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October 1, 2004European Journal of Heart FailureOpen Access

Nitric Oxide Synthase Inhibition Impairs Myocardial Efficiency and Ventriculo-Arterial Matching in Acute Ischemic Heart Failure

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Why the study?

Does NOS inhibition impair myocardial efficiency and hemodynamics in a porcine model of acute ischemic heart failure?

Population

14 anesthetized pigs with acute ischemic left ventricular failure induced by left coronary artery…

Comparison

N-Nitro-L-arginine-metyl ester 15 mg/kg vs Control group (n=7)

Design

Preclinical, randomized

Follow-up

15 min

Authors

DNDag NordhaugNorwegian University of Science and TechnologyTSTor SteensrudHesco (United States)EAEbrahim AghajaniUniversity Hospital of North Norway

Discussion

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Implication

Detrimental hemodynamic effects in porcine acute ischemic HF; leaves open human relevance of NOS pathway modulation.

Structured PICO

Does NOS inhibition impair myocardial efficiency and hemodynamics in a porcine model of acute ischemic heart failure?

P
Population
14 anesthetized pigs with acute ischemic left ventricular failure induced by left coronary artery microembolization
I
Intervention
N(omega)-Nitro-L-arginine-metyl ester (NOS inhibitor) 15 mg/kg
C
Comparator
Control group (n=7)
O
Outcome
Left ventricular (LV) function and energetics, and overall hemodynamics (cardiac output, stroke work, MVO2-PVA relationship, arterial elastance) measured 15 min after interventionsurrogate

In a porcine model of acute ischemic heart failure, NOS inhibition increased afterload, reduced cardiac output, and severely impaired mechanoenergetic efficiency.

Cite This Study

Nordhaug et al. (2004) studied this question.

synapsesocial.com/papers/6a11e923f7bd4f5c7da58b3dhttps://doi.org/10.1016/j.ejheart.2003.11.010
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