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ABSTRACT: Severe ischemia/reperfusion (IR) injury is associated with poor hepatic microperfusion. The aim of this study was to investigate the role of hepatic artery flow (HAF) and portal vein flow (PVF) in IR injury. From January 2004 to June 2008, 566 patients underwent orthotopic liver transplantation (OLT). The data were retrospectively reviewed via the transplant database. Patients with hepatic artery (HA) or portal vein (PV) thrombosis and retransplant patients were excluded. Intraoperative PVF and HAF values and graft weights were measured routinely, and the central venous pressure, mean arterial pressure, cardiac output, and cardiac index were recorded with hepatic blood flow measurements. Complete data were available for 312 primary OLT recipients (215 males and 97 females; mean age = 54 ± 10 years). The patients' follow-up ranged from 215 to 1746 days (705 ± 408 days). IR injury was defined by the aspartate aminotransferase (AST) level on postoperative day (POD) 2, and the patients were divided into 3 groups: (1) mild IR injury [AST < 500 U/L; n = 160 (51%)], (2) moderate IR injury [AST = 500-1000 U/L; n = 85 (27%)], and (3) severe IR injury [AST > 1000 U/L; n = 67 (21%)]. The demographics and pre-OLT variables (the Model for End-Stage Liver Disease score (MELD), platelet counts, PV thrombosis, transjugular intrahepatic portosystemic shunts, and shunts on computed tomography scans) were similar in all groups. The graft survival rate was 99% in group 1, 95.2% in group 2 (P = 0.02), and 92.3% in group 3 (P = 0.016). The patient survival rates were similar in the 3 groups. The cold ischemia time (CIT) was significantly higher in group 3 versus group 1 (P < 0.007). In the statistical analysis, low HAF, PVF, total liver blood flow (TLBF), and augmented HAF values were associated with a greater likelihood of elevated AST levels on POD 2. The strongest univariate predictors of AST were reduced augmented HAF (mL/minute/100 g) values (P < 0.001) and reduced TLBF (mL/minute/100 g) values (P < 0.001). In a covariate analysis with adjustments for CIT and donor variables, the blood flow parameters remained important predictors of graft function. In conclusion, this report demonstrates for the first time that reduced hepatic blood flow is a significant finding in patients with severe hepatic IR injury.
Liver Transplantation 08/2011; 17(12):1448-56. · 3.39 Impact Factor
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Xiaocheng Zhu,
John J Fung, Shunichi Nakagawa,
Lian-Fu Wang,
Samuel Irefin,
Andrei Cocieru,
Cristiano Quintini,
Teresa Diago,
Hiroaki Shiba,
Ivan Parra Sanchez,
Dympna M Kelly
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ABSTRACT: Elevated levels of norepinephrine (NE) have been reported in recipients of small-for-size liver (SFS) grafts in the perioperative period. The aim of the study is to test the hypothesis that although circulating catecholamines are elevated in recipients of SFS grafts, they are not the primary agents responsible for the hepatic artery (HA) vasospasm.
Female porcine recipients receiving a 20% (n = 10) partial liver graft were compared with a control group, using 60% partial liver transplanted grafts (n = 9). Hepatic blood flow (PVF, HAF) and levels of plasma catecholamines (epinephrine and NE) were measured at designated time points through postoperative day (POD) 7. Phentolamine (PA), an α-adrenergic blocker, was administered at doses of 1 to 112.5 ug/kg/min through an indwelling HA to the recipients of 20% group on POD1 (n = 5).
In the 20% group following reperfusion, HA vasospasm was found at 10, 60, and 90 min, and persisted on POD 3 and POD 7. Plasma NE levels increased after reperfusion in 20% and 60% groups and peaked at 6 h with 10- to 13-fold increased levels compared with baseline. In the 20% group, NE levels remained elevated up to POD 7. PA infusion at low (1-10 ug/kg/min) and high (12.5-112.5 ug/kg/min) doses did not reverse the reduced HAF observed in 20% group recipients.
Elevated serum NE does not appear to be the primary factor mediating HA vasospasm in the porcine SFS graft.
