Table 1.

Protection against reperfusion injury following chronic ethanol exposure: Effect of adenosine A₁ receptor antagonism

	Preischemia		Reperfusion
	Control	Ethanol	Control	Ethanol
Developed pressure, mmHg	112 ± 4	116 ± 3	35 ± 3*	60 ± 2*†
Diastolic pressure, mmHg	10 ± 0	10 ± 0	46 ± 4*	22 ± 2*†
Perfusion pressure, mmHg	70 ± 0	70 ± 0	75 ± 1*	75 ± 1*
Coronary flow, ml/min	36 ± 1	35 ± 1	25 ± 1*	24 ± 2*
(+)DPCPX
Developed pressure, mmHg	118 ± 4	113 ± 3	35 ± 6*	31 ± 4*‡
Diastolic pressure, mmHg	10 ± 0	10 ± 0	48 ± 6*	47 ± 5*‡
Perfusion pressure, mmHg	70 ± 0	70 ± 0	77 ± 1*	77 ± 1*
Coronary flow, ml/min	36 ± 1	34 ± 1	25 ± 1*	24 ± 2*

Isolated guinea pig hearts were subjected to 45 min of global ischemia and 48 min of reperfusion. Hearts from guinea pigs exposed to 10% ethanol in their drinking water for 6 weeks were compared to hearts from age-matched controls. Experiments were carried out in the presence and absence of the adenosine A₁ receptor antagonist, (+)DPCPX, (n = 10 for all groups). Data are presented as mean ± SEM. 

^*P < 0.05 versus preischemia value;  

^†P < 0.05 ethanol versus control value;  

^‡P < 0.05 (+)DPCPX versus (−)DPCPX value.