What question did this study set out to answer?

To determine whether functional alterations in the endocardial or vascular endothelium contribute to myocardial contractile depression following ischemia-reperfusion.

January 1, 1998Canadian Journal of Physiology and Pharmacology

Vascular endothelial dysfunction contributes to myocardial depression in ischemia-reperfusion in the rat

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Population

62 perfused rat hearts as Langendorff preparations

Comparison

Intracoronary Triton X100 injection, ischemia… vs No intervention (normal controls)

Design

Preclinical, Randomized to four groups

Authors

XQX L QiMontreal Heart Institute TNT L Nguyen LALuc AndriesCentre National de la Recherche Scientifique

Discussion

Member takes

Implication

Vascular endothelial dysfunction may contribute to ischemia-reperfusion myocardial depression; hypothesis-generating in this rat model and should not yet change practice.

Key Points

To determine whether functional alterations in the endocardial or vascular endothelium contribute to myocardial contractile depression following ischemia-reperfusion.
Randomized 62 Langendorff-perfused rat hearts into four groups: control, intracoronary Triton X-100 injection, 30-minute ischemia with 20-minute reperfusion, and ischemia-reperfusion followed by Triton X-100.
Assessed coronary endothelial reactivity using serotonin, vascular smooth muscle reactivity using sodium nitroprusside, and tissue injury via effluent creatine phosphokinase and morphology.
Measured isolated papillary muscle twitch tension and duration across extracellular calcium concentrations (0.7 to 7.0 mM) before and after endocardial endothelial removal.
Intracoronary Triton X-100 abolished serotonin-mediated vasodilation and reduced papillary muscle total tension compared to controls (4.0 vs. 4.6 g/mm², p << 0.01), a deficit corrected by increasing calcium to 3.25 mM.
Ischemia-reperfusion elevated creatine phosphokinase and caused persistent contractile depression, yet both ischemia-reperfusion and Triton X-100 groups showed a similar augmented calcium responsiveness (35% to 38% tension increase vs. 25% in controls).
Endocardial endothelial removal elicited identical contractile alterations across all groups, confirming that vascular, rather than endocardial, endothelial dysfunction mediates post-ischemic myocardial depression.

Structured PICO

Population

62 perfused rat hearts as Langendorff preparations

Intervention

Intracoronary Triton X100 injection, ischemia (30 min) - reperfusion (20 min), or ischemia-reperfusion followed by intracoronary Triton X100 injection

Comparator

No intervention (normal controls)

Outcome

Contractile characteristics (total tension and contraction duration) of excised papillary muscles at varying extracellular calcium concentrationssurrogate

Vascular, but not endocardial, endothelial dysfunction contributes to myocardial depression during ischemia-reperfusion injury in a rat model.

Cite This Study

Qi et al. (1998) studied this question.

synapsesocial.com/papers/6a766eec3da069e66cbd30f8 https://doi.org/10.1139/y97-185

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Implication

Vascular endothelial dysfunction may contribute to ischemia-reperfusion myocardial depression; hypothesis-generating in this rat model and should not yet change practice.

Vascular endothelial dysfunction contributes to myocardial depression in ischemia-reperfusion in the rat

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Vascular endothelial dysfunction contributes to myocardial depression in ischemia-reperfusion in the rat

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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