Hepatic microcirculatory failure.
Liver ischemia has been considered a frequent problem in medical practice, and can be associated to a number of surgical and clinical situations, such as massive hepatic resections, sepsis, liver trauma, circulatory shock and liver transplantation. After restoring blood flow, the liver is further subjected to an additional injury more severe than that induced by ischemia. On account of the complexity of mechanisms related to pathophysiology of ischemia and reperfusion (I/R) injury, this review deals with I/R effects on sinusoidal microcirculation, especially when steatosis is present. Alterations in hepatic microcirculation are pointed as a main factor to explain lower tolerance of fatty liver to ischemia-reperfusion insult. The employment of therapeutic strategies that interfere directly with vasoactive mediators (nitric oxide and endothelins) acting on the sinusoidal perfusion seem to be determinant for the protection of the liver parenchyma against I/R. These approaches could be very suitable to take advantage of marginal specimens as fatty livers, in which the microcirculatory disarrangements hamper its employment in liver transplantation.
Ramalho
Fernando Silva
FS
Department of Surgery and Anatomy, FMRP, USP, Brazil.
Fernandez-Monteiro
Izabel
I
Rosello-Catafau
Joan
J
Peralta
Carmen
C
D016232:Endothelins / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D008099:Liver / Q000098:blood supply; D008102:Liver Circulation / Q000502:physiology*; D016031:Liver Transplantation / Q000502:physiology; D008833:Microcirculation / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology*; D014664:Vasodilation / Q000502:physiology
D016232:Endothelins; D009569:Nitric Oxide