May 14, 2019Journal of Cardiothoracic SurgeryOpen Access

Ischemia time impacts on respiratory chain functions and Ca2+-handling of cardiac subsarcolemmal mitochondria subjected to ischemia reperfusion injury

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Why the study?

Despite cardioplegic arrest, ischemia reperfusion injury-associated cardiodepression is a major problem in heart surgery.

Population

Wistar rat hearts

Comparison

0, 15, 30, and 40 min of ischemia with 30 min of reperfusion

Design

Ex vivo Langendorff experiment

Follow-up

30 min of reperfusion

Authors

MLM. LeistnerUniversitätsklinikum Würzburg SSStefanie SommerHeart and Diabetes Center North Rhine-Westphalia PKPeer KanofskyUniversitätsklinikum Würzburg

Discussion

Member takes

Implication

Rat SSM changes with ischemia time suggest mitochondrial targets in surgical IR; leaves open translation to human cardioplegia.

Structured PICO

Population

Wistar rat hearts (cardiac subsarcolemmal mitochondria)

Intervention

Stop-flow induced warm global ischemia for 15, 30, or 40 minutes followed by 30 minutes of reperfusion using a pressure-controlled Langendorff system

Comparator

0 minutes of ischemia with 30 minutes of reperfusion (IR0/30)

Outcome

Respiratory chain (RC) function, inner membrane polarization, and Ca2+ homeostasis of cardiac subsarcolemmal mitochondriasurrogate

Increasing ischemia time progressively impairs respiratory chain function and calcium homeostasis in cardiac subsarcolemmal mitochondria, highlighting the need to minimize warm global ischemia during cardiac surgery.

Cite This Study

Leistner et al. (2019) studied this question.

synapsesocial.com/papers/6a90e8b58b76b10fb073cd94 https://doi.org/10.1186/s13019-019-0911-1

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