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T H Spaet

Publications and source records attributed to T H Spaet.

At least 55 records · Page 3Linked to original sources
PubMed1970

Vascular lesions: possible pathogenetic basis of the generalized Shwartzman reaction.

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.

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PubMedDate not supplied

In vitro synthesis of DNA, protein, and lipids by the de-endothelialized rabbit aorta.

The uptake of [3H] leucine, [3H] thymidine, [14C] acetate, and [14C] mevalonic acid by aortic intima media from normal rabbits and from rabbits subjected to a single balloon de-endothelialization as measured 6 days, 2 months, and 4 months after treatment to determine how long the injury-induced stimulation of incorporation of these precursors into tissue components persisted beyond 6 days, the time of maximum proliferative response of the smooth muscle cells. We found that [3H] thymidine incorporation (indicative of DNA synthesis and the potential for cell proliferation) was about three times greater in the de-endothelialized tissue than in the control tissue 6 days after vessel injury, but that by 2 months it was normal. Labeled leucine incorporation into the de-endothelialized tissue (a measure of protein synthesis) was eight times higher than normal at the time of maximum proliferative response to injury (6 days), and showed no decrease under identical incubation conditions in ballooned tissue obtained 2 months after de-endothelialization; it continued high at 4 months. Both [14C] acetate and [14C] mevalonate uptake into lipids by the aortic tissue were enhanced by the injury; this increased incorporation was still evident at 4 months. Thus, de-endothelialization of the aorta triggers a vessel wall response characterized by augmented protein synthesis and lipogenesis, which persists at least 4 months after injury and at least 2 months after DNA synthesis has normalized.

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