Effects of cardiac sympathetic nerve stimulation during adrenergic blockade on infarct size in anesthetized dogs

β-Adrenergic blockade has been shown to limit myocardial infarct size (IS) in anesthetized dogs. The objective of the present study was to determine whether sympathetic activation in the presence of β-adrenergic blockade would alter IS. Chloralose-anesthetized dogs were divided into five groups. Ail hearts were neurally decentralized and paced at 150 beats/min. The circumflex coronary artery was ligated distal to the first major branch. Group 1 (n = 5) had no treatment. Group 2 (n = 6) received timolol (0.2 mg/kg) intravenously before and throughout occlusion. Group 3 (n = 7) under-went left stellate stimulation (LSS; 8 Hz, 5 ms, 7-10 V) immediately following coronary artery occlusion and for the duration of occlusion. Group 4 (n = 5) received timolol in addition to LSS. Group 5 animais (n = 6) received prazosin (0.5 mg/kg i.v.) and timolol before circumflex occlusion and LSS following coronary artery occlusion. After 6 h, Evans blue dye was injected into the left atrium while the circumflex artery distal to the ligation was simultaneously perfused with saline. Hearts were rapidly excised, and the left ventricle was sliced and photographed. IS was determined and expressed as a percentage of the area at risk by planimetry. The following mean ± SEM values were measured: Group 1, 23.5 ± 5.3; Group 2, 34.2 ± 1.4; Group 3, 31.4 ± 7.8; Group 4, 59.3 ± 3.9; and Group 5, 25.6 ± 5.3%. Significant differences were found between Group 4 and ail other groups (p < 0.05). The data show that (a) without neural input, β-blockade did not limit IS following circumflex occlusion, (b) LSS during β-blockade increased IS, and (c) combined α- and β-blockade during LSS resulted in a significantly smaller IS compared with control values. Thus, with augmented levels of sympathetic input, α-receptors can play an important role in IS development following coronary artery occlusion, particularly when α-adrenergic vasoconstrictor effects are unopposed by β-receptor stimulation.