The aim was to determine whether treatment of rats with cyclosporin A (CsA) leads to deleterious side effects on heterotopically iso- or allotransplanted hearts when compared with recipient native in situ hearts. Four experimental groups were employed: inbred (Lewis) rats receiving either no immunosuppression or CsA at a dose of 15 mg.kg-1 per day for 7 days after surgery, and outbred (Wistar) rats receiving CsA at the same daily dose for either 7 or 21 days. One month following surgery, the mass of all transplanted hearts decreased and resulting atrophy was associated with relative myocardial fibrosis. Treatment with CsA significantly increased the concentration and content of collagen in the right and left ventricles of all transplanted and recipient hearts. No appreciable difference was observed between corresponding hearts of inbred and outbred groups receiving the identical dose of CsA, and between hearts in outbred groups treated for either 7 or 21 days. No signs of right ventricular mechanical dysfunction, as assessed on the isolated perfused "working' preparation, were observed after CsA treatment in both transplanted and recipient hearts. The maximal steady state developed pressure (RVDevP) and the rate of its development [(+dP/dt)max] were slightly higher in transplants than in the corresponding recipients, and in CsA-treated versus untreated hearts, while the index of contractile state [(+dP/dt)/P] was similar in all groups. The data suggest that treatment of rats with CsA can induce a similar degree of fibrosis both in heterotopic cardiac transplants and in recipient native hearts without impairment of their contractile performance.

Department of Developmental Cardiology Academy of Sciences of the Czech Republic Prague Czech Republic

Zobrazit více v PubMed

Transplantation. 1993 Oct;56(4):885-91 PubMed

Circulation. 1993 Apr;87(4):1368-77 PubMed

Cardiovasc Clin. 1990;20(2):179-88 PubMed

Int J Cardiol. 1991 Apr;31(1):15-22 PubMed

J Heart Transplant. 1988 Mar-Apr;7(2):145-51 PubMed

J Mol Cell Cardiol. 1994 Mar;26(3):279-92 PubMed

J Pharmacol Exp Ther. 1986 Oct;239(1):229-35 PubMed

Cardiovasc Res. 1993 Mar;27(3):341-8 PubMed

Transplant Proc. 1993 Aug;25(4):2735-7 PubMed

Am J Pathol. 1970 May;59(2):279-98 PubMed

Cardiovasc Res. 1993 Feb;27(2):172-5 PubMed

Cardiovasc Res. 1993 Jul;27(7):1244-7 PubMed

Eur J Pharmacol. 1993 Dec 1;248(4):341-4 PubMed

Hypertension. 1991 Oct;18(4):458-66 PubMed

J Pharmacol Exp Ther. 1991 Nov;259(2):905-15 PubMed

J Heart Lung Transplant. 1993 Mar-Apr;12 (2):199-204 PubMed

Mol Cell Biochem. 1993 Dec 22;129(2):121-31 PubMed

J Heart Transplant. 1987 May-Jun;6(3):180-5 PubMed

Transplantation. 1994 May 15;57(9):1382-8 PubMed

Kidney Int. 1994 Apr;45(4):1203-10 PubMed

J Pharm Pharmacol. 1990 Jul;42(7):525-7 PubMed

Circulation. 1989 Jan;79(1):66-75 PubMed

Hum Pathol. 1990 Apr;21(4):424-8 PubMed

J Hypertens Suppl. 1993 Dec;11(5):S122-3 PubMed

N Engl J Med. 1989 Dec 21;321(25):1725-38 PubMed

Circ Res. 1989 Oct;65(4):934-45 PubMed

Pflugers Arch. 1991 Sep;419(2):121-6 PubMed

Transplantation. 1988 Aug;46(2):285-92 PubMed

Agents Actions. 1984 Oct;15(3-4):306-27 PubMed

Hum Pathol. 1990 Jul;21(7):767-72 PubMed

Transplantation. 1989 Oct;48(4):720-3 PubMed

Cardiovasc Res. 1993 Oct;27(10):1845-54 PubMed

Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences

Sex-Linked Differences in Cardiac Atrophy After Mechanical Unloading Induced by Heterotopic Heart Transplantation

Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation