Abstract
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.
| Identifer | oai:union.ndltd.org:oulo.fi/oai:oulu.fi:isbn951-42-6401-0 |
| Date | 10 May 2001 |
| Creators | Spalding, M. (Michael) |
| Publisher | University of Oulu |
| Source Sets | University of Oulu |
| Language | English |
| Detected Language | English |
| Type | info:eu-repo/semantics/doctoralThesis, info:eu-repo/semantics/publishedVersion |
| Format | application/pdf |
| Rights | info:eu-repo/semantics/openAccess, © University of Oulu, 2001 |
| Relation | info:eu-repo/semantics/altIdentifier/pissn/0355-3221, info:eu-repo/semantics/altIdentifier/eissn/1796-2234 |
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