Key result
ACE inhibitors and kininogen significantly increased nitrite production and reduced cardiac O2 consumption in vitro (all P < .05), effects that were blocked by inhibitors of endogenous NO formation.
Why the study?
Do ACE inhibitors affect nitric oxide accumulation and myocardial oxygen consumption in vitro?
Population
In vitro tissue preparations of coronary microvessels and myocardium
Comparison
Kininogen and ACE inhibitors (captopril… vs Baseline/control without ACE inhibitors or…
Design
Preclinical
Authors
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Hypothesis-generating for NO-mediated ACE inhibitor effects on myocardial energetics; requires in vivo confirmation before clinical relevance.
Do ACE inhibitors affect nitric oxide accumulation and myocardial oxygen consumption in vitro?
p-value: p=< .05
ACE inhibitors increase local nitric oxide formation and reduce myocardial oxygen consumption in vitro, highlighting a potential mechanism for their therapeutic efficacy in cardiac disease.
Zhang et al. (1997) studied In vitro tissue preparations. ACE inhibitors (captopril, enalaprilat, ramiprilat) and kininogen vs. Baseline was evaluated on Nitrite production in coronary microvessels and O2 consumption in myocardium (p=< .05). ACE inhibitors and kininogen significantly increased nitrite production and reduced cardiac O2 consumption in vitro (all P < .05), effects that were blocked by inhibitors of endogenous NO formation.
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