Journal of Surgical Research 12/2010; 174(1):157-65. · 2.25 Impact Factor
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Dympna M Kelly,
Xiaocheng Zhu,
Hiroaki Shiba,
Samuel Irefin,
Loris Trenti,
Andrei Cocieru,
Teresa Diago,
Lian Fu Wang,
Cristiano Quintini,
Zhong Chen,
Joan Alster, Shunichi Nakagawa,
Charles Miller,
Anthony Demetris,
John J Fung
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ABSTRACT: The aim of the study is to define the role of the HABR in the pathophysiology of the SFS liver graft and to demonstrate that restoration of hepatic artery flow (HAF) has a significant impact on outcome and improves survival. Nine pigs received partial liver allografts of 60% liver volume, Group 1; 8 animals received 20% LV grafts, Group 2; 9 animals received 20% LV grafts with adenosine infusion, Group 3. HAF and portal vein flow (PVF) were recorded at 10 min, 60 min and 90 min post reperfusion, on POD 3 and POD 7 in Group 1, and daily in Group 2 and 3 up to POD 14. Baseline HAF and PVF (ml/100 g/min) were 29 +/- 12 (mean +/- SD) and 74 +/- 8 respectively, with 28% of total liver blood flow (TLBF) from the HA and 72% from the PV. PVF peaked at 10 mins in all groups, increasing by a factor of 3.8 in the 20% group compared to an increase of 1.9 in the 60% group. By POD 7-14 PVF rates approached baseline values in all groups. The HABR was intact immediately following reperfusion in all groups with a reciprocal decrease in HAF corresponding to the peak PVF at 10 min. However in the 20% group HAF decreased to 12 +/- 8 ml/100 g/min at 90 min and remained low out to POD 7-14 despite restoration of normal PVF rates. Histopathology confirmed evidence of HA vasospasm and its consequences, cholestasis, centrilobular necrosis and biliary ischemia in Group 2. HA infusion of adenosine significantly improved HAF (p < .0001), reversed pathological changes and significantly improved survival (p = .05). An impaired HABR is important in the pathophysiology of the SFSS. Reversal of the vasospasm significantly improves outcome.
Liver Transplantation 11/2009; 15(11):1448-57. · 3.39 Impact Factor
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ABSTRACT: Previous studies have shown that donor hypernatremia and possibly recipient hyponatremia negatively impact graft function after orthotopic liver transplant (OLT). The purpose of this retrospective investigation was to determine whether measured differences in serum sodium values between cadaveric donors and OLT recipients (DeltaNa(+)) influence immediate postoperative allograft function and short-term patient outcomes. Two hundred and fifty patients that underwent OLT from January 2001 to December 2005 were included in this study. The DeltaNa(+) for each donor recipient pair was correlated with standard postoperative liver function tests as well as recipient length of intensive care unit stay (LOICUS), length of hospital stay (LOHS) and recipient survival. The relationship between donor hypernatremia (serum sodium >or= 155 mEq/mL), recipient hyponatremia (serum sodium level <or= 130 mEq/mL), and postoperative outcomes were analyzed as well. Adjustments were made for baseline potential confounders, including model for end-stage liver disease (MELD) score, preservation solution used (HTK vs. UW), recipient and donor demographics and cold ischemia time (CIT). DeltaNa(+) as well as donor hypernatremia and recipient hyponatremia were not found to be associated with immediate postoperative allograft function, intraoperative blood product usage, LOICUS, LOHS or short-term patient survival. However, both the preoperative MELD score and HTK preservation solution used were significantly associated with several patient outcomes. A higher MELD score was associated with both increased red blood cell (RBC) (P < 0.001) and fresh frozen plasma (FFP) usage (P = 0.002), elevated postoperative total bilirubin levels (P < 0.001), increased LOHS (P = 0.04), and a higher 30-day post transplant mortality (P = 0.02). The use of HTK preservation solution was associated with higher mean postoperative aspartate aminotransferase levels (P = 0.02) and decreased mean RBC (P < 0.001) and FFP usage (P = 0.009) compared to UW preservation solution use.
Liver Transplantation 01/2008; 14(1):59-65. · 3.39 Impact Factor
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ABSTRACT: Hepatopulmonary syndrome (HPS) and portopulmonary hypertension (PPHTN) are distinct clinical entities that may complicate liver disease. Although HPS and PPHTN are different, several reports describe 6 patients in whom both conditions have occurred, either concurrently or sequentially, sometimes with the onset of PPHTN after liver transplantation. The current report extends this sparse experience by reporting 2 patients who underwent liver transplantation for HPS and who developed pulmonary hypertension after liver transplantation. This experience calls for better understanding of the pathogenesis of HPS and PPHTN and ways to better predict their occurrence.
Liver Transplantation 09/2006; 12(8):1278-82. · 3.39 Impact Factor
