Beta2-adrenergic activation via administration of atenolol/formoterol combination increases contractility and coronary blood flow in isolated rat hearts.

Introduction: Commonly used adrenergic agonists in low cardiac output scenarios rely primarily on beta1-adrenergic activation to stimulate cardiac function. Little is known about the use of beta2-adrenergic agonist administration for this purpose, although the associated vasodilation may be beneficial. This study was conducted in order to assess the efficacy of one such beta2-adrenergic agonist, formoterol, in augmenting cardiac function. Methods: The hearts of 8 anesthetized female Wistar rats were excised, and subsequently kept functional in an isolated heart preparation (Langendorff apparatus). After placement on the apparatus, hearts were subjected to the beta1-blocker, atenolol, and then to a combination of formoterol/atenolol. Left ventricular developed pressure (LVDP), heart rate (HR), and coronary flow (CF) were monitored. Results: CF showed a median increase of 16% (p<0.05) after formoterol/atenolol administration, with this effect lasting 20 min post-administration. Furthermore, statistically significant differences included an early 26% increase in LVDP and a late 21% increase in HR. The CF increase was independent of HR and LVDP changes. Conclusions: Our results indicate that the beta2-agonist formoterol not only successfully increases heart rate and contractility, but also increases coronary flow, most likely by means of beta2-mediated coronary vasodilation. This pharmacological profile may prove to be especially beneficial in situations where cardiac output must be increased, while adequate myocardial oxygen delivery needs to be maintained.