Mb. Spalding et al., The hemodynamic effects of adenosine infusion after experimental right heart infarct in young swine, J CARDIO PH, 35(1), 2000, pp. 93-99
Citations number
26
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
The use of a vasodilator selective to the pulmonary circulation may be bene
ficial in cases with right-ventricle failure, as it will decrease right-hea
rt afterload without concurrent systemic hypotension. Adenosine has recentl
y been advocated as such a drug, although its clinical efficacy in this res
pect is still in question. We therefore devised an experimental protocol of
right-heart infarct to test the efficacy of adenosine in alleviating sympt
oms 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 mu g/kg/min in a study group
of 10 animals, while the remaining seven were monitored as controls. Hemod
ynamic parameters were followed throughout the study, with particular atten
tion paid to pulmonary and systemic vascular resistance indices (PVRI and S
VRI), right ventricle ejection fraction (REF), cardiac index (CI), and hear
t rate (HR). Cardiac index (CI) showed a tendency to increase during the ad
enosine infusion, as did REF and stroke index (SI), whereas PVRI and mean p
ulmonary pressure (MPAP) were decreased. There was a marked decrease in SVR
I as a result of the adenosine, as there was in mean arterial pressure at t
he higher infusion rates. HR remained unchanged by the infusion. Discontinu
ation 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 arte
rial vasodilation, with a consequent unloading of right-heart afterload. It
s use may be beneficial in the treatment of increased pulmonary vascular re
sistance after right-heart failure.