What is the clinical evidence from this study?

Study design: Other. Population: Heart failure (n=19). Intervention: NOS inhibitor (L-NAME) vs. Isoproterenol alone. Primary outcome: Inotropic response to isoproterenol (increase in sarcomere shortening velocity from baseline) (p=< .05).

What does this research mean for the field?

Increased nitric oxide synthesis in failing myocytes attenuates the positive inotropic response to beta-adrenergic stimulation, contributing to beta-adrenergic hyporesponsiveness in heart failure. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

March 4, 1997Circulation

Role of Myocyte Nitric Oxide in β-Adrenergic Hyporesponsiveness in Heart Failure

Q: What are the key findings of this study?

Inhibition of nitric oxide synthase with L-NAME significantly augmented the inotropic response to isoproterenol in failing myocytes (140.6% vs 107.1% increase; P<0.05) but not in control myocytes.

Q: What does this research mean for the field?

Increased nitric oxide synthesis in failing myocytes attenuates the positive inotropic response to beta-adrenergic stimulation, contributing to beta-adrenergic hyporesponsiveness in heart failure. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

Inhibition of nitric oxide synthase with L-NAME significantly augmented the inotropic response to isoproterenol in failing myocytes (140.6% vs 107.1% increase; P<0.05) but not in control myocytes.

Population

Myocytes isolated from 11 dogs with rapid pacing-induced heart failure and 8 control dogs.

Comparison

NOS inhibitor plus isoproterenol vs Baseline, isoproterenol alone, and L-NAME alone

Design

Preclinical

Authors

SYShimako YamamotoRutgers, The State University of New Jersey HTHiroyuki TsutsuiHeart Failure & Transplant HTHirofumi TagawaNara Institute of Science and Technology

Discussion

Member takes

Overview

Should not change HF practice; hypothesis-generating for NOS inhibition restoring beta-adrenergic responsiveness in failing myocytes.

Structured PICO

Population

Myocytes isolated from 11 dogs with rapid pacing-induced heart failure (ejection fraction, 29 +/- 2%) and 8 control dogs (ejection fraction, 74 +/- 3%).

Intervention

NOS inhibitor (N pi-nitro-L-arginine methyl ester [L-NAME], 0.1 nmol/L) plus isoproterenol (ISO; 1 nmol/L)

Comparator

Baseline, isoproterenol alone, and L-NAME alone

Outcome

Sarcomere shortening velocity as an index of contractilitysurrogate

Main Result

Absolute Event Rate: 140.6% vs 107.1%

p-value: p=< .05

In a canine model of heart failure, nitric oxide synthase inhibition augmented the inotropic response to beta-adrenergic stimulation, suggesting myocyte NO contributes to beta-adrenergic hyporesponsiveness.

Cite This Study

Yamamoto et al. (1997) studied Heart failure (n=19). NOS inhibitor (L-NAME) vs. Isoproterenol alone was evaluated on Inotropic response to isoproterenol (increase in sarcomere shortening velocity from baseline) (p=< .05). Inhibition of nitric oxide synthase with L-NAME significantly augmented the inotropic response to isoproterenol in failing myocytes (140.6% vs 107.1% increase; P<0.05) but not in control myocytes.

synapsesocial.com/papers/6a14f5fa9ff8b2b0e129e02c https://doi.org/10.1161/01.cir.95.5.1111

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March 4, 1997Circulation

Role of Myocyte Nitric Oxide in β-Adrenergic Hyporesponsiveness in Heart Failure

View Full Paper

Ask AI

Bookmark

Key result

Inhibition of nitric oxide synthase with L-NAME significantly augmented the inotropic response to isoproterenol in failing myocytes (140.6% vs 107.1% increase; P<0.05) but not in control myocytes.

Population

Myocytes isolated from 11 dogs with rapid pacing-induced heart failure and 8 control dogs.

Comparison

NOS inhibitor plus isoproterenol vs Baseline, isoproterenol alone, and L-NAME alone

Design

Preclinical

Authors

SYShimako YamamotoRutgers, The State University of New Jersey HTHiroyuki TsutsuiHeart Failure & Transplant HTHirofumi TagawaNara Institute of Science and Technology

Discussion

Member takes

Overview

Should not change HF practice; hypothesis-generating for NOS inhibition restoring beta-adrenergic responsiveness in failing myocytes.

Structured PICO

Population

Myocytes isolated from 11 dogs with rapid pacing-induced heart failure (ejection fraction, 29 +/- 2%) and 8 control dogs (ejection fraction, 74 +/- 3%).

Intervention

NOS inhibitor (N pi-nitro-L-arginine methyl ester [L-NAME], 0.1 nmol/L) plus isoproterenol (ISO; 1 nmol/L)

Comparator

Baseline, isoproterenol alone, and L-NAME alone

Outcome

Sarcomere shortening velocity as an index of contractilitysurrogate

Main Result

Absolute Event Rate: 140.6% vs 107.1%

p-value: p=< .05

Cite This Study

synapsesocial.com/papers/6a14f5fa9ff8b2b0e129e02c https://doi.org/10.1161/01.cir.95.5.1111

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