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Adenosine and hypoxic pulmonary vasodilation.

J E Gottlieb, M D Peake, J T Sylvester

The American Journal of Physiology

|October 1, 1984

Summary

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Adenosine does not mediate hypoxic pulmonary vasodilation. Studies on isolated ferret lungs showed that adenosine deaminase, an enzyme that inactivates adenosine, did not affect hypoxic vasodilation, suggesting adenosine is not the mediator.

Area of Science:

Pulmonary Physiology
Cardiovascular Research
Hypoxia Studies

Background:

Isolated lungs exhibit vasoconstriction then dilation after hypoxic exposure (inspired O2 tension < 25 Torr).
Adenosine is a known vasodilator in systemic circulation and its lung concentration increases with hypoxia.
Previous research suggests adenosine may mediate hypoxic pulmonary vasodilation.

Purpose of the Study:

To test the hypothesis that adenosine mediates hypoxic pulmonary vasodilation.
To investigate the role of endogenous adenosine in the pulmonary vascular response to hypoxia.

Main Methods:

Isolated adult male ferret lungs were perfused with autologous blood.
Adenosine's vasodilatory effect was confirmed.
Adenosine deaminase (ADase) was added to the perfusate to inactivate adenosine during hypoxic exposure (inspiratory PO2 of 18 or 0 Torr).

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Main Results:

ADase treatment did not alter the time course of pulmonary arterial pressure during hypoxia compared to untreated lungs.
ADase prevented exogenous adenosine-induced vasodilation when vessels were pre-constricted, confirming enzyme activity in lung interstitium.
Hypoxic pulmonary vasodilation occurred even in the presence of active ADase.

Conclusions:

Adenosine is not the mediator of hypoxic pulmonary vasodilation in isolated ferret lungs.
The results suggest that endogenous adenosine, if released during hypoxia, is not responsible for the observed vasodilation, unless protected from ADase.