Cardiac output in mice overexpressing beta2-adrenoceptors or with myocardial infarct

1. The aims of the present study were to characterize cardiac output (CO) in transgenic mice that overexpress the beta2-adrenoceptor and to evaluate ultrasonic flowmetery for continuous CO measurement in the mouse in vivo. 2. Under conditions of anaesthesia, open chest and positive ventilation, CO was determined with a transonic flowmeter at baseline and during dobutamine administration and intravenous volume loading in wild-type mice (n = 17) and beta2-adrenoceptor transgenic (n = 9) and wild-type mice with chronic myocardial infarct (n = 16). 3. Compared with wild-type mice, beta2-adrenoceptor transgenic mice with markedly enhanced ventricular contractility had a significantly higher CO, heart rate (HR) and maximal acceleration of aortic flow. Both dobutamine and volume loading increased CO in the two groups and higher levels of CO were measured in transgenic mice during the interventions. At baseline or during interventions, stroke volume was similar between beta2-adrenoceptor transgenic and wild-type mice. Infarcted mice with impaired cardiac function had a significantly lower CO under basal and stress conditions. 4. Thus, beta2-adrenoceptor transgenic mice revealed higher CO that was largely attributable to a significantly higher HR but not to an increase in stroke volume. Transonic flowmetery can detect differences in CO among mice in various functional states and is suitable for evaluation of cardiac functional reserve in mice in vivo by continuous monitoring of CO responses to different interventions.