Portal Vein Flow (portal + vein_flow)

Distribution by Scientific Domains


Selected Abstracts


In vivo evaluation of an implantable portal pump system for augmenting liver perfusion

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 8 2000
L. R. Jiao
Background Increasing portal inflow in cirrhosis using a mechanical pump reduces portal venous pressure and improves liver function. A pump has been developed for portal vein implantation in human cirrhosis. This study describes the initial in vivo evaluation in a porcine model. Methods Five Large White pigs underwent laparotomy and exposure of the liver. Flow in the hepatic artery, portal vein and hepatic microcirculation was monitored continuously. Hepatic tissue oxygenation was measured by near-infrared spectroscopy. After baseline measurements the pump was inserted into the portal vein. Pump flow rate was then increased stepwise to 50 per cent over the baseline value for a period of 2 h. The pump was then stopped for 20 min and left in situ while continuing to collect systemic and hepatic haemodynamic data. The animal was killed and biopsies for histological examination were taken from the liver, small intestine and spleen. Results The baseline total hepatic blood flow was 626(39) ml/min; the hepatic artery supplied 18·4(2·1) per cent and the portal vein 81·6(2·1) per cent. The pump was inserted successfully in all animals without surgical complications. During surgical insertion of the pump, the temporary portal vein occlusion resulted in a significant rise in hepatic artery blood flow (22(3) per cent; P < 0·01 versus baseline). Portal vein flow was augmented by pumping; there was a significant correlation between the pump motor speed and portal vein flow (P < 0·0001). This inflow correlated directly with flow in the hepatic microcirculation and hepatic tissue oxygenation (P < 0·001). The pump ran satisfactorily throughout the study. Histological examination revealed no evidence of structural damage to the liver or ischaemic changes in the small intestine or spleen. Conclusion It is technically possible and safe to insert an implantable pump in the portal vein. Portal venous blood flow can be increased up to 50 per cent with a resultant increase in flow in the hepatic microcirculation and hepatic oxygenation and without adverse effects on either hepatic or systemic haemodynamics. © 2000 British Journal of Surgery Society Ltd [source]


PATIENT AGE IS A STRONG INDEPENDENT PREDICTOR OF 13C-AMINOPYRINE BREATH TEST RESULTS: A COMPARATIVE STUDY WITH HISTOLOGY, DUPLEX-DOPPLER AND A LABORATORY INDEX IN PATIENTS WITH CHRONIC HEPATITIS C VIRUS INFECTION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2006
Arne RJ Schneider
SUMMARY 1Noninvasive tests for the staging of chronic hepatitis C virus (HCV) infection would be an attractive alternative to liver biopsy. The 13C-aminopyrine breath test (ABT) has been proposed for the noninvasive assessment of hepatic function and partly correlates with fibrosis. We aimed to investigate causes for the lack of discriminatory power for different degrees of hepatic fibrosis. 2Eighty-three patients (median age 49 years (28,78 years)) with chronic HCV infection underwent the ABT after an oral load of 75 mg N,N-dimethyl- 13C-aminopyrine. Portal vein flow was assessed by duplex-Doppler and a laboratory index (aspartate aminotransferase to platelet ratio index or APRI) was calculated. Parameters were compared with liver histology. 3The cumulative 13C-recovery differed significantly between patients without relevant fibrosis (fibrosis score 0,2) and cirrhosis (5,6), beginning after 30 min of sampling (P < 0.05). The ABT did not discriminate patients with fibrosis scores 3,4 from the remaining two patient groups. Sensitivity and specificity for the prediction of cirrhosis was 73.4,82.8% and 63.2,68.4%, depending on the sampling time. Compared with the fibrosis score (P = 0.04), patient age was a highly significant independent predictor for the 13C-recovery (P < 0.0001). Aspartate aminotransferase to platelet ratio index and duplex-Doppler predicted cirrhosis with 76.6%vs. 87.5% sensitivity and 63.2%vs. 68.4% specificity. 4Our data suggest an age-dependent decrease of cytochrome P450 activity which probably accounts for the large overlap of ABT results that preclude clear differentiation. This is also consistent with former pharmacodynamic trials. Age-adapted reference ranges could improve ABT results. [source]


Venous hemodynamics in living donor right lobe liver transplantation

LIVER TRANSPLANTATION, Issue 9 2002
Gabriel E. Gondolesi MD
We evaluated the influence of portal and hepatic venous hemodynamics on the immediate and 3-month postoperative function of living donor right lobe grafts. Portal velocity was measured prospectively by ultrasound in 14 consecutive donor/recipient pairs. Velocity was converted to flow with the Moriyasu formula. Measurements were taken in donors in the operating room and in recipients at 1 hour after reperfusion and 3 months after transplant. Recipient liver function tests were measured postoperatively. Prereperfusion and postreperfusion liver biopsies were evaluated and correlated with the hemodynamic and biochemical results. There were 11 male (78.6%) and 3 female donors (mean age, 38.9 ± 9.8 years) for 10 male (71.4%) and 4 female recipients (mean age, 49.3 ± 14 years). The mean graft/recipient weight ratio was 1.22 ± 0.3. The mean right portal vein pressure was 8 ± 1.8 mm Hg in donors versus 13 ± 4.7 mm Hg in recipients (P < .05). The mean peak flow velocity (Vmax) in the portal vein in donors was 47.6 ± 12.8 cm/sec (normal, 44 cm/sec). One hour after graft reperfusion in the recipient, the mean portal Vmax was significantly higher at 94.7 ± 28.4 cm/sec (P = .004), but by 3 months follow-up, mean portal Vmax had fallen to 58.8 ± 37.8 (P = .01). Recipient portal vein Vmax highly correlated with portal flow (r = 0.7, P = .01). Increased recipient total bilirubin on postoperative day 2 correlated highly with higher recipient portal flow one hour after transplant (r = 0.6; P = .03). Portal vein velocity/flow dramatically increases after reperfusion, returning to baseline about 3 months after transplant. Evaluation of hepatic and portal venous flow is a relatively easy skill to acquire. Intraoperative ultrasound may enable the surgeon to predict graft dysfunction and possibly, may be used to implement pre-emptive therapies. [source]


