Alpha 1 antitrypsin defective Lewis rats injected with heparin: comparison of the glomerular changes with those of Lewis rats produced anti BSA antibody.

Heparin effects were studied on Lewis rats with alpha 1 antitrypsin (AT) defect. Among 8 rats that were born at the same birth, three rats were shown to have mild defect of alpha 1 AT. Heparin was injected repeatedly into all the 8 rats. Interstitial pneumonia and localized periodic acid-Schiff (PAS) stain of hepatocytes were found in alpha 1 AT defective male. One of the three alpha 1 AT defective rats had about a half of normal alpha 1 AT level. Antithrombin (AT) III level was slightly low in the alpha 1 AT defective female with splenomegaly. Lung electron micrograph of the other alpha 1 AT defective female showed edematous changes of capillaries and alveolar basement membranes and also proliferated collagen fibers. In the lung of alpha 1 AT defective male, many thrombocytes adhered to alveolar degenerated smooth muscles that were recognized as Masson bodies. Extracted platelet-activating factor (PAF) in the plasma of the alpha 1 AT defective male was shown to trigger T lymphocyte chemotaxis. Five normal Lewis rats were immunized with bovine serum albumin (BSA). IgG1 antibody to BSA was produced in all the rats. The rats with high titers of IgG1 anti BSA antibody showed more strongly atrophic changes of glomerulus than those of the mild alpha 1 AT defective rats treated with heparin.