Endogenously released adenosine causes pulmonary vasodilation during the acute phase of pulmonary embolization in dogs.

Background: Endogenous adenosine levels increase under stress in various organs. Exogenously administered adenosine is a well-known pulmonary vasodilator. However, the physiology and therapeutic potential of endogenous adenosine during alteration in pulmonary hemodynamics such as pulmonary embolism is not elucidated. We hypothesized that the adenosine level increases following an acute elevation of pulmonary resistance, resulting in pulmonary vasodilation.

Methods: We induced acute pulmonary embolization by injecting plastic beads in anesthetized dogs. Plasma adenosine levels, defined as the product of plasma adenosine concentration and simultaneous cardiac output, were assessed from blood samples from the superior vena cava, main pulmonary artery (MPA), and ascending aorta 1 and 10 min following injection. Hemodynamics were assessed with ( = 3) and without ( = 8) administration of the adenosine receptor blocker, 8-(-sulfophenyl)theophylline (8SPT).

Results: Mean pulmonary arterial pressure (PAP) increased from 11 ± 1 mmHg, peaking at 28 ± 4 mmHg at 52 ± 13 s after injection. During this period, total pulmonary resistance (TPR) elevated from 11 ± 1 to 33 ± 6 Wood unit. Plasma adenosine levels increased in the MPA from 14.5 ± 2 to 38.8 ± 7 nmol/min 1 min after injection. TPR showed greater elevation under 8SPT treatment, to 96 ± 12 Wood unit at PAP peak.

Conclusions: Endogenously released adenosine after acute pulmonary embolization is one of the initial pulmonary vasodilators. The immediate surge in plasma adenosine levels in the MPA could lead to a hypothesis that adenosine is released by the right heart in response to pressure overload.