What question did this study set out to answer?

To evaluate whether heart failure enhances sensitivity to beta 2-adrenergic stimulation in canine cardiomyocytes and confirm functional beta 2-adrenergic receptors in failing human ventricular myocytes.

September 15, 1995Circulation

Response of Failing Canine and Human Heart Cells to β 2 -Adrenergic Stimulation

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Why the study?

Does beta-2-adrenergic stimulation with zinterol increase intracellular calcium transients in failing canine and human ventricular cardiomyocytes?

Population

Isolated ventricular cardiomyocytes from healthy dogs, dogs with tachypacing-induced heart failure, and…

Comparison

Zinterol administration during electric field… vs Healthy canine myocytes, or baseline without…

Design

Preclinical

Authors

RARuth A. AltschuldUniversity of Maryland, Baltimore RSRandall C. StarlingHeart Failure & Transplant RHRobert L. HamlinElectrophysiology

Discussion

Member takes

Implication

May support beta-2-mediated inotropy in failing myocytes; leaves open clinical translation from animal and ex vivo data.

Key Points

To evaluate whether heart failure enhances sensitivity to beta 2-adrenergic stimulation in canine cardiomyocytes and confirm functional beta 2-adrenergic receptors in failing human ventricular myocytes.
Isolated ventricular myocytes from healthy dogs, dogs with pacing-induced heart failure, and human transplant recipients were loaded with calcium indicators and electrically stimulated with the selective beta 2-agonist zinterol.
Measurements included intracellular calcium transients, isotonic twitches, L-type calcium currents via patch clamping, cAMP accumulation, and phospholamban phosphorylation.
Zinterol significantly increased intracellular calcium transient amplitudes across all groups, with failing canine myocytes exhibiting significantly greater sensitivity than control cells.
In healthy canine myocytes, zinterol elevated L-type calcium currents and twitch amplitudes, an effect fully blocked by the beta 2-antagonist ICI 118,551.
Zinterol did not induce detectable increases in cAMP production or phospholamban phosphorylation in either healthy or failing canine myocytes.

Structured PICO

Does beta-2-adrenergic stimulation with zinterol increase intracellular calcium transients in failing canine and human ventricular cardiomyocytes?

Population

Isolated ventricular cardiomyocytes from healthy dogs, dogs with tachypacing-induced heart failure, and failing human ventricles from transplant recipients

Intervention

Zinterol (highly selective beta-2-adrenergic agonist) administration during electric field stimulation

Comparator

Healthy canine myocytes, or baseline without zinterol

Outcome

[Ca2+]i transient amplitudessurrogate

Failing human and canine ventricular cardiomyocytes possess functional beta-2-adrenergic receptors that mediate positive inotropic responses independent of cAMP increases.

Cite This Study

Altschuld et al. (1995) studied this question.

synapsesocial.com/papers/6a7f22f8eadf0d493516c080 https://doi.org/10.1161/01.cir.92.6.1612

Topics

Heart failure HFrEF treatment

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Response of Failing Canine and Human Heart Cells to β 2 -Adrenergic Stimulation

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Response of Failing Canine and Human Heart Cells to β 2 -Adrenergic Stimulation

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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Topics

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