William E. Neville

Mechanisms of blood-vascular reactions of the primate lung to acute endotoxemia

Abstract Previous studies have related structural and functional changes of the lung in shock to the syndrome of pulmonary leukocytosis (SPL) which is defined as rapid sequestration, degranulation and fragmentation of PMN-leukocytes in the pulmonary vascular bed. In the present study, in vivo and in vitro experiments were performed to investigate the mechanism and significance of ultrastructural changes associated with endotoxin-induced SPL. In rhesus monkeys infused with E. coli endotoxin (5 or 10 mg/kg), sequestered PMN-leukocytes revealed numerous digestive vacuoles containing characteristic membranous particles which were positively identified as particulate endotoxin. In places endotoxin particles were found to be incorporated in the matrix of leukocytic granules as well as in digestive vacuoles released intra-vascularly from fragmented leukocytes. These changes were associated with progressive degranulation of the PMN-leukocytes as well as multifocal damage to the endothelium of capillaries and arterioles which was demonstrable before the onset of significant leukocytic fragmentation. In addition, formation of digestive vacuoles and degranulation were found to be more prominent in sequestered rather than in circulating PMN-leukocytes. Platelet aggregates and fibrinous deposits in lung capillaries were virtually absent. In vitro endotoxin-leukocyte interaction reproduced all changes seen in sequestered PMN-leukocytes with the exception of leukocyte fragmentation. The results suggest that endotoxin-induced SPL in associated with early development of endothelial damage, and it is largely a manifestation of increased phagocytosis of endotoxin by the marginating PMN-leukocytes. The findings also provide strong ultrastructural evidence that phagocytized endotoxin results in direct injury to leukocyte lysosomes, which has not been reported to occur with phagocytosis of inert particles. The above evidence is consistent with previous biochemical data which indicated that endotoxin-induced enzyme release, and potential tissue injury, is greater than that observed with simple phagocytosis.

Peripheral pulmonary artery stenosis secondary to chronic pulmonary thromboembolic disease

Abstract A patient is described with chronic thromboembolic pulmonary disease and clinical and cardiac catheterization findings indicating stenosis of a branch of the right pulmonary artery. A continuous murmur over the lung, present in this case, may serve as a clue to the diagnosis and should be looked for in patients with recurrent pulmonary thromboembolism. Although symptoms and exercise tolerance improved after pulmonary thromboembolectomy, severe pulmonary hypertension persisted and hemodynamics were unchanged.

CARDIOPULMONARY BYPASS WITH LARGE VOLUME NONBLOOD PERFUSATE. EXPERIMENTAL AND CLINICAL OBSERVATIONS.

Experimental and clinical data have been presented which support the efficacy of using a large-volume nonblood perfusate for cardiopulmonary bypass. Dogs have consistently survived hemodilution of 100 to 120 ml/kg body wt when manifest hypoxic acidosis has been ameliorated with THAM (tris [hydroxymethyl] aminomethane) or sodium bicarbonate.Fifty-eight patients have undergone total bypass with the disc oxygenator totally primed with 2,500 to 3,000 ml of buffered Ringers or Ringers lactate solution. Normothermia and moderate hypothermia have been employed with a hemodilution of 33 to 60 ml/kg body wt and a mean perfusion hematocrit of 24%. Despite the decrease in oxygen-carrying capacity of the blood, acidosis has not been observed during prolonged perfusions at median flow rates. Following oxygenator reinfusion, the postoperative total blood volume has been normal. However, a decrease in red cell mass was observed which necessitated the administration of “packed red cells.” With this technique, the clottingtime was more readily restored to normal, and kidney function was markedly improved over a comparable series of patients perfused with donor blood.

Surgical Treatment of Pulmonary Disease Due to Mycobacterium kansasii

Abstract Over a period of thirteen years, 35 patients at the Veterans Administration Hospital, Hines, Ill., have undergone thirty-eight surgical procedures, including thirty-four pulmonary resections and four collapse procedures, for pulmonary disease due to Mycobacterium kansasii. Major complications following operation occurred in 2 patients; 1 died from staphylococcal empyema. All patients with positive sputum cultures achieved prompt bacteriological conversion following operation. Long-term follow-up ranging from one to more than eleven years following operation was available in 31 of the 35 patients. All patients achieved a quiescent or inactive status. There were 2 late deaths due to unrelated causes.