Dietary coenzyme Q(10) supplement renders swine hearts resistant to ischemia-reperfusion injury

Citation
N. Maulik et al., Dietary coenzyme Q(10) supplement renders swine hearts resistant to ischemia-reperfusion injury, AM J P-HEAR, 278(4), 2000, pp. H1084-H1090
Citations number
36
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
278
Issue
4
Year of publication
2000
Pages
H1084 - H1090
Database
ISI
SICI code
0363-6135(200004)278:4<H1084:DCQSRS>2.0.ZU;2-N
Abstract
To examine whether nutritional supplementation of coenzyme Q(10) (CoQ(10)) can reduce myocardial ischemia-reperfusion injury, a group of swine was fed a regular diet supplemented with CoQ(10) (5 mg kg(-1).day(-1)) for 30 days . Another group of pigs that were fed a regular diet supplemented with plac ebo served as a control. After 30 days, isolated in situ pig hearts were pr epared and hearts were perfused with a cardiopulmonary pump system. Each he art was subjected to 15 min of regional ischemia by snaring of the left ant erior descending coronary artery, followed by 60 min of hypothermic cardiop legic global ischemia and 120 min of reperfusion. After the experiments wer e completed, myocardial infarct size was measured by triphenyltrazolium chl oride staining methods. Postischemic left ventricular contractile function was better recovered in the CoQ(10) group than in the control group of pigs . CoQ(10)-fed pigs revealed less myocardial infarction and less creatine ki nase release from the coronary effluent compared with control pigs. The exp erimental group also demonstrated a smaller amount of malonaldehyde in the coronary effluent and a higher content of the endogenous antioxidants ascor bate and thiol. Significant induction of the expression of ubiquitin mRNA w as also found in the hearts of the CoQ(10)-fed group. The results of this s tudy demonstrate that nutritional supplementation of CoQ(10) renders the he arts resistant to ischemia-reperfusion injury, probably by reducing the oxi dative stress.