Veränderung von Perfusion und hepatisch-oxidativem Stress nach Hirntod

Abstract

Brain death [BD] is an important, multifactorial variable contributing to the donor specific damage of the liver. Our study aimed at assessing the specific influence of hemodynamic instability on systemic and hepatic parameters of perfusion and oxidative stress in a porcine model of brain death. Method: BD was induced in 16 pigs (German landrace,18 – 28 kg) in 2 groups (hypotension [HYPO-BD]: (n = 8; normotension [NORM-BD]: n = 8) and compared to controls/living donors [LD]: n = 6) over a period of 2 h. We analyzed systemic hemodynamic parameters and oxidative stress (total glutathione in erythrocytes [tGSH_E]), and compared them to hepatic parameters of perfusion (hepatic artery [HAF] and portal venous [PVF] flow, microperfusion [MP]) and liver oxidative stress (rGSH_L, GSSG_L). Results: Independent of the hemodynamic stability, liver macro- and microcirculation dropped ([HYPO-BD]: 79 ± 6 to 69 ± 10 ml/100 g/min, [NORM-BD]: 81 ± 10 to 73 ± 7 ml/100 g/min, p <0,05). Hepatocellular damage (AST: [NORM-BD]: 49 ± 20 U/L; [HYPO-BD]: 170 ± 140 U/L, p<0.01) and hepatic oxidative stress increased ([rGSH_L]/ [GSSG_L]: [NORM-BD]: 29.4 ± 2.3 to 13.0 ± 1.3 [HYPO-BD]: 29.4 ± 2.3 to 9.05 ± 0.81; p < 0.001) in both BD-groups. Systemic oxidative stress was increased in HYPO-BD only ([tGSH_E]: 2.65 ± 0.25 to 0.15 ± 0.25 mM; p < 0.01). Conclusion: During BD, liver specific parameters (portal venous flow, microperfusion, AST, hepatic oxidative stress) were compromized independent of the hemodynamic Status. Hence, the systemic hemodynamic Status does not reflect the functional Status of the liver during brain death.