Key result
K ATP channel blockade with glibenclamide did not prevent locally mediated metabolic increases in coronary blood flow accompanying myocardial O2 consumption during pacing tachycardia.
Why the study?
Does K ATP channel blockade with glibenclamide reduce coronary blood flow during pacing tachycardia in anesthetized closed-chest dogs?
Does K ATP channel blockade with glibenclamide reduce coronary blood flow during pacing tachycardia in anesthetized closed-chest dogs?
K ATP channels are not required for locally mediated metabolic increases in coronary blood flow during pacing tachycardia without catecholamines.
Answers are grounded in this paper and cite their sources.
Questions K ATP channel necessity for metabolic coronary vasodilation in dogs; leaves open relevance to humans or catecholamine states.
ATP-sensitive potassium ([Formula: see text]) channels have been shown to play a role in the maintenance of basal coronary vascular tone in vivo. [Formula: see text] channels are also involved in the coronary vasodilator response to adenosine. The aim of this study was to determine the role of[Formula: see text] channels in local metabolically mediated increases in coronary blood flow during cardiac electrical paired pacing without catecholamine effects. In 10 anesthetized closed-chest dogs, coronary blood flow was measured in the left circumflex coronary artery, and myocardial O 2 consumption was calculated using the arteriovenous O 2 difference. Cardiac interstitial adenosine concentration was estimated from coronary venous and arterial plasma adenosine measurements using a previously described, multicompartmental, axially distributed, mathematical model. Paired stimulation increased heart rate from 57 to 120 beats/min, myocardial O 2 consumption 88%, and coronary blood flow 76%. During[Formula: see text] channel blockade with glibenclamide, baseline coronary blood flow decreased in relation to myocardial O 2 consumption and thus coronary sinus O 2 tension fell. Paired-pulse pacing with glibenclamide resulted in increases in myocardial O 2 consumption and coronary blood flow similar to those during control pacing. Coronary venous and estimated interstitial adenosine concentration did not increase sufficiently to overcome the glibenclamide blockade. In conclusion, [Formula: see text] channels are not required for locally mediated metabolic increases in coronary blood flow that accompany myocardial O 2 consumption during pacing tachycardia without catecholamines, and adenosine levels do not increase sufficiently to overcome the glibenclamide blockade.
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Richmond et al. (1999) studied this question. K ATP channel blockade with glibenclamide vs. Control pacing was evaluated on Coronary blood flow and myocardial O2 consumption during paired-pulse pacing. K ATP channel blockade with glibenclamide did not prevent locally mediated metabolic increases in coronary blood flow accompanying myocardial O2 consumption during pacing tachycardia.
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