caa a22 4500 477061850 CHVBK 20180405111403.0 cr unu---uuuuu 170330e19960901xx s 000 0 eng 10.1007/BF00181659 doi (NATIONALLICENCE)springer-10.1007/BF00181659 Acute ethanol does not protect against ischemic/ reperfusion injury in rabbit myocardium [Elektronische Daten] [Stephen Bellows, Sharon Hale, Robert Kloner] Moderate use of alcohol has shown protective effects in coronary artery disease, while excessive use has been associated with cardiomyopathy and hypertension. Since alcohol is a vasodilator, we postulated that it might have protective effects when administered acutely in the setting of ischemia/reperfusion. Therefore, we studied the acute effects of alcohol on myocardial infarction in a rabbit model. Anesthetized, open chest rabbits were subjected to a 30 minute coronary artery occlusion followed by 4 hours of reperfusion. Rabbits were randomized to a control group (n = 20), receiving an infusion of 10 ml normal saline, intravenously, over 10 minutes via a Harvard pump, or an alcohol group (n = 20), receiving a diluted solution of 100% ethanol (1 ml/kg diluted in normal saline to 10 ml total solution) infused in a similar fashion. This infusion regimen resulted in an average blood alcohol level of 110 mg/dl (range 77-129) tested in five rabbits within the study. Ten minutes after infusion, a marginal branch of the circumflex artery was occluded. Regional myocardial blood flow during coronary occlusion and reperfusion was measured using radioactive microspheres. Myocardial ischemic area at risk (AR) was assessed by blue dye injection and myocardial necrosis (AN) by triphenyltetrazolium chloride (TTC) staining. The mean regional coronary blood flow in ischemic tissue was 0.04 ± 0.01 ml/min/g in the control group versus 0.03 ± 0.01 ml/min/g in the experimental group (p = NS) and averaged 1.74 ml/min/g (control) to 1.98 ml/min/g (alcohol) in the nonischemic tissue. All rabbits received comparable ischemic insult: Collateral blood flow and AR were similar in both groups. An overall analysis showed no significant reduction in infarct size (expressed as the percent of necrotic tissue within the area at risk) in the alcohol group (23 ± 3%) compared with the control group (27 ± 4%). In conclusion, alcohol did not reduce infarct size in the rabbit model. Kluwer Academic Publishers, 1996 alcohol nationallicence myocardial infarction nationallicence myocardial infarct size nationallicence Bellows Stephen Heart Institute, Good Samaritan Hospital, Los Angeles, California aut Hale Sharon Heart Institute, Good Samaritan Hospital, Los Angeles, California aut Kloner Robert Section of Cardiology, University of Southern California, Los Angeles, California aut Journal of Thrombosis and Thrombolysis Kluwer Academic Publishers 3/3(1996-09-01), 181-184 0929-5305 3:3<181 1996 3 11239 https://doi.org/10.1007/BF00181659 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00181659 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Bellows Stephen Heart Institute, Good Samaritan Hospital, Los Angeles, California aut NATIONALLICENCE 700 1- Hale Sharon Heart Institute, Good Samaritan Hospital, Los Angeles, California aut NATIONALLICENCE 700 1- Kloner Robert Section of Cardiology, University of Southern California, Los Angeles, California aut NATIONALLICENCE 773 0- Journal of Thrombosis and Thrombolysis Kluwer Academic Publishers 3/3(1996-09-01), 181-184 0929-5305 3:3<181 1996 3 11239 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer