Effects of changes in pH and P-CO2 on wall tension in isolated rat intrapulmonary arteries

We examined mean (+/- S.E.M.) changes in wall tension in isolated rat intra pulmonary arteries on switching from control conditions (pH 7.38 +/- 0.01; P-CO2, 34.4 +/- 0.5 mmHg) to hypercapnia acidosis (pH change, -0.24 +/- 0.0 1; P-CO2 change, +27.5+/-0.9 mmHg), isohydric hypercapnia (pH change, -0.02 +/- 0.01; P-CO2 change +28.5 +/- 0.8 mmHg) and normocopnic acidosis (pH ch ange, -0.24 +/- 0.01; P-CO2 change, -0.5 +/- 0.3). Arteries were submaximal ly preconstricted with prostaglandin F-2 alpha and changes in tension are e xpressed as a percentage of the 80 mM KCl- induced contraction (%P-o). Mean changes in wall tension on switching to hypercapnic acidosis (+4.4 +/- 3.7 %P-o), isohydric hypercapnia (+1.9 + 2.2 %P-o) and normocapnic acidosis (- 1.5 +/- 1.9%P-o) were not significantly different from the change observed on switching to control conditions (+3.5 +/- 1.1 %P-o), and were unaltered by endothelial removal. In isolated carotid preparations, the change in ten sion in isohydric hypercapnia (-6.8 +/- 7.1 %P-o,) was not significantly di fferent from that observed in control switches (+ 8.6 +/- 3.2 %P-o). Signif icant reductions in tension (P < 0.001) were observed in hypercapnic (-42.9 +/- 7.8 %P-o,) and normocapnic acidosis (-36.4 +/- 9.0 % P-o). These data suggest that intrapulmonary arteries are resistant to the vasodilator effec ts of extracellular acidosis observed in systemic (carotid) vessels.