Inhibition of the graft-versus-host response by BCGcw-induced suppressor cells or prostaglandin E1.

Immunization of C57BL/6 mice with BCGcw stimulated a population of "suppressor cells" which had a decreased capacity to induce the graft-versus-host response. The graft-versus-host response was quantitated using the Simonsen splenomegaly assay. F1 mice (C57BL/6 X CBA) were inoculated intraperitoneally with 1 X 10(8) parental (C57BL/6) or (CBA) spleen cells. The F1 mice were sacrificed 13 days later and the resulting splenomegaly was 3-4 times the normal amount. F1 mice which were injected with parental BCGcw-primed C57BL/6 spleen cells had a 50% inhibition of splenomegaly, whereas BCGcw-primed CBA spleen cells (a strain which does not develop suppressor cells) did not show this inhibition. In vitro results also confirmed that only C57BL/6 mice and not CBA mice developed suppressor cells after BCGcw immunization. A second study showed that X-irradiated (1000 R) BCGcw-primed "suppressor cells" could inhibit splenomegaly caused by the inoculation of normal parental C57BL/6 cells into F1 mice. The mechanism by which BCGcw-primed "suppressor cells" caused this inhibition of splenomegaly was delineated and found to be dependent upon the secretion of prostaglandin (PGE-1). Indomethacin and aspirin, potent inhibitors of prostaglandin synthesis, blocked the activity of C57BL/6 BCGcw "suppressor cells" and splenomegaly resulted. Systemic administration of the prostaglandin (15S)-15-methyl PGE-1 reduced splenomegaly approximately 50% in F1 mice which were injected with C57BL/6 or CBA cells. These results indicated that immunization with BCGcw stimulated a population of "suppressor cells" which could cause a decrease in graft-versus-host response and that the secretion of prostaglandin was responsible for this inhibition.

Sequential treatment of deep leg vein thrombosis with porcine plasmin and low dose streptokinase.

Sequential treatment of deep leg vein thrombosis with porcine plasmin and low dose streptokinase (10,000-20,000 U/h) produces strong systemic fibrinolysis as demonstrated by the sustained decrease of euglobulin lysis time, of thromboplastin time values in percent, fibrinogen and factor V levels. There is a statistically significant negative correlation between thrombolytic results and euglobulin lysis time. Treatment period below 3 days are unlikely to give satisfactory results. Occluded vein segments with an apparent median age of 4 days including thrombi older than 10 days (20% of cases) are cleared with an average chance of 50%. Complete dissolution of all thrombi proximal to the crural veins has been demonstrated in 47/114 = 41.2%, some thrombolytic effects in 31/114 = 27.2% and treatment failure in 36/114 = 31.6%. The data favour laboratory monitoring of thrombolytic therapy.