Heparin from degranulating mast cells influences a wide range of cellular and humoral reactions associated with allergic inflammation and asthma. Agents that inhibit mast cell degranulation may therefore compromise the moderating effects of heparin in the tissues and result in worsening inflammation and other associated pathology. This study measures heparin release from allergen-challenged human lung tissue and compares the effect of the mast cell stabilizing beta 2-agonists, salbutamol and fenoterol, and a non-beta 2-agonist, sodium cromoglycate, on the release of heparin. Pieces of lung tissue 2 to 3 mm3 were sensitized with high titer Dermatoaphagoides pteronyssinus-specific IgE serum and challenged with D. pteronyssinus allergen, with and without prior addition of salbutamol, fenoterol, or sodium cromoglycate. Dextran sulfate was added to the mixture to prevent the binding of heparin to tissue proteins. Heparin was released together with histamine after challenge. The mean and 95% confidence interval of prechallenge and postchallenge heparin concentrations in the lung tissue filtrates were 0.10 IU/ml (0.07, 0.12) and 0.24 IU/ml (0.17, 0.30), respectively (P < 0.001). Addition of the beta 2-agonists produced a mean inhibition of released heparin of 71% (50, 92), and 73% (55, 91), respectively. Sodium cromoglycate gave a 35% (20, 51) inhibition that was significantly less than that produced by the beta 2-agonists (P < 0.01). The beta 2-agonists salbutamol and fenoterol strongly inhibited heparin release from mast cells. The therapeutic use of mast cell stabilizing agents may therefore be potentially detrimental to the control of allergic inflammation and other associated pathologies.

This study is a multifactorial analysis of 389 transplants performed from June 1977 to December 1981. Analysis of the effects of transfusions antilymphocyte serum (ALS), histocompatibility testing, gender, and patient risk factors (presence of concomitant disease, greater than 50 years of age, etc.) was done. Two-hundred fifty-three patients received cadaver kidneys and 136 patients obtained kidneys from a relative. Two-hundred eighty-three (73%) patients received blood transfusions prior to transplantation. Our data showed that recipients receiving transfusions prior to transplantation had a significantly higher graft survival than those who were not transfused in both cadaveric and related graft recipients. Two-hundred twenty-one (56%) patients received ALS following the transplant. This group had a 15% higher graft survival than a comparable group. Analysis of histocompatibility testing data shows approximately 5% higher functional graft survival between each match grade. Surprisingly, female patients receiving kidneys from living related donors had a 16% higher graft survival than male patients. In cadaver recipients female patients had a 10% higher patient survival as compared to male patients. The risk factor status of recipients affected not only graft survival but patient survival, which probably is due to the consequences of immunotherapy. The authors' conclusion is that the above mentioned factors may be additive in nature. Further, multivariable analysis is necessary in order to correctly transplant data.