Pulmonary oedema in rats given dehydromonocrotaline: a topographic and electron-microscope study.
Study of cleared, histological and electron-microscope specimens shows that increased vascular permeability plays a major role in the formation of the pulmonary oedema and pleural effusions that occur in rats following the intravenous injection of a large dose of dehydromonocrotaline. There is a latent interval of 6-8 hr between injection of the dehydroalkaloid and the start of increased permeability which appears to be due to a direct damaging effect of the toxin on the endothelium of pulmonary capillaries and small venules. The endothelial injury does not cause permanent disruption of small blood vessels, and 2 days after injury all vessels are patent and lined by a complete layer of endothelium. Large numbers of mononuclear cells are present in the interstitial tissues of the lung 44 hr after injury. These cells appear to be emigrated blood monocytes but the cause of their emigration and their role in the subsequent progression of this type of injury to the lung are not clear.
D000818:Animals; D002199:Capillary Permeability; D002465:Cell Movement; D004727:Endothelium / Q000187:drug effects; D005260:Female; D008168:Lung / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D009000:Monocytes / Q000187:drug effects; D011654:Pulmonary Edema / Q000139:chemically induced* / Q000473:pathology; D011763:Pyrrolizidine Alkaloids / Q000633:toxicity*; D051381:Rats
D011763:Pyrrolizidine Alkaloids