Abstract
Heparin effects were studied on Lewis rats with α1 antitrypsin (AT) defect. Among 8 rats that were born at the same birth, three rats were shown to have mild defect of α1 AT. Heparin was injected repeatedly into all the 8 rats. Interstitial pneumonia and localized periodic acid-Schiff (PAS) stain of hepatocytes were found in α1 AT defective male. One of the three α1 AT defective rats had about a half of normal α1 AT level. Antithrombin (AT) III level was slightly low in the α1 AT defective female with splenomegaly. Lung electron micrograph of the other α1 AT defective female showed edematous changes of capillaries and alveolar basement membranes and also proliferated collagen fibers. In the lung of α1 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 α1 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 α1 AT defective rats treated with heparin.
