Chronic Ethanol-induced Myocardial Protection Requires Activation of Mitochondrial KATPChannels

Zhu, Peili; Zhou, Hui-Zhong; Gray, Mary O.

doi:10.1006/jmcc.2000.1233

Cited by 35 publications

(24 citation statements)

References 14 publications

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“…Canine (31) and rodent (25,26,47) models confirm the benefits observed in human studies and they exhibit sustained cardioprotection for 10 mo or longer (47) with continued oral administration of alcohol. Chronic ethanol (EtOH) feeding of guinea pigs (27) upregulates protein kinase C (PKC)⑀, a signal transduction molecule required for the cardioprotective effects of acute ischemic preconditioning (38).…”

supporting

confidence: 62%

“…Chronic ethanol (EtOH) feeding of guinea pigs (27) upregulates protein kinase C (PKC)⑀, a signal transduction molecule required for the cardioprotective effects of acute ischemic preconditioning (38). EtOH activates ATP-sensitive K ϩ channels, putative end effectors of cardioprotection (31,47). Therefore, animal models of moderate alcohol consumption may be useful for identification of novel therapeutic targets for sustained protection against coronary heart disease in humans.…”

mentioning

confidence: 99%

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Moderate alcohol consumption induces sustained cardiac protection by activating PKC-ε and Akt

Zhou

Karliner

Gray

2002

American Journal of Physiology-Heart and Circulatory Physiology

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C57BL/6 mice were fed 18% ethanol (vol/vol) in drinking water for 12 wk. Isovolumic hearts were subjected to 20 min of ischemia and 30 min of reperfusion on a Langendorff apparatus. There were no differences in baseline hemodynamic function between hearts from ethanol (EtOH)-fed mice and controls. However, prior alcohol consumption doubled recovery of left ventricular developed pressure (68 ± 8 vs. 33 ± 8 mmHg for controls; n = 10, P < 0.05) and reduced creatine kinase release by half (0.26 ± 0.04 vs. 0.51 ± 0.08 U · min−1 · g wet wt−1 for controls; n = 10, P < 0.05). EtOH feeding doubled expression of activated protein kinase C epsilon (PKC)ε ( n = 6, P < 0.05); whereas PKC inhibition blocked protection during ischemia-reperfusion. EtOH feeding also increased expression of Akt three- to fivefold ( n = 6, P < 0.05), whereas PKC inhibition prevented increases in Akt kinase activity. We conclude that signaling pathways involving PKC-ε are critical for sustained EtOH-mediated cardioprotection and that Akt may be a downstream effector of resistance to myocardial reperfusion injury.

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confidence: 62%

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confidence: 99%

Moderate alcohol consumption induces sustained cardiac protection by activating PKC-ε and Akt

Zhou

Karliner

Gray

2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…Animal studies support these observations by demonstrating that sustained oral administration of low doses of ethanol provides protection against ischemia-reperfusion injury (60). Similarly, acute exposure of isolated cardiomyocytes and isolated hearts to physiological levels of ethanol also provides protection against ischemic damage (4).…”

mentioning

confidence: 86%

“…In experimental systems, cardiac apoptosis has been associated with ischemia and reperfusion injury (7,14), hypertrophy (54), aging (23,30), vascular wall remodeling (41), and TNF-␣ exposure (27). Intracellular accumulation of lipid within the heart is also associated with cardiomyopathy and increased cardiomyocyte apoptosis (60). Clinically high levels of circulating fatty acids are seen acutely after myocardial ischemia (35,40).…”

mentioning

confidence: 99%

Attenuation of fatty acid-induced apoptosis by low-dose alcohol in neonatal rat cardiomyocytes

Sparagna¹,

Jones²,

Hickson-Bick³

2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…For example, in vivo experiments in the brain indicate that ethanol pretreatment attenuates cerebral I/R injury (27). It has also been reported that both acute and chronic ethanol consumption prevent I/R injury in the heart (17,23,39). Given the inconsistency in the I/R responses to ethanol pretreatment among different tissues, we chose to systematically examine the effects of both low-and high-dose ethanol consumption on the hepatic microvascular and inflammatory responses to gut I/R.…”

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confidence: 99%

Ethanol modulates gut ischemia/reperfusion-induced liver injury in rats

Yamagishi

Horie

Kato

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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Whereas both ethanol and gut ischemia/reperfusion (I/R) are known to alter hepatic microvascular function, little is known about the influence of ethanol consumption on the hepatic microvascular responses to I/R. The objective of this study was to determine whether acute ethanol administration exacerbates the hepatic microvascular dysfunction induced by gut I/R. Rats were exposed to gut ischemia for 30 min followed by reperfusion. Intravital videomicroscopy was used to monitor leukocyte recruitment and the number of nonperfused sinusoids (NPS). Plasma alanine aminotransferase (ALT), tumor necrosis factor-α (TNF-α), and endotoxin concentrations were monitored. In separate experiments, ethanol was administered 15 min or 24 h before gut ischemia. In control rats, gut I/R increased the number of stationary leukocytes and NPS. It also elevated the plasma ALT, TNF-α, and endotoxin with a corresponding increase in intestinal mucosal permeability. Low-dose ethanol consumption 15 min before gut ischemia blunted the gut I/R-induced leukostasis and elevations in plasma TNF-α and ALT. However, high-dose ethanol consumption aggravated the gut I/R-induced increases in leukostasis and increases in plasma endotoxin and ALT. When ethanol was administered 24 h before, high-dose ethanol aggravated the gut I/R-induced hepatocellular injury, but low-dose ethanol did not have any effects on it. These results suggest that low-dose ethanol consumption shortly before gut ischemia attenuates the hepatic inflammatory responses, microvascular dysfunction, and hepatocellular injury elicited by gut I/R, whereas high-dose ethanol consumption appears to significantly aggravate these gut I/R-induced responses.

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Chronic Ethanol-induced Myocardial Protection Requires Activation of Mitochondrial KATPChannels

Cited by 35 publications

References 14 publications

Moderate alcohol consumption induces sustained cardiac protection by activating PKC-ε and Akt

Moderate alcohol consumption induces sustained cardiac protection by activating PKC-ε and Akt

Attenuation of fatty acid-induced apoptosis by low-dose alcohol in neonatal rat cardiomyocytes

Ethanol modulates gut ischemia/reperfusion-induced liver injury in rats

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