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Influence of adenosine and prostacyclin on hypoxia‐induced pulmonary hypertension in the anaesthetized pig
Author(s) -
Öwall A.,
Davilén J.,
Sollevi A.
Publication year - 1991
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1991.tb03304.x
Subject(s) - medicine , hypoxia (environmental) , prostacyclin , vascular resistance , adenosine , pulmonary artery , cardiac output , vasodilation , pulmonary hypertension , anesthesia , hemodynamics , blood pressure , cardiology , oxygen , chemistry , organic chemistry
The effects of adenosine and prostacyclin (PGI 2 ) infusions on hypoxia‐induced pulmonary hypertension in the pulmonary and systemic circulatory systems of nine pigs were compared. The animals received the drugs in random order, and they were allowed to recover between each experimental sequence. Hypoxia was induced by reducing Fio 2 to 0.12–0.13 so as to result in an arterial Po 2 of approximately 6 kPa. Dose rates of adenosine or PGI 2 during hypoxia were individualized in order to achieve a maximal reduction of 15% in the mean arterial blood pressure. Adenosine and PGI 2 produced a fall in pulmonary vascular resistance of 36 ± 4% (s.e.mean P <0.01) and 37 ± 6% ( P <0.01), respectively. The mean pulmonary artery pressure was reduced by 19 ± 3% ( P <0.01) during adenosine infusion and by 36 ± 4% ( P <0.01) during PGI 2 infusion. The systemic haemodynamic responses to the two drugs were similar but adenosine produced a 7 ± 2% ( P <0.01) increase in cardiac output. Arterial Po 2 during hypoxia and vasodilator treatment did not differ from the hypoxic situation without drug infusion. It is concluded that adenosine and PGI 2 counteract hypoxia‐induced increases in pulmonary vascular resistance similarly, but the reduction in pulmonary artery pressure was greater with PGI 2 at infusion rates, causing minor systemic haemodynamic changes.