Journal of Applied Physiology, Vol 58, Issue 4 1107-1114, Copyright © 1985 by American Physiological Society
Reversal of reflex pulmonary vasoconstriction induced by main pulmonary arterial distension
C. E. Juratsch, R. F. Grover, C. E. Rose, J. T. Reeves, W. F. Walby and M. M. Laks
Distension of the main pulmonary artery (MPA) induces pulmonary
hypertension, most probably by neurogenic reflex pulmonary
vasoconstriction, although constriction of the pulmonary vessels has not
actually been demonstrated. In previous studies in dogs with increased
pulmonary vascular resistance produced by airway hypoxia, exogenous
arachidonic acid has led to the production of pulmonary vasodilator
prostaglandins. Hence, in the present study, we investigated the effect of
arachidonic acid in seven intact anesthetized dogs after pulmonary vascular
resistance was increased by MPA distention. After steady-state pulmonary
hypertension was established, arachidonic acid (1.0 mg/min) was infused
into the right ventricle for 16 min; 15-20 min later a 16-mg bolus of
arachidonic acid was injected. MPA distension was maintained throughout the
study. Although the infusion of arachidonic acid significantly lowered the
elevated pulmonary vascular resistance induced by MPA distension, the
pulmonary vascular resistance returned to control levels only after the
bolus injection of arachidonic acid. Notably, the bolus injection caused a
biphasic response which first increased the pulmonary vascular resistance
transiently before lowering it to control levels. In dogs with resting
levels of pulmonary vascular resistance, administration of arachidonic acid
in the same manner did not alter the pulmonary vascular resistance. It is
concluded that MPA distension does indeed cause reflex pulmonary
vasoconstriction which can be reversed by vasodilator metabolites of
arachidonic acid. Even though this reflex may help maintain high pulmonary
vascular resistance in the fetus, its function in the adult is obscure.
