Lung Microvascular Pressure Profile in Acute Lung Injury.

Abstract

To clarify the role of microvessels in the development of pulmonary hypertension of acute lung injury, we induced lung edema by oleic acid (OA) in ten artificially perfused cat lungs and measured microvascular pressure. Pulmonary artery pressure (Ppa) and pressure of 30-50 microns arteriole (Parteriole) increased from 19.2 +/- 1.4 and 15.7 +/- 1.0 cmH2O before to 30.5 +/- 5.0 cmH2O and 22.7 +/- 2.4 cmH2O after edema, respectively. Pressure of 30-50 microns venule (Pvenule) and venous occlusion pressure (Pvo) did not change significantly after edema. Double occlusion pressure (Pdo) which represents pulmonary microvascular pressure increased from 14.5 +/- 0.6 to 17.7 +/- 2.0 cmH2O. Pressure gradient in the artery, i.e., between Ppa and Parteriole and in the microvessels, i.e., between Parteriole and Pvenule increased when lung became edematous. Pressure gradient in vein, i.e., between Pvenule to left atrium was not affected by edema. Pdo was in the midst of Parteriole and Pvenule in both edematous and non-edematous lung. In acute lung injury, increase of microvascular resistance was followed by an increase of arterial resistance and caused pulmonary hypertension.

Feline pulmonary hypertension: are we overlooking an important comorbidity?

“…There are numerous experimental studies in which cats are used as a model for PH. In one study designed to assess the role of microvascular pressure in the development of PH, 68 oleic acid was used to induce acute lung injury in artificially perfused feline lungs. The authors demonstrated that in this model of acute lung injury an increase in microvascular resistance was followed by an increase in the arterial resistance and PAH.…”