Xamoterol recruits an inotropic reserve in the acutely failing, reperfused canine myocardium without detrimental effects on its subsequent recovery.

The present study tested (1) whether xamoterol recruits an inotropic reserve in reperfused myocardium and (2) whether acute inotropic stimulation by xamoterol has deleterious consequences on the long-term recovery of the reperfused myocardium. Sixteen anaesthetized, open-chest dogs were bilaterally vagotomized and heart rate kept constant by left atrial pacing. The distal left circumflex coronary artery was occluded for 15 min and then reperfused for 8 h. The coronary occlusion resulted in regional myocardial dyskinesia and myocardial function remained severely depressed after release of the occlusion. At 10 min reperfusion, 8 dogs received xamoterol (100 micrograms/kg i.v.), whereas the remaining 8 dogs served as controls and received saline. Xamoterol increased mean systolic wall thickening velocity (from 1.47 +/- 2.34 (SD) mm/s at 10 min reperfusion to 7.13 +/- 3.55 mm/s at 30 min reperfusion and 7.64 +/- 2.48 mm/s at 1 h reperfusion, respectively, both P less than 0.05). In the control group, only a slow recovery of mean systolic wall thickening velocity was observed (from 3.14 +/- 3.30 mm/s to 2.96 +/- 3.74 mm/s and 4.03 +/- 3.00 mm/s at 10 min, 30 min, and 1 h reperfusion, respectively). At 8 h reperfusion, mean systolic wall thickening velocity was similar in both groups (7.97 +/- 4.23 mm/s in the xamoterol-group and 6.87 +/- 4.00 mm/s in the placebo-group). Histological examination revealed no difference in the extent of necrosis between the two groups after 8 h reperfusion. We conclude that (1) xamoterol recruits an inotropic reserve in reperfused myocardium, and (2) this recruitment of an inotropic reserve does not compromise functional recovery and structural integrity of the reperfused myocardium.