Jon F. Moran

Surgical treatment of acute ascending aortic dissection.

Since adopting a policy of immediate operation on patients with acute dissection of the ascending aorta, 42 men and 6 women (ages 18–67 years) have been managed surgically. Thirty-two patients had graft replacement of the ascending aorta and resuspension of the incompetent aortic valve. One of these had a coronary graft. There were five deaths in this group. Eight patients required aortic valve replacement because of a diseased aortic valve as well as grafting of the ascending aorta, with one death. Three patients had resuspension of the aortk valve and primary repair of their dissection without mortality. Two patients were managed successfully with an intraluminal prosthesis and resuspension of the aortic valve. Another patient had successful repair with a valved conduit and reimplantation of the coronaries. Two patients dissected 4 and 6 years after aortic valve replacement and neither survived operative repair. Of the surviving patients, one required dialysis, one a femoral-femoral bypass graft, and one an axillo-femoral bypass graft. One patient required a pacemaker for heart block, and two underwent successful repair of suture line aneurysms, both occurring three years after operation. On the basis of this experience prompt surgical intervention for acute ascending aortic dissection is the treatment of choice. A variety of techniques are available to repair the dissected aorta. Long-term results for resuspension of the aortic valve in acute ascending aortic dissection have been excellent and emphasize that valve replacement should be reserved for those patients found at operation to have a primary abnormality of the aortic valve.

Reversible pulmonary oxygen toxicity in the primate.

: In order to investigate the effects of high concentrations of oxygen on the lung, experiments were performed on 18 baboons exposed to a humidified environment of 95% oxygen for five days. Open lung biopsies for biochemical assay, histologic and electron microscopic analysis and measurement of tissue respiration were performed before and after oxygen exposure. Pulmonary function was evaluated by measurement of arterial blood gases, compliance, closing capacity (CC), functional residual capacity (FRC), total lung capacity (TLC), residual volume (RV) and vital capacity (VC) before and after exposure and then at seven and 14 days in the animals which recovered. Six baboons removed from the oxygen environment after 96--110 hours and exposed to room air died within three to 20 hours of profound hypoxemia (PaO2 40 +/- 6). The remaining 12 baboons were successfully weaned to room air over a three day period with a return of ABGs to control values (PaO2 89+/- 2). Electron microscopic analysis of alveolar membranes exposed to 120 hours of hyperoxia demonstrated endothelial cell swelling, interstitial alveolar membrane edema, and an increased predominance of Type II pneumocytes. Lung volume measurements showed significant decreases in TLC (25%), VC (34%), CC/TLC (28%) and dynamic compliance (47%). Biochemical studies indicated a shift toward anaerobic metabolism with a decrese in tissue oxygen consumption, reduced cytochrome oxidase activity, and increased lung lactic acid production. These changes were all found to be reversible in the 12 baboons slowly weaned back to room air.

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 > 0.95 for 48–70 hours. Radioactive 8–10 μ 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 < 0.0001) during 70 hours. Left atrial pressure fell from 9 ± 2 mm Hg to 3 ± 3 mm Hg (p < 0.0001), but cardiac output was constant at 2.7 ± 0.1/min. Pulmonary arteriolar resistance increased from 183 ± 20 dynes-sec-CM−5 to 791 ± 30 at 70 hours (p < 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.

Reversible Pulmonary Oxygen Toxicity in the Primate

In order to investigate the effects of high concentrations of oxygen on the lung, experiments were performed on 18 baboons exposed to a humidified environment of 95% oxygen for five days. Open lung biopsies for biochemical assay, histologic and electron microscopic analysis and measurement of tissue respiration were performed before and after oxygen exposure. Pulmonary function was evaluated by measurement of arterial blood gases, compliance, closing capacity (CC), functional residual capacity (FRC), total lung capacity (TLC), residual volume (RV) and vital capacity (VC) before and after exposure and then at seven and 14 days in the animals which recovered. Six baboons removed from the oxygen environment after 96--110 hours and exposed to room air died within three to 20 hours of profound hypoxemia (PaO2 40 +/- 6). The remaining 12 baboons were successfully weaned to room air over a three day period with a return of ABGs to control values (PaO2 89+/- 2). Electron microscopic analysis of alveolar membranes exposed to 120 hours of hyperoxia demonstrated endothelial cell swelling, interstitial alveolar membrane edema, and an increased predominance of Type II pneumocytes. Lung volume measurements showed significant decreases in TLC (25%), VC (34%), CC/TLC (28%) and dynamic compliance (47%). Biochemical studies indicated a shift toward anaerobic metabolism with a decrese in tissue oxygen consumption, reduced cytochrome oxidase activity, and increased lung lactic acid production. These changes were all found to be reversible in the 12 baboons slowly weaned back to room air.