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Am J Physiol Heart Circ Physiol 281: H1575-H1582, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 4, H1575-H1582, October 2001

Na+/H+ exchange subtype 1 inhibition reduces endothelial dysfunction in vessels from stunned myocardium

J. David Symons1 and Saul Schaefer1,2

1 Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis 95616; and 2 Sacramento Veterans Administration Medical Center, Sacramento, California 95655

Myocardial ischemia and reperfusion cause myocyte and vascular dysfunction, frequently termed "stunning." We hypothesized that inhibiting the Na+/H+ exchanger subtype 1 isoform (NHE1) during ischemia and reperfusion limits myocardial and coronary microvascular stunning. Anesthetized rats completed 2 × 10-min coronary artery occlusions separated by 5-min of reperfusion, followed by 15 or 60 min of reperfusion. Vehicle (saline) or the NHE1 inhibitor cariporide (HOE-642) was administered 15 min before ischemia and was continued throughout each protocol. After reperfusion, hearts were excised, and the reactivity of resistance arteries (internal diameter, ~120 µm) was assessed. The first derivative of left ventricular (LV) pressure, LV developed pressure, and LV systolic wall thickening were depressed (P < 0.05) similarly in vehicle- and cariporide-treated rats during ischemia and after 15 or 60 min of reperfusion compared with sham-operated animals that were not exposed to ischemia (i.e., controls). In vessels obtained after 15 min of reperfusion, the maximal response to acetylcholine-induced relaxation (10-8-10-4 M) was blunted (P < 0.05) in vessels from vehicle- (~35%) and cariporide-treated rats (~55%) compared with controls (~85%). However, the percent relaxation to acetylcholine was greater (P < 0.05) in cariporide-treated rats compared with vehicle-treated rats. Maximal contractile responses to endothelin-1 (10-11-10-7 M) were increased (P < 0.05) similarly in vehicle- and cariporide-treated rats compared with controls. Relaxation to sodium nitroprusside (10-4 M) was not different among groups. Results were similar in vessels obtained from animals after 60 min of reperfusion. These findings suggest that NHE1 inhibition before coronary occlusion lessens ischemia-induced microvascular dysfunction for 15-60 min after reperfusion but does not alter myocardial contractile function in the area at risk.

coronary resistance vessels; myocardial function; endothelium; vascular smooth muscle; acetylcholine; myocardial ischemia; myocardial stunning


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