ArticleExperimental and clinical cardiology2003
Relationship between basal nitric oxide and ventricular repolarization in an intact heart.
Article in Experimental and clinical cardiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 2 citations in OpenAlex.
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Abstract
Recent studies suggest that endogenous nitric oxide (NO) attenuates ischemia- or reperfusion-induced shortening in the action potential duration of ventricular myocytes. The effect of basal NO on ventricular repolarization in an intact heart remains unclear. The activation-recovery interval was measured from 32 epicardial electrocardiograms in six anesthetized, open-chest sheep. Intravenous administration of N(G)-nitro-L-arginine, a NO synthase inhibitor, increased left ventricular systolic pressure from 101+/-7 mmHg to 118+/-10 mmHg (P=0.02), and left ventricular end diastolic pressure from 6.3+/-1.5 mmHg to 8.8+/-1.8 mmHg (P<0.01) without changing the heart rate (96+/-4 beats/min versus 94+/-3 beats/min, P=0.06). The average activation-recovery interval from the 32 ventricular sites remained unchanged in each animal after the administration of N(G)-nitro-L-arginine (P>0.05). The pooled activation-recovery interval in the six animals before and 60 min after drug administration was 287+/-21 ms and 288+/-27 ms, respectively (P>0.05). It was concluded that basal NO is important in maintaining hemodynamics but has limited impact on ventricular repolarization.
Indexed as
Identifiers
19644580PMC2716192W213694986What OpenQuestion holds
Registered trials
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