Effects of Complement Suppression on Xenograft Survival in Hyperacute Rejection

To examine the significance of complement in discordant cardiac xenograft rejection, morphological changes in the rejection reaction were investigated following administration of FUT-175 (FUT), an anticomplement reagent. Guinea pigs were the cardiac donors, and Wistar rats were the recipients. Four groups of rats were constituted as follows: Group 0 was the control group. FUT of 40 mg/kg was injected intraperitoneally in group I. It was followed by continuous intravenous infusion (20 and 40 mg/kg/hr) in groups II and III. In one series, the effects of FUT on complement suppression was examined. In the FUT groups of rats (groups I to III), the serum levels of CH50 and ACH50 were measured at 0, 1, 2 and 4 hr following injection of FUT. In the second series of rats with identical treatments, the graft heart beating time following cardiac transplantation was measured. Cardiac transplantation into untreated rats was also performed as a control (group 0). In another series, the graft hearts in the FUT groups were extracted after 15, 30, 60 and 90 min of coronary reperfusion for morphological examination with scanning electron microscopy.　　 The complement levels decreased significantly in the FUT-treated rats in a dose-dependent manner. Although the graft heart beating times in the FUT-treated groups were significantly longer than in group 0 (103, 106, and 112 min versus 14.7 min, p<0.01), there was no significant difference in the graft heart beating time or in the morphological changes among the three FUT groups. Our results suggest the presence of factors other than complements contribute to the cardiac xenograft rejection

A Heterotopic Cardiac Transplantation Model for Evaluation of Rejection Using Transvenous Endomyocardial Biopsy

A model of heterotopic cardiac transplantation for diagnosis of rejection is described. Heterotopic cardiac transplantations were performed in the thorax using the left innominate artery as an arterial supply with venous return into the superior vena cava. Six pairs of mongrel dogs underwent cardiac transplantation using this technique. Two dogs died postoperatively on the 2nd and 3rd day due to respiratory failure. Another four donor hearts arrested their beats in 6 to 8 postoperative days (mean 6.3 days) resulting from acute cardiac rejection. Serial echocardiographic recordings were found to be a reliable measure of acute cardiac rejection, since the left ventricular wall thickness of the donor heart increased until the donor heart stopped by rejection. Endomyocardial biopsy was easy to perform by passage of flexible cardiac biotome into the right ventricle of the donor and the recipient heart through the right internal jugular vein. Pathological findings revealed that early changes of the donor heart were interstitial edema caused by myocardial ischemia. This was followed by lymphocyte infiltration around peripheral coronary arteries and acute rejection resulting in myocyte necrosis.This study was presented in the seventh annual meeting of Japan Cardiac Transplantation Research, May 1989.Financial contribution was granted by Tsuchiya Memorial Medical Foundation (President Dr. Taro Tsuchiya)

A Functional New Experimental Bi ventricular Model of Heterotopic Cardiac Transplantation

A heterotopic cardiac transplantation model in which the donor heart was able to maintain the systemic and pulmonary circulation of the recipient was devised, which did not require extracorporeal circulation or heparinization. All donor hearts in five pairs of adult mongrel dogs were resuscitated, and the systemic and pulmonary circulations maintained by the donor hearts alone were studied hemodynamically up to 3 hr after resuscitation, although long-term survival was not achieved

Rupture of Donor Ascending Aorta following Heart Transplantation

Among 81 patients who underwent orthotopic heart transplantation between July 1986 and December 1990, we found rupture of the donor ascending aorta in three patients, all with severe ventricular dysfunction secondary to aortic valvular disease. The mechanism for this may be compliance mismatch between the recipient ascending aorta and the donor ascending aorta. This situation is a unique complication in heart transplantation for the recipients who have severe athero-sclerotic changes in the systemic aortic wall, especially for those with valvular diseases caused by calcification