Immunologically induced coronary artery stenosis in allografts after heart and heart-lung transplantation in rats.

The role of the lung in suppressing immunologically induced coronary artery stenosis after heterotopic allograft transplantation was studied in rats. Thirty-nine recipients were divided into two groups: untreated and treated. The untreated group was divided into two subgroups--the heart allograft TH group and the heart-lung allograft THL group. The treated group was divided further into four subgroups depending on when the graft was harvested, after 30 days or 60 days (T30-H and T30-HL group, and T60-H, T60-HL, respectively). Rejection was assessed by Lurie's classification. The percent of intraluminal stenosis (PIS) was determined by planimetry. All treated animals received cyclosporin A 10 mg/kg/day intramuscularly for 20 days. In the untreated group, heart-lung allograft survival was longer than heart allograft survival. In the treated group, all grafts were still beating when the animals were killed. The rejection grade score in the T30-H and T30-HL groups were lower than those in the T60-H or T60-HL groups. The PIS in the THL group was slightly lower than that in the TH group. However the PIS increased over time in both the TH and THL groups. This study demonstrates that the lung suppresses but does not abolish immunologically induced coronary atherosclerosis-like occlusive lesions after cardiac transplantation.