Assessment of Cardiac Function by Echocardiography in Conscious and Anesthetized Mice

Abstract

In this study, the authors sought to evaluate the mechanisms responsible for echocardiographically determined differences in cardiac structure and function between conscious and anesthetized mice to determine whether such differences were more or less evident in diseased states. Cardiac parameters were determined by transthoracic echocardiography. Mice anesthetized with a mixture of ketamine and xylazine showed reductions in heart rate (HR, 252 +/- 16 beats/min versus 734 +/- 9 beats/min) and fractional shortening (FS, 35% +/- 2% versus 59% +/- 2%) compared with conscious mice. Conscious mice responded little to the beta-agonist isoproterenol or atropine, but showed profound reductions in HR and FS in response to the beta(1)-antagonist atenolol. In contrast, both isoproterenol and atropine led to increases in HR and FS in anesthetized mice. The stress in conscious animals was reduced by the sedative midazolam, leading to partial restoration of responses to isoproterenol. Mice with constitutive activation of the beta-adrenergic system, due to cardiac overexpression of beta(2)-adrenergic receptors or with heart disease (myocardial infarct and pressure-overload hypertrophy) showed few differences in functional parameters between conscious and anesthetized states, attributable to pre-existing activation of the sympathetic and beta-adrenergic systems, even during anesthesia. The results indicate that the autonomic nervous system plays a critical role in the observed differences in cardiac structure and function between anesthetized and conscious mice.

Preserved left ventricular structure and function in mice with cardiac sympathetic hyperinnervation

“…The present findings of intact functional responses to isoproterenol in TG mice in vivo by catheter and by echocardiography strongly indicate intact ␤-AR signaling in the left ventricles of TG mice. Because there is strong evidence that the response to sympathoadrenergic stimulation is largely mediated by ␤ 1 -ARs (2,8,38), these results indicate that enhanced NGF activity leading to sympathetic hyperinnervation is not associated with ␤-AR dysfunction, a finding that Fig. 4.…”

“…In vivo heart function and chamber dimensions were assessed with two-dimensional targeted M-mode echocardiography while mice were under light anesthesia (6 mg/100 g ketamine, 1.5 mg/100 g xylazine, and 0.045 mg/100 g atropine ip) using a Hewlett-Packard Sonos 5500 ultrasonograph with a 15-MHz linear array as described previously (38). Measurements of left ventricular (LV) end-diastolic dimension (EDD), end-systolic dimension (ESD), and wall thickness at end diastole were made from captured freeze frames of M-mode images by applying the leading-edge convention of the American Society of Echocardiography.…”

Impact of Anesthesia on Echocardiographic Evaluation of Systolic and Diastolic Function in Rats

“…Therefore the choice of anesthetic agent has the potential to significantly alter echocardiographic parameters. Despite the reported differential effects of anesthetic agents on cardiac function and echocardiograms in mice ( [18][19][20][21][22][23][24][25] ) , much less is known about the impact of the choice of the anesthetic agent on the echocardiogram of sedated healthy or sick rats, especially if the animals suffer from a cardiac disease that is significantly affecting pre-load and afterload. Therefore the present study was performed to assess the differential impact of two types of anesthetic regimens (intraperitoneal ketamine-xylazine or inhaled isoflurane) on basic echocardiographic measurements 1) in healthy male adult rats and 2) in rats suffering from chronic aortic valve regurgitation (AR).…”

Preferable Anesthetic Conditions for Echocardiographic Determination of Murine Cardiac Function

“…In the measurement of cardiac function in experimental animals, various anesthetic agents such as pentobarbital (1,11), urethane (12 -14), and ketamine (1,5,6,10,13,15) have been employed to induce sedation and immobility. Apparently, the anesthetic agents directly and indirectly affect cardiac performance and hemodynamics (5,11,15).…”