Effects of vasopressin on right ventricular function in an experimental model of acute pulmonary hypertension*
| Autor: | Noor Berends, Patrick Wouters, Eugene Vandermeersch, Patrick Segers, H. A. Leather |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Vasopressin
Hypertension Pulmonary Ventricular Dysfunction Right Critical Care and Intensive Care Medicine Phenylephrine Dogs medicine.artery medicine Animals Vasoconstrictor Agents Prospective Studies Analysis of Variance business.industry Hemodynamics Stroke Volume medicine.disease Pulmonary hypertension Arginine Vasopressin Preload medicine.anatomical_structure Ventricle Anesthesia Shock (circulatory) Acute Disease Pulmonary artery Ventricular pressure Vascular resistance Vascular Resistance medicine.symptom business |
| Zdroj: | Critical Care Medicine. 30:2548-2552 |
| ISSN: | 0090-3493 |
| DOI: | 10.1097/00003246-200211000-00024 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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