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J Am Coll Cardiol, 2001; 37:601-607
© 2001 by the American College of Cardiology Foundation
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Acute ethanol exposure fails to elicit preconditioning-like protection in in situ rabbit hearts because of its continued presence during ischemia

Maike Krenz, MD*, Christopher P. Baines, PhD*, Xi-Ming Yang, MD*, Gerd Heusch, MD, FACC, FESC* {ddagger}, Michael V. Cohen, MD, FACC* {dagger} and James M. Downey, PhD*

* Department of Physiology, University of South Alabama, Mobile, Alabama, USA
{dagger} Department of Medicine, University of South Alabama, Mobile, Alabama, USA
{ddagger} Department of Pathophysiology, University of Essen Medical School, Essen, Germany



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Figure 1 Experimental protocols in in situ preparations (part A). Timing of the different interventions is shown in relation to the index ischemia. IPC = ischemic preconditioning.

 


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Figure 2 Experimental protocols in the in vitro and hybrid preparations (parts B and C). Timing of the different interventions is shown in relation to the index ischemia.

 


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Figure 3 Effect of ethanol (E) on infarct size in the in situ preparation (part A). Open symbols, individual experiments; closed symbols, group means ± SEM. If the 10-min ethanol infusion were started 20 min prior to ischemia, infarct size was not affected. In contrast, a 10-min infusion of 0.35 g/kg ethanol started 1 h prior to ischemia significantly reduced infarct size in comparison to control. *p < 0.05 vs. Control.

 


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Figure 4 Effects of ethanol (E) alone or with staurosporine (S) + genistein (G) on infarct size in the in situ preparation (part A). Open symbols, individual experiments; closed symbols, group means ± SEM. Combining genistein and staurosporine did not affect infarct size either in the absence or presence of ethanol.

 


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Figure 5 Effects of ethanol (E), ischemic preconditioning (IPC), and diazoxide (D) on infarct size in the in situ preparation (part A). Open symbols, individual experiments; closed symbols, group means ± SEM. Ethanol abolished the reduction in infarct size induced by either IPC or diazoxide. *p < 0.05 vs. Control.

 


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Figure 6 Effects of ethanol (E) on infarct size in the in vitro preparation (part B). Open symbols, individual experiments; closed symbols, group means ± SEM. Ten, 20, and 50 mmol/liter ethanol reduced infarct size when washed out prior to ischemia, whereas protection was lost when ethanol (10 or 50 mmol/liter) was continued throughout ischemia. *p < 0.05 vs. Control.

 


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Figure 7 Effects of ethanol infusion in the open-chest rabbit followed by an ischemic insult in the Langendorff mode (hybrid preparation, part C). Open symbols, individual experiments; closed symbols, group means ± SEM. Ethanol exposure before excision of the hearts did confer protection as compared to hearts removed from untreated rabbits.

 




 
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