FRIDAY, March 5 (HealthDay News) -- Rosuvastatin protects against injury from ischemia and reperfusion through a cyclooxygenase (COX)-2-dependent mechanism, which may explain why COX-2 inhibitors have negative cardiovascular side-effects, according to a study in the March 9 issue of the Journal of the American College of Cardiology.
Andrew Liuni, of the University of Toronto, and colleagues conducted a study of 20 volunteers who were randomized to receive either a 40 mg oral dose of rosuvastatin or placebo and 24 hours later underwent measurement of endothelium-dependent, flow-mediated dilation (FMD) of the radial artery before and after ischemia and reperfusion (IR). Another 18 volunteers received a five-day course of twice-daily 200 mg celecoxib and were randomized to the rosuvastatin or control groups on day four.
Participants in both groups had similar FMD before IR but, post-IR, rosuvastatin prevented the impairment of FMD seen in the control group, the researchers found. When they looked at the impact of celecoxib, the investigators found that it wiped out the protective effect of rosuvastatin.
"We demonstrate that rosuvastatin administration exerts potent endothelial protection against IR injury in conduit vessels via activation of COX-2. These results represent the first human evidence of a direct endothelial pharmacological pre-conditioning effect by rosuvastatin and may provide a mechanistic explanation to previous observations from clinical settings." the authors conclude.
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