CyA Treatment Research Articles

Early change of myocardial water during acute cardiac allograft rejection.

To determine the changes in myocardial water during acute cardiac rejection and the effects of Ciclosporin (CYA) on the myocardial water, 90 heterotopic cardiac transplants were performed in rats which were divided into 3 groups, namely those receiving 1) Lewis X Lewis isografts, 2) Lewis X Brown Norway allografts and 3) CYA treated allografts (15 mg/kg/day). The water content was measured in both recipient and donor hearts at 2, 4, 6 and 8 days after transplant. Pathological specimens were examined by light and electron microscopy, and scored on a 0 to 4+ scale of increasing evidence of rejection. The water content of the isografts showed no significant change throughout the post operative period. In contrast, the allografts had significant increase of water content as early as 2 days after transplant, compared to the isografts and recipients hearts. A significant difference in cellular infiltration was noted between isograft and allograft 4 days after transplant. CYA suppressed significantly the increase of myocardial water and cellular infiltration in the allografts. These data suggest that myocardial edema may precede cellular infiltration during the rejection process and it may be suppressed with CYA treatment. The measurement of myocardial water may be useful in early detection of acute cardiac allograft rejection and for examining the therapeutic effects of CYA.

In vivo effects of cyclosporin A: abrogation of the induction of experimental allergic orchitis and sparing of the generation of suppressor cells.

Cyclosporin A (CyA; 10 mg/kg/day) administration for 14 days, starting on the day of immunization with testicular antigen (TA) in complete Freund's adjuvant (CFA), almost completely abrogated the induction of experimental allergic orchitis (EAO), delayed skin reactivities to both TA and purified protein derivative of tuberculin (PPD), and antisperm antibody response in strain 13 guinea pigs when examined 2 weeks after immunization. The unresponsive state induced was of a transitory nature. After cessation of CyA treatment, EAO-eliciting capability and cellular immune responsiveness recovered in relatively short time, while restoration of humoral immune responsiveness was delayed. Transfer of lymph node cells taken from CyA-treated, EAO-suppressed animals at 2 weeks postimmunization into normal syngeneic recipients inhibited the induction of EAO and delayed skin response. The suppressor cell activity appeared to be at least in part antigen-specific. It seems likely, therefore, that the profound suppression of EAO by CyA could be explained as due to the additive effect of the inhibition of helper/inducer T cell generation and the sparing or activation of suppressor cell populations.