Effects of Hypercapnia on Steady State, Phenylephrine-Induced Tension in Isolated Rings of Rat Pulmonary Artery

Abstract

One of the primary functions of the lung is the exchange of oxygen and carbon dioxide with the environment. In order for this task to be carried out, matching of regional blood flow to ventilation is essential. To achieve this matching, the pulmonary vasculature has developed functional properties, which are significantly different from those of the systemic circulation. The best known of these is hypoxic pulmonary vasoconstriction; the response of systemic vessels to a reduction in PO₂ is dilatation (Fishman, 1985). Standard teaching suggests that a second specialization seen in the pulmonary circulation is a vasoconstrictor response to hypercapnic acidosis (Barnes & Liu, 1995). However, review of the original literature reveals much disagreement on this issue. Acidosis has been variably reported as potentiating (Rudolph & Yuan, 1966), inhibiting (Marshall et al, 1984), or having no effect on HPV (Housley et al, 1970). Alkalosis has been found to leave HPV unaffected (Silove et al, 1968) to reduce (Marshall et al, 1984) or to enhance it (Gordon et al, 1993). Brimioulle et al (1979) have suggested that elevation of PCO₂ exerts a pH independent vasodilator effect on the pulmonary circulation. This finding is similar to the vasodilator effect of CO₂ reported in systemic arteries (Carr et al, 1993) but contrasts with the enhanced contraction seen in other smooth muscle preparations in these circumstances (Liston et al, 1991).