Reduction in nonparenchymal cell injury and vascular endothelial dysfunction after cold preservation of the liver by gaseous oxygen
Reintroduction of oxygen to previously anoxic tissue may result in severe cell injury (oxygen paradox) and contribute to the socalled reperfusion damage of ischemic organs. Our study investigated the influence of simple gaseous oxygen supply during ischemia on nonparenchymal cell alterations upon reperfusion of the liver. Livers from male Wistar rats were isolated, rinsed blood-free and stored for 48 h at 4°C in UW-preservation solution (group 1; n = 6). Gaseous oxygen was insufflated into a second group of livers (group 2; n = 6) during the storage period via the inferior caval vein at a pressure limited to 18 mmHg. To simulate the period of slow rewarming of the organ during surgical implantation in vivo, all livers were incubated at 25°C in saline solution for 30 min prior to reperfusion. Reperfusion was carried out in vitro in a recirculating system with Krebs-Henseleit buffer. A control group was perfused immediately after harvest. The technique of aerobic storage (group 2) resulted in normal vascular perfusion characteristics without elevation of portal venous pressure (PVP) above control values, in contrast to group 1 livers which showed a significantly elevated PVP, averaging between 1.5 and 2 times the values of the control. Hepatic efflux of NO (nmol/ml) after 10 min of reperfusion was massively increased in group 1, while only low concentrations were found in group 2 and in control livers. Kupffer cell activation after ischemia was shown by a huge increase in acid phosphate release upon reperfusion compared with the control, with significantly lower values in group 2 after 10 min of reperfusion than in group 1. Thus, aerobic ischemia by gaseous oxygen persufflation seems an appropriate tool for long-term organ preservation, preventing vascular and parenchymal dysfunction upon reperfusion.
Key wordsPersufflation Aerobic ischemia Oxygen Preservation Liver
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- 4.Evans T, Carpenter A, Kinderman H, Cohen J (1993) Evidence of increased nitric oxide production in patients with the sepsis syndrome. Circ Shock 41: 7781Google Scholar
- 10.Isselhard W, Denecke H, Stelter W, Berger M, Sachweh D, Witte J, Fischer JH (1973) Function and metabolism of canine kidneys after aerobic ischemia by orthograde persufflation with gaseous oxygen. Res Exp Med 159: 288297Google Scholar
- 11.Jin MB, Kobayashi Y, Ochiai T, Yasui J, Ohsada S, Nakano K, Yamagishi H, Hironaka T, Oka T (1994) Relationship between nitric oxide and endothelin-1 during the perioperative phase in canine orthotopic liver transplantation (abstract). Eur Surg Res 26 [Suppl 1]: 27Google Scholar
- 13.Manax WG, Largiader F, Lillehei RC (1966) Whole canine organ preservation. Prolongation in vitro by hypothermia and hyperbaria. JAMA 196: 11211124Google Scholar
- 17.Minor T, Osswald B, Krauss TW, July N, Isselhard W, Klar E (1995) Determination of plasma activities of purine nucleoside phosphorylase by high performance liquid chromatography: estimates of nonparenchymal cell injury after porcine liver transplantation. J Chromatogr B 670: 332 - 336CrossRefGoogle Scholar