Cardiac output in mice overexpressing beta(2)-adrenoceptors or with myocardial infarct

1. The aims of the present study were to characterize cardiac output (CO) i n transgenic mice that overexpress the beta (2)-adrenoceptor and to evaluat e 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 dobutamin e administration and intravenous volume loading in wild-type mice (n = 17) and beta (2)-adrenoceptor transgenic (n = 9) and wild-type mice with chroni c myocardial infarct (n = 16). 3. Compared with wild-type mice, beta (2)-adrenoceptor transgenic mice with markedly enhanced ventricular contractility had a significantly higher CO, heart rate (HR) and maximal acceleration of aortic flow. Both dobutamine a nd volume loading increased CO in the two groups and higher levels of CO we re measured in transgenic mice during the interventions. At baseline or dur ing interventions, stroke volume was similar between beta (2)-adrenoceptor transgenic and wild-type mice. Infarcted mice with impaired cardiac functio n had a significantly lower CO under basal and stress conditions. 4. Thus, beta (2)-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 mic e in various functional states and is suitable for evaluation of cardiac fu nctional reserve in mice in vivo by continuous monitoring of CO responses t o different interventions.