Hepatic arterial flow becomes the primary supply of sinusoids following partial portal vein ligation in rats

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2006
Yukihiro Yokoyama
Abstract Background and Aim:, Partial portal vein ligation (PPVL) is a commonly used procedure to induce prehepatic portal hypertension in animal models. The aim of this study was to test the hypothesis that the hepatic arterial flow becomes the primary source feeding the sinusoids in the liver after PPVL. Methods:, Sprague,Dawley rats underwent either sham operation or partial portal vein ligation (PPVL). The number of vessels in the liver at 2 weeks postoperatively was determined by factor VIII immunolocalization and the gene expression of angiogenic factors was assessed by RT-PCR. The total hepatic arterial supply to the liver was measured using the fluorescent microsphere injection technique. To further test the hypothesis, two additional groups of rats underwent hepatic artery ligation (HAL) or PPVL plus HAL (PPHAL). The integrity of hepatic microcirculation was then evaluated in all four groups by intravital microscopy. Results:, At 2 weeks after operation, the number of vessels detected by factor VIII staining was significantly higher in PPVL compared to sham. Densitometric analysis of RT-PCR bands revealed a significant increase of vascular endothelial growth factor gene expression in PPVL compared to sham. Arterial flow to the liver measured by fluorescent microspheres was increased by 190% in PPVL compared to sham. When all four groups were compared, no prominent histological abnormality was observed in sham, HAL, and PPVL groups; however, PPHAL livers showed focal necrosis and inflammatory cell infiltration around the portal triads. Additionally, only the PPHAL livers showed a decreased sinusoidal diameter and significantly lower perfusion index (PPHAL 42.9 ± 6.1; sham 85.7 ± 7.0, PPVL 80.2 ± 6.5, HAL 70.9 ± 4.5). Conclusions:, These results suggest that the hepatic artery flow becomes the primary source for the blood supply of sinusoids and the compensatory change in the hepatic arterial system plays a critical role in maintaining microcirculatory perfusion following the restriction of the portal vein flow by PPVL. [source]


Adenosine restores the hepatic artery buffer response and improves survival in a porcine model of small-for-size syndrome,

LIVER TRANSPLANTATION, Issue 11 2009
Dympna M. Kelly
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/100g/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 Transpl 15:1448,1457, 2009. © 2009 AASLD. [source]


In vivo evaluation of an implantable portal pump system for augmenting liver perfusion

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 8 2000
L. R. Jiao
Background Increasing portal inflow in cirrhosis using a mechanical pump reduces portal venous pressure and improves liver function. A pump has been developed for portal vein implantation in human cirrhosis. This study describes the initial in vivo evaluation in a porcine model. Methods Five Large White pigs underwent laparotomy and exposure of the liver. Flow in the hepatic artery, portal vein and hepatic microcirculation was monitored continuously. Hepatic tissue oxygenation was measured by near-infrared spectroscopy. After baseline measurements the pump was inserted into the portal vein. Pump flow rate was then increased stepwise to 50 per cent over the baseline value for a period of 2 h. The pump was then stopped for 20 min and left in situ while continuing to collect systemic and hepatic haemodynamic data. The animal was killed and biopsies for histological examination were taken from the liver, small intestine and spleen. Results The baseline total hepatic blood flow was 626(39) ml/min; the hepatic artery supplied 18·4(2·1) per cent and the portal vein 81·6(2·1) per cent. The pump was inserted successfully in all animals without surgical complications. During surgical insertion of the pump, the temporary portal vein occlusion resulted in a significant rise in hepatic artery blood flow (22(3) per cent; P < 0·01 versus baseline). Portal vein flow was augmented by pumping; there was a significant correlation between the pump motor speed and portal vein flow (P < 0·0001). This inflow correlated directly with flow in the hepatic microcirculation and hepatic tissue oxygenation (P < 0·001). The pump ran satisfactorily throughout the study. Histological examination revealed no evidence of structural damage to the liver or ischaemic changes in the small intestine or spleen. Conclusion It is technically possible and safe to insert an implantable pump in the portal vein. Portal venous blood flow can be increased up to 50 per cent with a resultant increase in flow in the hepatic microcirculation and hepatic oxygenation and without adverse effects on either hepatic or systemic haemodynamics. © 2000 British Journal of Surgery Society Ltd [source]