Beta2-adrenergic activation via administration of atenolol/formoterol combination increases contractility and coronary blood flow in isolated rat hearts.
Commonly used adrenergic agonists in low cardiac output scenarios rely primarily on beta1adrenergic 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. 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. 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. 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.