|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
J Thorac Cardiovasc Surg 2001;121:401
© 2001 The American Association for Thoracic Surgery
Letters to the Editor |
Division of Cardiac Surgery
Brigham and Women's Hospital Boston, MA 02115
Reply to the Editor:
We read with interest the letter from Beranek regarding our previously published articles on pig-to-primate cardiac xenograft rejection,
1,2 and we appreciate his identification of myocardial apoptosis in our figures.
An important mechanism in hyperacute rejection involves the binding of porcine galactose
-1,3 (
-Gal) by primate immunoglobulin M antibodies, which activate the complement membrane attack complex (MAC) and induces microvascular thrombosis and graft loss. Beranek has previously commented that apoptosis-induced cardiomyocyte damage may be another potential mechanism of xenograft rejection
3-6: vascular leakage during hyperacute rejection allows immunoglobulin M and MAC to attack bystander cardiomyocytes, inducing apoptosis and myocardial defects.
Although we agree that apoptosis may play a role in xenograft rejection, we are uncertain whether this phenomenon is the result of vascular leakage of immunoglobulin M and MAC. Ischemia and reperfusion alone can induce apoptosis.
7 In the setting of hyperacute rejection where the graft is rejected minutes after implantation, the contribution of ischemia/reperfusion versus immunoglobulin M/MAC in the induction of cardiomyocyte apoptosis remains unclear. Although we agree that apoptosis may occur after transplantation, we do not necessarily agree that vascular leakage of immunologic proteins is the mechanism.
12/8/111201
doi:10.1067/mtc.2001.111201
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |