Potential Deleterious Effect of β-Adrenergic Stimulation During Warm-Blood Cardioplegia in Rabbit Hearts.

We hypothesized that β-adrenergic stimulation with isoproterenol during continuous normothermic cardioplegic arrest would enhance the regenerative and regulatory function of the myocardium, resulting in improved cardiac function. We studied isolated rabbit hearts paced at ~200 beats per minute (bpm) and perfused by a support rabbit. We measured ventricular pressure over a range of ventricular volumes to determine maximal elastance (E[sub max]) at baseline and 20 and 45 min after discontinuation of cardioplegia. Myocardial oxygen consumption (MVO[sub 2]) measurements were performed simultaneously and during cardioplegic arrest. Hearts were prospectively randomized to receive either isoproterenol at 0.1 M or control in blinded fashion for 10 min during a 1-h continuous warm-blood cardioplegic arrest. Compared to control hearts, isoproterenol-treated hearts had trends toward longer time to first spontaneous heartbeat (control 141 ± 43 vs. isoproterenol 200 ± 74 s, p = .07), and longer time to capture of atrial pacing (control 214 ± 52 vs. isoproterenol 288 ± 91 s, p = .06). There was no difference observed in the MVO[sub 2] between isoproterenol-treated and control groups of hearts. MVO[sub 2] decreased during cardioplegia (p < .01), but there was no significant change in MVO[sub 2] during isoproterenol infusion during cardioplegic arrest. There was a significant reduction in E[sub max] compared to baseline 20 min after discontinuation of cardioplegic arrest in both groups (control 7.3 ± 1.7 mm Hg/μL vs. 9.0 ± 1.7 mm Hg/μL, p = .02, isoproterenol-treated 6.8 ± 2.8 mm Hg/μL vs. 8.2 ± 2.6 mm Hg/μL, p = .01, respectively), with recovery of E[sub max] by 45 min in control hearts only. We conclude that exposure of hearts to isoproterenol during warm cardioplegic arrest has a deleterious effect that may be mediated through mechanisms independent of increased myocardial oxygen consumption. [ABSTRACT FROM AUTHOR]