The experiment was designed to test whether the ability of heparin to prevent vascular 'fibrinoid' necrosis in severe hypertension is related to its effects on vascular permeability. Hypertension was produced by infusion of angiotensin II into rats for 1 or 4 hours; some rats were treated with heparin and others not. Native ferritin was used as a tracer, and small arteries of the intestine were examined by light and electron microscopy. Rats not subjected to angiotensin II were used as controls. Half were treated with heparin, and half were not. Arteries from normotensive animals showed no signs of permeability to ferritin, damage to the vessel wall, or irregularities in caliber. Vessels from hypertensive rats had alternating zones of constriction and dilatation. Ferritin penetration and vessel wall damage were found only in dilated zones; these were focal in the 1-hour experiments and more extensive in the 4-hour experiments. No differences were observed between heparin-treated and non-heparin-treated rats with respect to permeability to ferritin or to vessel wall damage. However, in the 4-hour experiments, non-heparin-treated animals had occasional fibrinlike deposits at sites of severe medial damage; these were never found in heparin-treated animals. The findings suggest that although heparin does not appear to affect vascular permeability or medial damage during acute hypertension, it may prevent polymerization of fibrin in damaged vessel walls - presumably a result of the drug's anticoagulant properties.
|Original language||English (US)|
|Number of pages||13|
|Journal||American Journal of Pathology|
|State||Published - Jan 1 1983|
ASJC Scopus subject areas
- Pathology and Forensic Medicine