What question did this study set out to answer?

To assess how varying durations of myocardial ischemia followed by reperfusion affect cholinergic vasodilator and alpha-adrenergic vasoconstrictor responses in coronary vessels.

February 1, 1995AJP Heart and Circulatory Physiology

Cholinergic and alpha-adrenergic coronary vasomotion [corrected] with increasing ischemia-reperfusion injury

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Why the study?

Does increasing duration of ischemia-reperfusion injury alter cholinergic and alpha-adrenergic coronary vasomotion in an open-chest dog model?

Population

30 open-chest dogs

Comparison

Left circumflex coronary artery occlusion for 15… vs 15 minutes versus 60 minutes of occlusion…

Design

Preclinical

Authors

TEThomas EhringLMU Klinikum MKMladen KrajcarZabok General Hospital DBDietrich BaumgartMayo Clinic

Discussion

Member takes

Implication

Impaired cholinergic coronary vasodilation after prolonged ischemia in dogs; leaves open selective endothelial effects and clinical translation to human reperfusion injury.

Key Points

To assess how varying durations of myocardial ischemia followed by reperfusion affect cholinergic vasodilator and alpha-adrenergic vasoconstrictor responses in coronary vessels.
In 30 open-chest dogs, the left circumflex coronary artery was occluded for either 15 minutes or 60 minutes prior to reperfusion.
Responses to intracoronary acetylcholine, the alpha-1 agonist methoxamine, and the alpha-2 agonist BHT-933 were measured (n = 10 per group).
Triphenyltetrazolium chloride (TTC) staining was employed in the 60-minute occlusion group to identify reversibly (TTC+) versus irreversibly (TTC-) injured myocardial layers.
Vasodilation to acetylcholine remained intact after 15 minutes of ischemia but was significantly attenuated after 60 minutes in TTC+ subendocardium and midmyocardium, suffering further loss across all layers in TTC- myocardium.
Vasoconstrictor responses to methoxamine and BHT-933 were unaffected after both 15-minute and 60-minute occlusions across all myocardial tissue layers.
Posterior wall thickening was unaltered by the administration of acetylcholine, methoxamine, or BHT-933 under all experimental conditions.

Structured PICO

Does increasing duration of ischemia-reperfusion injury alter cholinergic and alpha-adrenergic coronary vasomotion in an open-chest dog model?

Population

30 open-chest dogs

Intervention

Left circumflex coronary artery occlusion for 15 or 60 minutes followed by reperfusion, with intracoronary administration of acetylcholine, methoxamine, or BHT-933 (n=10 each)

Comparator

15 minutes versus 60 minutes of occlusion; reversibly (TTC+) versus irreversibly (TTC-) injured myocardium

Outcome

Coronary vasomotor responses (vasodilator response to acetylcholine and vasoconstrictor responses to methoxamine and BHT-933)surrogate

Increasing ischemia-reperfusion injury impairs cholinergic coronary vasodilation but does not enhance alpha-adrenergic vasoconstriction in a canine model.

Cite This Study

Ehring et al. (1995) studied this question.

synapsesocial.com/papers/6a90e925fae915895c360f6c https://doi.org/10.1152/ajpheart.1995.268.2.h886

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Implication

Impaired cholinergic coronary vasodilation after prolonged ischemia in dogs; leaves open selective endothelial effects and clinical translation to human reperfusion injury.

Cholinergic and alpha-adrenergic coronary vasomotion [corrected] with increasing ischemia-reperfusion injury

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Cholinergic and alpha-adrenergic coronary vasomotion [corrected] with increasing ischemia-reperfusion injury

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider