.1177","volume":"27","author":[{"given":"Saema S","family":"Beg","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jacob A","family":"Hansen-Schwartz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Petter 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