The hemodynamic effects of aminophylline, adenosine, losartan and nitric oxide administered shortly after right heart infarct in a porcine model
1University of Oulu, Faculty of Medicine, Department of Anaesthesiology
|Online Access:||PDF Full Text (PDF, 1.3 MB)|
|Persistent link:|| http://urn.fi/urn:isbn:9514264010
|Publish Date:|| 2001-05-10
|Thesis type:||Doctoral Dissertation
|Defence Note:||Academic Dissertation to be presented with the assent of the Faculty of Medicine, University of Oulu, for public discussion in the Auditorium 7 of the University Hospital of Oulu, on August 17th, 2001, at 2 p.m.
Docent Raimo Kettunen
Docent Juhani Rämö
Right heart failure may be caused by several etiologic factors such as pulmonary embolism, post coronary bypass, chronic obstructive pulmonary disease (COPD) and right heart infarction. Traditionally, treatment has consisted of fluid loading (volume expansion) and the use of inotropic agents. In the present series of studies, an experimental model of acute right heart failure was developed using right heart infarct. Treatment with drugs chosen to specifically improve right heart performance was then evaluated. The drugs used in this series were aminophlline, adenosine, nitric oxide (NO) and losartan.
Aminophylline transiently improved cardiac index and pulmonary vascular resistance, but simultaneously caused an increase in heart rate and a decrease in stroke volume. Although it may reduce right heart afterload, aminophylline did not improve overall cardiac function in this experimental model of right heart infarction.
Adenosine affected an increase in cardiac index during the adenosine infusion and in stroke index, while pulmonary vascular resistance and mean pulmonary pressure were decreased. There was a marked decrease in systemic vascular resistance as a result of the drug. Heart rate remained unchanged by the infusion. Discontinuation of the drug resulted in a rapid reversal of the hemodynamic changes. The continuous infusion of adenosine therefore appears to cause an effective arterial vasodilation, with a consequent unloading of right heart afterload.
NO treatment significantly reduced right heart afterload. A significant deterioration was observed in cardiac output as well as in left and right ventricle stroke work indices. The use of NO in this model of right heart infarct affected a decrease in both right heart afterload and left heart preload, with an overall deterioration in global hemodynamics.
Losartan was shown to decrease central venous pressure and wedge pressure, while cardiac output, left ventricle stroke work and stroke volume all showed improvement. Compared to the control animals, pulmonary vascular resistance, systemic vascular resistance and systemic pressures were unaffected by the drug, as was heart rate. An inhibition of angiotensin II action may therefore be of benefit in the treatment of right heart failure symptoms during the first hours after right heart infarct.
Acta Universitatis Ouluensis. D, Medica
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