Hemodynamic effects of prolonged hyperoxia.
Experimental studies have consistently demonstrated the development of perivascular edema in the dog lung following prolonged exposure to 95% oxygen. This pathological change has been thought to result from capillary injury, but a direct effect secondary to left ventricular dysfunction has not yet been excluded. To evaluate the latter possibility, ten trained, awake dogs were prepared with monitoring of right and left atrial, systemic and pulmonary artery pressures, cardiac output, and mixed venous and arterial blood gases. Animals were exposed to an F1O2 greater than 0.95 for 48-70 hours. Radioactive 8-10 mu microspheres (141Ce, 51Cr, 85Sr, 46Sc) were injected into the left atrium at zero, six, 24, and 48 hours. PaO2 was 480 +/- 10 mm Hg during exposure, and the pulmonary shunt fraction increased from 11.3% to 16.9% (p less than 0.0001) during 70 hours. Left atrial pressure fell from 9 +/- 2 mm Hg to 3 +/- 3 mm Hg (p less than 0.0001), but cardiac output was constant at 2.7 +/- 0.1 l/min. Pulmonary arteriolar resistance increased from 183 +/- 20 dynes-sec-CM-5 to 791 +/- 30 at 70 hours (p less than 0.0001). Histologic sections of the lungs demonstrated the characteristic perivascular edema. Of particular interest was the fact that myocardial perfusion was significantly increased to all three layers of the ventricular wall at 24 and 48 hours. These data indicate that perivascular edema developing after exposure to high concentrations of oxygen is secondary to pulmonary capillary endothelial damage with no evidence that myocardial dysfunction occurs during this period.
Hemodynamic effects of prolonged hyperoxia. Experimental studies have consistently demonstrated the development of perivascular edema in the dog lung following prolonged exposure to 95% oxygen. This pathological change has been thought to result from capillary injury, but a direct effect secondary to left ventricular dysfunction has not yet been excluded. To evaluate the latter possibility, ten trained, awake dogs were prepared with monitoring of right and left atrial, systemic and pulmonary artery pressures, cardiac output, and mixed venous and arterial blood gases. Animals were exposed to an F1O2 greater than 0.95 for 48-70 hours. Radioactive 8-10 mu microspheres (141Ce, 51Cr, 85Sr, 46Sc) were injected into the left atrium at zero, six, 24, and 48 hours. PaO2 was 480 +/- 10 mm Hg during exposure, and the pulmonary shunt fraction increased from 11.3% to 16.9% (p less than 0.0001) during 70 hours. Left atrial pressure fell from 9 +/- 2 mm Hg to 3 +/- 3 mm Hg (p less than 0.0001), but cardiac output was constant at 2.7 +/- 0.1 l/min. Pulmonary arteriolar resistance increased from 183 +/- 20 dynes-sec-CM-5 to 791 +/- 30 at 70 hours (p less than 0.0001). Histologic sections of the lungs demonstrated the characteristic perivascular edema. Of particular interest was the fact that myocardial perfusion was significantly increased to all three layers of the ventricular wall at 24 and 48 hours. These data indicate that perivascular edema developing after exposure to high concentrations of oxygen is secondary to pulmonary capillary endothelial damage with no evidence that myocardial dysfunction occurs during this period.