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Nitric oxide production during the hyperacute vascular rejection
J Castillo1, J R Berrazueta, L Herrera
1Department of General Surgery, Hospital Universitario "Marqués de Valdecilla," Avda de Valedecilla s/n, Spain.
The Journal of Surgical Research
|July 1, 1996
Summary
Cytotoxic nitric oxide (NO) may contribute to hyperacute rejection in xenotransplantation. Studies show inducible NO synthase activation in transplanted kidneys, suggesting NO
Area of Science:
- Transplantation immunology
- Xenotransplantation
- Vascular rejection mechanisms
Background:
- Hyperacute rejection remains a significant barrier in xenotransplantation.
- Nitric Oxide (NO) produced by cytokine-induced NO synthase exhibits cytotoxic activity.
- Understanding NO's role is crucial for preventing hyperacute vascular rejection.
Purpose of the Study:
- To investigate the release of cytotoxic nitric oxide (NO) during hyperacute rejection in pig-to-dog kidney xenotransplantation.
- To determine the involvement of inducible NO synthase (iNOS) in the transplanted organ.
Main Methods:
- Performed 20 heterotopic pig-to-dog kidney xenotransplantations.
- Measured plasma nitrites and cyclic guanosine monophosphate (cGMP) levels in graft artery and vein.
- Assessed NO synthase activity in renal artery and tissue samples.
Main Results:
- Inducible NO synthase (iNOS) was activated in the transplanted kidney post-xenotransplantation.
- Elevated nitrites and cGMP levels suggest NO production.
- Findings indicate NO's potential role in mediating tissue damage.
Conclusions:
- Inducible NO synthase activation occurs during hyperacute rejection in pig-to-dog kidney xenografts.
- Nitric Oxide (NO) is implicated as a mediator of host tissue damage in this rejection process.
- Further research into NO modulation may offer strategies to prevent xenograft rejection.