April 17, 2018Microcirculation
Endothelium‐dependent hyperpolarization‐mediated vasodilatation compensates nitric oxide‐mediated endothelial dysfunction during ischemia in diabetes‐induced canine coronary collateral microcirculation in vivo
Key result
In dogs, NO-mediated vasodilatations of small coronary arteries during coronary occlusion are impaired in diabetes mellitus but compensated by endothelium-dependent hyperpolarization of arterioles.
Population
Canine model undergoing 90 minutes of left anterior descending coronary artery occlusion (n=18, 6 per group)
Comparison
Diabetes mellitus with or without L-NMMA + KCa… vs Control (non-diabetic) dogs
Design
Preclinical
Follow-up
90 minutes
Authors
Discussion
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Implication
EDH may compensate for impaired NO function in diabetic ischemia; leaves open human relevance.
Structured PICO
P
Population
18 dogs undergoing 90 minutes of left anterior descending coronary artery occlusion to study coronary microcirculation in diabetes mellitus.
I
Intervention
Diabetes mellitus with or without L-NMMA + KCa channel blockade
C
Comparator
Control (non-diabetic) dogs
O
Outcome
Coronary vasodilatation to bradykinin and levels of caveolin-1, eNOS, and caspase-3surrogate
Endothelium-dependent hyperpolarization compensates for impaired NO-mediated endothelial function during coronary ischemia in a diabetic canine model.
Cite This Study
Yada et al. (2018) studied Diabetes mellitus during coronary occlusion (n=18). Diabetes mellitus and KCa channel blockade vs. Control was evaluated on NO-mediated coronary vasodilatations of small arteries to bradykinin. In dogs, NO-mediated vasodilatations of small coronary arteries during coronary occlusion are impaired in diabetes mellitus but compensated by endothelium-dependent hyperpolarization of arterioles.