What question did this study set out to answer?

To determine whether dysfunctional coronary vascular endothelium alters the contractile characteristics of adjacent myocardium and whether these effects parallel or add to endocardial endothelial dysfunction.

April 1, 1993Circulation Research

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

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Population

Rabbit hearts (n = 54) mounted in a Langendorff preparation

Comparison

Triton X-100 injected as a bolus into the… vs Control Langendorff-perfused hearts and control…

Design

Preclinical

Authors

KLK LiMontreal Heart Institute JRJ L RouleauUniversité de Sherbrooke LALuc AndriesCentre National de la Recherche Scientifique

Discussion

Member takes

Implication

May impair myocardial contractility in endothelial dysfunction; extends endocardial observations in animals but leaves open human translation.

Key Points

To determine whether dysfunctional coronary vascular endothelium alters the contractile characteristics of adjacent myocardium and whether these effects parallel or add to endocardial endothelial dysfunction.
Rabbit hearts (n = 54) were excised and mounted on a Langendorff perfusion apparatus, with vascular endothelial dysfunction induced in one group via an intracoronary bolus of Triton X-100.
Endothelial dysfunction was verified by loss of acetylcholine-mediated vasodilation while preserving smooth muscle responsiveness to nitroprusside, compared against control perfused hearts and non-perfused controls (n = 18).
Right ventricular papillary muscles were subsequently excised from all groups to quantify myocardial mechanics, including twitch duration, total tension, dT/dt, and maximum shortening velocity (Vmax).
Coronary perfusion rate increased from 8.9 ± 0.4 to 11.0 ± 0.3 ml/g/min in response to acetylcholine in control hearts (p < 0.01), but this vasodilatory response was abolished in Triton X-100-treated hearts.
Papillary muscles from Triton X-100-perfused hearts showed significantly shorter twitch duration (363 ± 16 vs. 449 ± 9 msec, p < 0.01) and decreased total tension (2.2 ± 0.2 vs. 2.9 ± 0.2 g/mm², p < 0.01) compared with perfused controls.
Vascular endothelial dysfunction significantly decreased dT/dt (9 ± 1 vs. 12 ± 1 g/mm²/sec, p < 0.05) and Vmax (0.89 ± 0.06 vs. 1.14 ± 0.07 Lmax/sec, p < 0.05), matching the mechanical impairments observed after endocardial endothelial removal.

Structured PICO

Population

Rabbit hearts (n = 54) mounted in a Langendorff preparation

Intervention

Triton X-100 injected as a bolus into the coronaries to render the vascular endothelium dysfunctional

Comparator

Control Langendorff-perfused hearts and control hearts without Langendorff perfusion

Outcome

Myocardial mechanical characteristics (twitch duration, total tension, dT/dt, and maximum velocity of unloaded muscle shortening)surrogate

Vascular endothelial dysfunction alters myocardial contractile characteristics similarly to endocardial endothelial removal in isolated rabbit hearts.

Cite This Study

Li et al. (1993) studied this question.

synapsesocial.com/papers/6a766eec3da069e66cbd30fb https://doi.org/10.1161/01.res.72.4.768

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Implication

May impair myocardial contractility in endothelial dysfunction; extends endocardial observations in animals but leaves open human translation.

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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