Systemic vascular effects during acute rejection of lung
allografts.
Scherst[acute]en, Henrik, Henry D. Tazelaar, Alexander R. J. Cale,
Virginia M. Miller, Christopher G. A. McGregor.
Departments of Surgery, Pathology, Physiology and Biophysics, Mayo
Clinic and Foundation, Rochester, Minnesota
APStracts 3:0118H, 1996.
Circulating leukocytes activated during rejection of organ allografts
could potentially have generalized affects on systemic blood vessels
of the transplant recipient. Experiments were designed, therefore, to
determine the function of the endothelium and smooth muscle of
arteries from nontransplanted organs in dogs who received single lung
transplants. Dogs underwent single lung allotransplantation and were
immunosuppressed for five days. Immunosuppression was then withheld
for three days allowing rejection to occur. Dogs were studied at this
time (rejecting) or following treatment for rejection for a further
six - eight days (treated). Arteries from unoperated, untreated dogs
also were studied to provide baseline responses of healthy tissue.
Rings cut from left circumflex coronary, nonoperated native pulmonary
and renal arteries were suspended in organ chambers for measurement
of isometric force. Endothelium-dependent relaxations to the calcium
ionophore A23187 were not affected by rejection in any of the
arteries. Contractions to angiotensin-1 were reduced significantly
only in native pulmonary arteries. Contractions to KCl and
endothelin-1 increased in renal arteries with endothelium during
rejection. These contractions in renal arteries were reduced
following treatment of rejection. None of the responses of the
coronary arteries were affected significantly by rejection of the
lung allograft. These results demonstrate that contractions to
arteries in the transplant recipient's native organs are altered
during rejection of lung allografts. The effects are organ specific,
may include production of endothelium-derived contractile factors in
renal arteries and can be partially reversed by treatment of
rejection.
Received 2 December 1994; accepted in final form 30 October 1995.
APS Manuscript Number H1059-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96