Da. Fullerton et al., ADENOSINE EFFECTIVELY CONTROLS PULMONARY-HYPERTENSION AFTER CARDIAC OPERATIONS, The Annals of thoracic surgery, 61(4), 1996, pp. 1118-1123
Background. Pulmonary hypertension secondary to increased pulmonary va
scular resistance may greatly complicate the perioperative management
of patients having cardiac operations. Adenosine may have a therapeuti
c role as a selective pulmonary vasodilator. The purpose of this study
was to examine the pulmonary hemodynamic effects of a central venous
infusion of adenosine in cardiac operative patients with pulmonary hyp
ertension. Methods. Ten cardiac patients with pulmonary hypertension (
age, 62 +/- 6 years) were studied in the operating room under general
anesthesia after weaning from cardiopulmonary bypass. Cardiac output,
pulmonary vascular resistance, systemic vascular resistance, mean pulm
onary arterial pressure, and mean systemic arterial pressure were dete
rmined before, during, and after central venous infusion of adenosine
(50 mu g . kg(-1). min(-1)) for 15 minutes. Statistical analysis was b
y analysis of variance, and significance was accepted at p < 0.05. Res
ults. Adenosine produced significant pulmonary vasodilation. Mean pulm
onary arterial pressure was lowered from 36 +/- 1 to 28 +/- 2 mm Hg (p
< 0.05), and pulmonary vascular resistance was lowered from 560 +/- 3
0 to 260 +/- 30 dynes . s . cm(-5) (p < 0.05) during adenosine adminis
tration. At the same time, cardiac output rose from 4.0 +/- 0.6 to 6.2
L/min (p < 0.05). Pulmonary vascular resistance, mean pulmonary arter
ial pressure, and cardiac output returned to baseline after the adenos
ine infusion was stopped. There was no change in systemic mean arteria
l pressure during adenosine infusion. Conclusions. Adenosine may be us
ed clinically as a selective pulmonary vasodilating agent to optimize
pulmonary hemodynamic indices without adverse systemic hemodynamic eff
ects in patients with pulmonary hypertension having cardiac operations
. It may be particularly valuable in patients with right heart dysfunc
tion by selectively lowering right ventricular afterload.