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November 1, 1995European Heart Journal18 citations

Functional and ultrastructural alterations of canine myocardium subjected to very brief coronary occlusions

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FPFrancisco PomarJCJuan CosínMPManuel Portolés

Key Points

  • To evaluate the impact of brief, repeated coronary artery occlusions and reperfusions on regional myocardial contractile function and subendocardial ultrastructure.
  • Conducted an open-chest experiment in 23 anesthetized dogs subjected to twenty 2-minute complete occlusions of the left anterior descending coronary artery, separated by 3-minute reperfusion intervals.

Structured PICO

Do very brief and recurrent coronary occlusions reduce regional systolic function and alter ultrastructure in a canine model?

P
Population
23 anaesthetized dogs with open thorax
I
Intervention
Twenty 2-minute total occlusions in the left anterior descending coronary artery, with 3-minute recovery intervals (reperfusion) between occlusions
C
Comparator
Control (non-ischaemic) myocardial segment
O
Outcome
Myocardial regional shortening fraction and ultrastructural changes (mitochondrial volume and damage)surrogate

Very brief, recurrent coronary occlusions induce prolonged regional systolic dysfunction and mitochondrial damage in a canine model, suggesting a mechanism for ischemic dysfunction without infarction.

Abstract

The effects of very brief and recurrent coronary occlusions on myocardial regional shortening and its ultrastructure have been analysed. Ultrasonic crystals were implanted in the left ventricular subendocardium of 23 anaesthetized dogs with the thorax open, to measure the shortening fractions of an ischaemic and a control segment. Twenty 2 min total occlusions were provoked in the left anterior descending coronary artery, with 3 min recovery intervals (reperfusion) between occlusions. The shortening fraction decreased progressively with each occlusion, reaching a value 18.9% lower than the basal after the last ischaemic episode (P < 0.05); 32.3% after 4 h of reperfusion (P < 0.01), and 28.6% after 24 h (P < 0.01). Qualitative and quantitative ultrastructural analysis showed an increase in the mitochondrial volume of the ischaemic tissue (158% vs control, P < 0.001) with significant damage to the cell components (7.7-fold increases vs control mitochondria). These results show that when the myocardium is subjected to very brief and repeated coronary occlusions, there is progressive deterioration of systolic function with structural alterations, mainly at the mitochondrial level. These modifications are still observable 24 h after the end of ischaemic stimulation and could be the cause of transitory and/or chronic systolic dysfunctions in the absence of previous heart attack.

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Cite This Study

Pomar et al. (1995) studied this question.

synapsesocial.com/papers/6a912cff69f7e599b311f8achttps://doi.org/10.1093/oxfordjournals.eurheartj.a060768
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