Assessment of dexmedetomidine effects on left ventricular function using pressure-volume loops in rats

The role of dexmedetomidine on left ventricular function is ambiguous. We analyzed pressure-volume loops to investigate whether dexmedetomidine has a myocardial depressive effect.

Thirty-two Sprague-Dawley rats were anesthetized and a pressure-volume loop catheter was advanced into the left ventricle. Rats were divided into four groups (n = 8 each). The control group received a 10-min infusion of 0.1 ml of normal saline, and the other three groups received 1.0 (Dex1.0 group) , 2.5 (Dex2.5 group), and 5.0 μg/kg (Dex5.0 group) dexmedetomidine in a similar fashion to the control group. Steady-state hemodynamic parameters were recorded. The inferior vena cava was occluded intermittently to assess preload-independent indices.

Compared with the control group, changes in the Dex1.0 group were insignificant. In the Dex2.5 group, only the systolic blood pressure was higher (vs control, P = 0.03), and other parameters were insignificant. The Dex5.0 group exhibited a lower heart rate, higher systolic blood pressure, higher arterial elastance (vs control, all P < 0.001), and unaltered cardiac output. The Dex5.0 group showed steeper slopes of end-systolic pressure increment and end-systolic pressure-volume relationship than the control, Dex1.0, and Dex2.5 groups (all P < 0.001). Slopes of end-diastolic pressure decrement and end-diastolic pressure-volume relationship did not differ among groups.

Dexmedetomidine had no direct myocardial depressant effect in the rat heart in doses that are similar to those encountered under clinical conditions. Dexmedetomidine did not significantly alter the ability of the heart to cope with bradycardia and greatly increased afterload. Their potentially negative impact on cardiac output was effectively attenuated by improved myocardial contractility and preserved diastolic function in healthy subjects.