Key result
Diabetes mellitus was associated with significantly greater bradykinin-induced dilation in coronary arterioles compared to non-diabetic patients (77% vs 38%, P<0.05), mediated by COX-2 expression.
Why the study?
Does diabetes mellitus increase COX-2-dependent prostaglandin-mediated dilation in human coronary arterioles?
Population
Coronary arterioles dissected from right atrial appendages obtained at the time of cardiac surgery from…
Comparison
Bradykinin administration with or without COX… vs Coronary arterioles from patients without…
Design
Preclinical
Authors
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May indicate compensatory microvascular function in diabetes; hypothesis-generating and should not yet change practice.
Observational
Does diabetes mellitus increase COX-2-dependent prostaglandin-mediated dilation in human coronary arterioles?
Absolute Event Rate: 77% vs 38%
p-value: p=<0.05
Diabetes mellitus increases COX-2 expression and dilator prostaglandin synthesis in human coronary arterioles, which may serve as a compensatory mechanism to maintain adequate cardiac perfusion.
Szerafin et al. (2006) conducted an observational in Diabetes Mellitus. Diabetes Mellitus vs. No documented diabetes was evaluated on Arteriolar dilation to bradykinin (10 nmol/L) (p=<0.05). Diabetes mellitus was associated with significantly greater bradykinin-induced dilation in coronary arterioles compared to non-diabetic patients (77% vs 38%, P<0.05), mediated by COX-2 expression.
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