• M B Spalding, T I Ala-Kokko, K Kiviluoma, H Ruskoaho, and S Alahuhta.
• Department of Anesthesiology, Biocenter Oulu, University of Oulu, and University Hospital of Oulu, Finland. spami@sun3.oulu.fi
• J. Cardiovasc. Pharmacol. 2000 Jan 1;35(1):93-9.

AbstractThe use of a vasodilator selective to the pulmonary circulation may be beneficial in cases with right-ventricle failure, as it will decrease right-heart afterload without concurrent systemic hypotension. Adenosine has recently been advocated as such a drug, although its clinical efficacy in this respect is still in question. We therefore devised an experimental protocol of right-heart infarct to test the efficacy of adenosine in alleviating symptoms of right-heart failure. Right-heart infarct was induced experimentally in 17 young pigs. After hemodynamics had stabilized, preload was optimized with a dextrose-based colloid solution. A continuous infusion of adenosine was then begun at doses of 25, 50, 75, and 100 microg/kg/min in a study group of 10 animals, while the remaining seven were monitored as controls. Hemodynamic parameters were followed throughout the study, with particular attention paid to pulmonary and systemic vascular resistance indices (PVRI and SVRI), right ventricle ejection fraction (REF), cardiac index (CI), and heart rate (HR). Cardiac index (CI) showed a tendency to increase during the adenosine infusion, as did REF and stroke index (SI), whereas PVRI and mean pulmonary pressure (MPAP) were decreased. There was a marked decrease in SVRI as a result of the adenosine, as there was in mean arterial pressure at the higher infusion rates. HR remained unchanged by the infusion. Discontinuation of the drug resulted in a rapid increase in MAP, SVRI, MPAP, HR, left ventricle stroke work index (LVSWI), and PVRI and in a modest decrease in CI. The continuous infusion of adenosine appears to cause an effective arterial vasodilation, with a consequent unloading of right-heart afterload. Its use may be beneficial in the treatment of increased pulmonary vascular resistance after right-heart failure.

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