What is the clinical evidence from this study?

Study design: Other. Population: Normal dogs. Intervention: L-NAME (NG-nitro-L-arginine methyl ester) vs. D-enantiomer. Primary outcome: Responses of left ventricular (LV) dP/dt, regional wall thickening in LCX region and LCX blood flow to graded intracoronary doses of isoproterenol.

What does this research mean for the field?

Inhibition of nitric oxide synthesis significantly reduces baseline coronary blood flow and its response to β-adrenergic stimulation, but does not alter basal cardiac contractility or its response to β-adrenergic stimulation. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To assess whether endogenous nitric oxide regulates baseline cardiac contractility and coronary blood flow, as well as their responses to beta-adrenergic stimulation in the intact canine heart.

February 1, 1996Journal of Cardiovascular Pharmacology

Inhibition of Nitric Oxide Synthesis Reduces Coronary Blood Flow Response But Does Not Increase Cardiac Contractile Response to β-Adrenergic Stimulation in Normal Dogs

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Key result

Inhibition of nitric oxide synthesis with L-NAME significantly reduced baseline coronary blood flow and its response to isoproterenol in normal dogs, but did not alter basal cardiac contractility.

Why the study?

Does NO synthase inhibition with L-NAME alter basal cardiac contractility, coronary blood flow, and their responses to beta-adrenergic stimulation in normal dogs?

Population

Normal dogs

Comparison

Intracoronary NG-nitro-L-arginine methyl ester… vs D-enantiomer administered into left circumflex…

Design

Preclinical

Authors

HKHaruo KanekoToho University TETakao EndoOsaka Women's and Children's Hospital KKKaname KiuchiHarvard University

Discussion

Member takes

Implication

NO regulates coronary flow but not contractility in normal dogs; leaves open relevance to human disease states.

Key Points

To assess whether endogenous nitric oxide regulates baseline cardiac contractility and coronary blood flow, as well as their responses to beta-adrenergic stimulation in the intact canine heart.
Administered low and high doses of L-NAME (10 and 100 μg/kg/min for 10 min) or its inactive D-enantiomer directly into the left circumflex coronary artery of normal dogs.
Measured left ventricular dP/dt, regional wall thickening, and left circumflex blood flow during graded intracoronary infusions of isoproterenol (0.002–0.016 μg/kg/min).
Intracoronary L-NAME caused dose-dependent reductions in acetylcholine-mediated vasodilation, significantly decreasing baseline left circumflex blood flow and blunting the hyperemic response to isoproterenol.
L-NAME had no effect on baseline left ventricular contractility (evaluated by LV dP/dt and wall thickening) and did not enhance the contractile response to isoproterenol.
Infusion of the inactive D-enantiomer caused no significant changes in baseline coronary blood flow or the coronary flow response to isoproterenol.

Structured PICO

Does NO synthase inhibition with L-NAME alter basal cardiac contractility, coronary blood flow, and their responses to beta-adrenergic stimulation in normal dogs?

Population

Normal dogs

Intervention

Intracoronary NG-nitro-L-arginine methyl ester (L-NAME) (10 and 100 μg/kg/min for 10 min) and graded intracoronary doses of isoproterenol (ISO 0.002-0.016 μg/kg/min)

Comparator

D-enantiomer administered into left circumflex (LCX) artery

Outcome

Left ventricular (LV) dP/dt, regional wall thickening in LCX region, and LCX blood flowsurrogate

Constitutive NO formation regulates basal coronary vascular tone and resistance during beta-adrenergic stimulation, but does not influence basal cardiac contractility or its response to beta-adrenergic stimulation in normal dogs.

Cite This Study

Kaneko et al. (1996) studied Normal dogs. L-NAME (NG-nitro-L-arginine methyl ester) vs. D-enantiomer was evaluated on Responses of left ventricular (LV) dP/dt, regional wall thickening in LCX region and LCX blood flow to graded intracoronary doses of isoproterenol. Inhibition of nitric oxide synthesis with L-NAME significantly reduced baseline coronary blood flow and its response to isoproterenol in normal dogs, but did not alter basal cardiac contractility.

synapsesocial.com/papers/6a14f5fa9ff8b2b0e129e02e https://doi.org/10.1097/00005344-199602000-00011

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February 1, 1996Journal of Cardiovascular Pharmacology

Inhibition of Nitric Oxide Synthesis Reduces Coronary Blood Flow Response But Does Not Increase Cardiac Contractile Response to β-Adrenergic Stimulation in Normal Dogs

View Full Paper

Ask AI

Bookmark

Key result

Inhibition of nitric oxide synthesis with L-NAME significantly reduced baseline coronary blood flow and its response to isoproterenol in normal dogs, but did not alter basal cardiac contractility.

Why the study?

Does NO synthase inhibition with L-NAME alter basal cardiac contractility, coronary blood flow, and their responses to beta-adrenergic stimulation in normal dogs?

Population

Normal dogs

Comparison

Intracoronary NG-nitro-L-arginine methyl ester… vs D-enantiomer administered into left circumflex…

Design

Preclinical

Authors

HKHaruo KanekoToho University TETakao EndoOsaka Women's and Children's Hospital KKKaname KiuchiHarvard University

Discussion

Member takes

Implication

NO regulates coronary flow but not contractility in normal dogs; leaves open relevance to human disease states.

Key Points

To assess whether endogenous nitric oxide regulates baseline cardiac contractility and coronary blood flow, as well as their responses to beta-adrenergic stimulation in the intact canine heart.
Administered low and high doses of L-NAME (10 and 100 μg/kg/min for 10 min) or its inactive D-enantiomer directly into the left circumflex coronary artery of normal dogs.
Measured left ventricular dP/dt, regional wall thickening, and left circumflex blood flow during graded intracoronary infusions of isoproterenol (0.002–0.016 μg/kg/min).
Intracoronary L-NAME caused dose-dependent reductions in acetylcholine-mediated vasodilation, significantly decreasing baseline left circumflex blood flow and blunting the hyperemic response to isoproterenol.
L-NAME had no effect on baseline left ventricular contractility (evaluated by LV dP/dt and wall thickening) and did not enhance the contractile response to isoproterenol.
Infusion of the inactive D-enantiomer caused no significant changes in baseline coronary blood flow or the coronary flow response to isoproterenol.

Structured PICO

Does NO synthase inhibition with L-NAME alter basal cardiac contractility, coronary blood flow, and their responses to beta-adrenergic stimulation in normal dogs?

Population

Normal dogs

Intervention

Intracoronary NG-nitro-L-arginine methyl ester (L-NAME) (10 and 100 μg/kg/min for 10 min) and graded intracoronary doses of isoproterenol (ISO 0.002-0.016 μg/kg/min)

Comparator

D-enantiomer administered into left circumflex (LCX) artery

Outcome

Left ventricular (LV) dP/dt, regional wall thickening in LCX region, and LCX blood flowsurrogate

Cite This Study

synapsesocial.com/papers/6a14f5fa9ff8b2b0e129e02e https://doi.org/10.1097/00005344-199602000-00011

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