Evidence of vascular injury was found in rabbits after a single small dose of endotoxin from Escherichia coli. Eighty percent of the treated animals developed circulating endothelial cells, leukopenia, and thrombocytopenia, and 50 percent had aortic endothelial lesions as determined by electron microscopy. Prior anticoagulation with heparin did not prevent this response. No control animals showed these abnormalities.

A patient with CML is presented in whom Gaucher’s cells were seen in the bone marrow and other tissues. Biochemical and electron microscopic studies established the similarity of these cells to those found in Gaucher’s disease. Evidence is presented which indicates that the granulocyte is normally the major source of sphingolipid and that the Gaucher’s cells seen in CML arise from excessive granulocyte turnover.

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This study examines the role of neutrophils (PMN) in the pathogenesis of the endothelial lesion induced by a single sublethal dose of endotoxin. It is intended to clarify whether the margination of PMN on endothelium after endotoxin causes intimal injury or is a response to it. Neutropenic rabbits had mean PMN counts of 33/cu mm 72 hr after nitrogen mustard (HN2). They were heparinized and given either intravenous endotoxin or saline and were sacrificed 30-60 min later. Preterminal blood samples were positive for the presence of endothelium in 77% of endotoxin-treated neutropenic rabbits, in 87% of endotoxin-treated normal rabbits, and in only 12% of neutropenic rabbits given saline. Sections of aorta revealed marked abnormalities of endothelium in rabbits receiving endotoxin, whether neutropenic (90% had lesions) or normal (85% had lesions). Endothelial abnormalities included vacuolation and lysis, marked subendothelial edema, and desquamation. Similar lesions in control neutropenic rabbits were not found, and mild abnormalities were seen only rarely. These data indicate that neutropenia does not protect rabbits from endothelial injury due to endotoxin. They further suggest that HN2 may cause endothelial damage either directly or secondary to the effects of neutropenia.

No abstract