Nitric oxide production during the hyperacute vascular rejection.
A complete understanding of the biological mechanisms that take part in the hyperacute vascular rejection is necessary to prevent its development. Nitric Oxide (NO) release by the graft could be one of those mechanisms as cytokine induction of NO synthase in reticuloendothelial cells produces NO with cytotoxic activity. We have performed 20 heterotopic pig-to-dog kidney xenotransplantations in order to determine if cytotoxic NO is released during the hyperacute rejection. Nitrites and cGMP levels were determined in plasma samples taken from the graft artery and vein until vessel thromboses. NO synthase activity was measured in pieces from renal artery and renal tissue. The results show that after discordant xenotransplantation, inducible NO synthase is activated in the transplanted organ, indicating that NO can mediate host tissue damage during the hyperacute rejection.
Castillo
J
J
Department of General Surgery, Hospital Universitario "Marqués de Valdecilla," Avda de Valedecilla s/n, Spain.
Berrazueta
J R
JR
Herrera
L
L
Val-Bernal
J F
JF
Gómez
J
J
Sánchez
M J
MJ
Riestra
A
A
García-Unzueta
M T
MT
Amado
J A
JA
Salas
E
E
Gómez-Fleitas
M
M
D000208:Acute Disease; D000818:Animals; D004285:Dogs; D004789:Enzyme Activation; D004790:Enzyme Induction; D006084:Graft Rejection / Q000378:metabolism*; D007668:Kidney / Q000201:enzymology; D016030:Kidney Transplantation; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000097:blood; D019001:Nitric Oxide Synthase / Q000097:blood; D012077:Renal Artery / Q000201:enzymology; D012082:Renal Veins; D013552:Swine; D014183:Transplantation, Heterologous
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase