Erschienen in:
05.11.2016 | Original Article
Assessment of dexmedetomidine effects on left ventricular function using pressure–volume loops in rats
verfasst von:
Kyuho Lee, Hye Jeong Hwang, Ok Soo Kim, Young Jun Oh
Erschienen in:
Journal of Anesthesia
|
Ausgabe 1/2017
Einloggen, um Zugang zu erhalten
Abstract
Purpose
The role of dexmedetomidine on left ventricular function is ambiguous. We analyzed pressure–volume loops to investigate whether dexmedetomidine has a myocardial depressive effect.
Methods
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.
Results
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.
Conclusion
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.