In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 277, No. 5 ( 1999-11-01), p. H1708-H1717
Abstract:
Although protein kinase C (PKC) plays a pivotal role in ischemic preconditioning, it is not clear what the end effector is that protects the myocardium. In isolated, paced (1.25 Hz, 36–37°C) adult rat cardiomyocytes, the effects of PKC preactivation by diacylglycerol on cell motion, intracellular Ca 2+ concentration ([Ca 2+ ] i ; indo 1), and intracellular pH (pH i ; seminaphthorhodafluor-1) during simulated ischemia-reperfusion (I/R) were investigated. The degree of reperfusion-induced contracture was significantly attenuated in the myocytes pretreated with 10 μM 1,2-dioctanoyl- sn-glycerol (DOG; n = 19) compared with the untreated myocytes ( n = 23, P 〈 0.02). There were no differences in twitch amplitude, end-diastolic [Ca 2+ ] i , or peak-systolic [Ca 2+ ] i during I/R between the DOG-pretreated and untreated myocytes. Although there were no differences in pH i during ischemia, the pH i overshoot during reperfusion was significantly delayed in the DOG-pretreated myocytes compared with the untreated myocytes ( n = 17 for each, P 〈 0.01). Chelerythrine completely abolished the favorable effects of DOG on the reperfusion-induced contracture and the pH i overshoot. These data suggest that diacylglycerol attenuates I/R injury in isolated, paced cardiomyocytes, which may be related to the slower pH i overshoot during reperfusion.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.1999.277.5.H1708
Language:
English
Publisher:
American Physiological Society
Publication Date:
1999
detail.hit.zdb_id:
1477308-9
SSG:
12
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