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This Article Full Text Full Text (PDF) All Versions of this Article: 297/1/H466    most recent 01317.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Gragasin, F. S. Articles by Davidge, S. T. PubMed PubMed Citation Articles by Gragasin, F. S. Articles by Davidge, S. T.

The effects of propofol on vascular function in mesenteric arteries of the aging rat

Departments of ¹Anesthesiology and Pain Medicine and ²Physiology and ³Obstetrics and Gynecology, University of Alberta, Edmonton, Canada

Submitted 22 December 2008 ; accepted in final form 18 May 2009

Hypotension following administration of propofol, an anesthetic agent, is strongly predicted by advanced age and is partly due to direct vasodilation. We hypothesized that propofol increases nitric oxide (NO)-mediated vasodilation by enhancing its bioavailability in the aged adult vasculature, leading to greater vasodilation than in the young adult. Small mesenteric arteries from rats aged 13–15 versus 3 to 4 mo were compared in this study. Reactivity to propofol (1–100 µM) alone and with the addition of acetylcholine (ACh; 0.1–10 µM) in endothelial-intact and dunuded arteries following phenylephrine constriction was assessed using myography. N^G-nitro-L-arginine methyl ester (L-NAME) and meclofenamate (Meclo) were used to inhibit NO and prostaglandin synthesis, respectively. Superoxide dismutase (SOD) and catalase were used as antioxidants during ACh relaxation and were compared with propofol in aging arteries. Propofol alone induced greater relaxation in 1) endothelial-intact compared with denuded arteries and 2) aged compared with young arteries, which were inhibited by L-NAME. ACh-induced relaxation was greater in young compared with aged control arteries; however, propofol pretreatment increased this relaxation in aged but not in young arteries. Additionally, propofol inhibited ACh-induced relaxation in arteries treated with L-NAME + Meclo [relaxation attributed to endothelium-derived hyperpolarizing factor (EDHF)]. Pretreatment with SOD and catalase increased relaxation to ACh in aged arteries similar to propofol. In conclusion, propofol causes relaxation in small mesenteric arteries in an endothelial-dependent and independent manner and increases ACh-induced relaxation in aged arteries. Interestingly, propofol inhibits EDHF-mediated relaxation but increases availability of NO, which leads to overall vascular relaxation.

nitric oxide; endothelium-derived hyperpolarizing factor; oxidative stress