Arginine vasopressin caused a 31% decrease in right ventricular contractility, whereas contractility was preserved with phenylephrine, in a canine model of acute pulmonary hypertension.
Does arginine vasopressin improve right ventricular function compared to phenylephrine in an experimental model of acute pulmonary hypertension?
Arginine vasopressin exerts a negative inotropic effect on the right ventricle and causes pulmonary vasoconstriction in an experimental model of acute pulmonary hypertension, suggesting caution in its use when RV function is compromised.
OBJECTIVE: Arginine vasopressin is a promising systemic vasopressor in settings such as vasodilatory shock and cardiopulmonary resuscitation. The evidence that arginine vasopressin may also have a pulmonary vasodilatory effect makes it an attractive drug for the treatment of circulatory shock secondary to right ventricular failure and pulmonary hypertension. In the present study, we evaluated the effects of arginine vasopressin on right ventricular function and ventriculovascular coupling in the setting of moderate acute pulmonary hypertension and compared these effects with those of phenylephrine. DESIGN: Prospective laboratory investigation using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: Seven adult beagle dogs weighing 8-14 kg. INTERVENTIONS: After acute instrumentation to measure right ventricular pressure and volume with the conductance technique and pulmonary artery flow and pressure with high-fidelity transducers, the stable thromboxane analogue U46619 was infused continuously to obtain stable pulmonary hypertension. Phenylephrine and arginine vasopressin were administered consecutively in continuous infusions at doses titrated to achieve a 25% increase in aortic pressure. MEASUREMENTS AND MAIN RESULTS: Phenylephrine and arginine vasopressin both increased total pulmonary vascular resistance and arterial elastance without influencing characteristic impedance. Both drugs decreased cardiac output and stroke volume. Right ventricular hydraulic power output was reduced by arginine vasopressin but not by phenylephrine. Most importantly, arginine vasopressin caused a 31% decrease in right ventricular contractility measured as the slope of the preload recruitable stroke work relationship, whereas contractility was preserved during phenylephrine infusion. CONCLUSIONS: In the present model, arginine vasopressin causes pulmonary vascular constriction and exerts an important negative inotropic effect on the right ventricle. These findings suggest that one should be cautious in the use of arginine vasopressin when right ventricular function is compromised.
Leather et al. (Fri,) conducted a other in Acute pulmonary hypertension (n=7). Arginine vasopressin vs. Phenylephrine was evaluated on Right ventricular contractility measured as the slope of the preload recruitable stroke work relationship. Arginine vasopressin caused a 31% decrease in right ventricular contractility, whereas contractility was preserved with phenylephrine, in a canine model of acute pulmonary hypertension.
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