Abstracts
1999 Digestive Disease Week

# 2128 HEMODYNAMICS OF THE HARVESTED LIVER
R Ricciardi, S H Quarfordt, T McLaughlin, S E Donohue, S M Wheeler, D P Foley, William C Meyers, Univ of MA Med Ctr, Worcester, MA

Introduction: An inverse correlation exists between hepatic vascular resistance (HVR)/portal vein pressure (PVP) with secretory function of the harvested liver. Increased PVP/HVR likely reflects endothelial cell damage from cold ischemia, potentially a rapid marker of this damage. Hepatic hemodynamics were sequentially determined insitu, in the isolated liver, and after cold ischemia (harvested liver). Methods: Hepatic vascular resistance was determined from portal vein pressure and hepatic blood flow recordings in the same liver, insitu, in isolation, and after two hours of cold ischemia. Vasoconstriction (norepinephrine), and vasodilatation (nitroprusside), and flow affects were compared in the three models. Statistical significance was determined with Student's t Test and Anova. Results: At baseline portal vein flow (PVF), the PVP and HVR of the insitu and isolated liver were similar (8.2 vs. 8.0mmHg; n = 5, p = 0.8) (HVR 0.014 vs. 0.015; n = 5, p = 0.7). Norepinephrine similarly increased PVP and HVR in the insitu liver (9.0 to 16.5mmHg; n = 4, p = 0.001) (HVR 0.01 to 0.016; n = 4, p = 0.04) and isolated liver (8.0 to 14.0mmHg; n = 4, p = 0.016) (HVR 0.015 to 0.024; n =4, p = 0.03). Nitroprusside decreased PVP in the insitu liver (8.8 to 5.5mmHg; n = 4, p = 0.05) and the isolated liver (8.8 to 3.8mmHg; n = 4, p = 0.001). HVR was decreased in the isolated liver ((0.016 to 0.007; n = 4, p = 0.0007) during nitroprusside infusion. After cold ischemia PVP and HVR were significantly elevated compared to the insitu and isolated liver (12.6 vs. 8.2 vs. 8.0mmHg; n =5, p = 0.008) (HVR 0.022 vs. 0.014 vs. 0.015; n = 5, p= 0.013). Nitroprusside reduced PVP and HVR after cold ischemia (10.0 to 6.7mmHg; n = 3, p = 0.015) (HVR 0.020 to 0.013; n = 3 p = 0.007). However, after cold ischemia, the change in PVP and HVR to norepinephrine was blunted (12.5 to 17.0mmHg; n = 4, p = 0.5) (HVR .023 to .030; n = 4, p = 0.5). Doubling of PVF minimally increased PVP in insitu and isolated livers but significantly increased PVP in the harvested liver (2, 3, 6mmHg respectively; n = 4, p = 0.03). Conclusions: Alterations in PVP/HVR in harvested livers are due to cold ischemia and not loss of neurologic input. Pressure responses to flow and vasoactive agonists are similar in insitu and isolated livers, but modified by cold ischemia. Rapid evaluation of hepatic hemodynamics may predict transplant function and survival. Vasodilatation of a harvested liver prior to transplant, may be beneficial in the early function of the organ.

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