[Renal neuroadrenergic effects. Part I. Renal ischemia caused by sympathetic stimulation and risk factors of cadaver donor].
Functional impairment of transplanted kidneys may occur due to circumstances related either directly or indirectly to the donor, the graft or the receptor. In most publications, renal damage is frequently attributed to ischaemia phenomena, mainly host ischaemia, either because of intraoperative interruption of blood flow for an exceedingly long interval, until perfusion and cooling of the removed kidneys, by the duration of cold ischaemia for organ preservation, or during the implant procedure. Also due to the activation of neuroadrenergic reflexes as a consequence of the mechanical stimulation of sympathetic nervous endings during dissection of the vascular pedicle. Earlier studies in animals have demonstrated that direct, low frequency electric stimulation of the splanchnic nerve involves reversible changes in sodium renal excretion, but it does not modify glomerular filtration; when nerve stimulation is done with high frequency there is a decline of renal blood flow and glomerular filtration. The present study tries to associate some of the causes of hot ischaemia during the agony of the corpse donor and to evaluate those that may be caused by sympathetic efference during removal.
García Matilla
F
F
Servicio de Urología, Hospital Universitario Virgen del Rocío, Sevilla.
García Montes
F
F
D002102:Cadaver; D006801:Humans; D007511:Ischemia; D007668:Kidney / Q000098:blood supply / Q000294:innervation* / Q000502:physiology; D016030:Kidney Transplantation / Q000379:methods; D012307:Risk Factors; D013564:Sympathetic Nervous System / Q000502:physiology