No Direct Postconditioning Effect of Poloxamer 188 on Mitochondrial Function after Ischemia Reperfusion Injury in Rat Isolated Hearts

被引：5

作者：

Eskaf, Josephine ^{[1
,2
]}

Cleveland, William J. ^{[1
]}

Riess, Matthias L. ^{[1
,3
,4
]}

机构：

[1] Vanderbilt Univ, Med Ctr, Dept Anesthesiol, Nashville, TN 37232 USA

[2] Univ Med Greifswald, Dept Anesthesiol, D-17475 Greifswald, Germany

[3] Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37232 USA

[4] TVHS VA Med Ctr, Anesthesiol, Nashville, TN 37212 USA

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2021年 / 22卷 / 09期

关键词：

ATP synthesis; calcium retention capacity; cardiac; cardiac arrest; copolymer; mitochondria; myocardial infarction; oxygen consumption; P188; PEG; MEMBRANE PERMEABILIZATION; CARDIOVASCULAR-DISEASE; BLOCK-COPOLYMER; DAMAGE; CELL; TRANSITION; REDUCTION; F-68;

D O I：

10.3390/ijms22094879

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Myocardial infarction is a leading cause for morbidity and mortality worldwide. The only viable treatment for the ischemic insult is timely reperfusion, which further exacerbates myocardial injury. Maintaining mitochondrial function is crucial in preserving cardiomyocyte function in ischemia reperfusion (IR) injury. Poloxamer (P) 188 has been shown to improve cardiac IR injury by improving cellular and mitochondrial function. The aim of this study was to show if P188 postconditioning has direct protective effects on mitochondrial function in the heart. Langendorff prepared rat hearts were subjected to IR injury ex-vivo and reperfused for 10 min with 1 mM P188 vs. vehicle. Cardiac mitochondria were isolated with 1 mM P188 vs. 1 mM polyethylene glycol (PEG) vs. vehicle by differential centrifugation. Mitochondrial function was assessed by adenosine triphosphate synthesis, oxygen consumption, and calcium retention capacity. Mitochondrial function decreased significantly after ischemia and showed mild improvement with reperfusion. P188 did not improve mitochondrial function in the ex-vivo heart, and neither further P188 nor PEG induced direct mitochondrial protection after IR injury in this model.

引用

页数：21

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