Key result
Experimental hypercholesterolemia in pigs enhanced coronary vasoconstriction to ET-1 (CBF -88% vs -45% at baseline, P<.05) and attenuated the response to endogenous NO inhibition.
Why the study?
Does experimental hypercholesterolemia alter coronary vasomotor responses to endothelin and endogenous NO inhibition in pigs?
Population
Pigs subjected to a cholesterol diet for 10 weeks to induce experimental hypercholesterolemia
Comparison
Infusion of Endothelin-1 at 5 ng/kg/min or… vs Baseline responses before the 10-week…
Design
Preclinical
Follow-up
10 weeks
Authors
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May support coronary vasomotor dysfunction in hypercholesterolemia; leaves open human translation.
Does experimental hypercholesterolemia alter coronary vasomotor responses to endothelin and endogenous NO inhibition in pigs?
Absolute Event Rate: -88% vs -45%
p-value: p=<.05
Experimental hypercholesterolemia in pigs enhances coronary vasoconstriction to endothelin and attenuates basal nitric oxide activity, indicating altered coronary vascular reactivity.
Mathew et al. (1997) studied Experimental hypercholesterolemia. Endothelin-1 (ET-1) and N(G)-monomethyl-L-arginine (L-NMMA) vs. Baseline (before cholesterol diet) was evaluated on Decrease in coronary blood flow (CBF) with ET-1 (p=<.05). Experimental hypercholesterolemia in pigs enhanced coronary vasoconstriction to ET-1 (CBF -88% vs -45% at baseline, P<.05) and attenuated the response to endogenous NO inhibition.
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