OBJECTIVETo examine the effect of different infusion volume on hemodynamics of portal hypertension (PHT) canines after hemorrhagic shock (HS).

METHODSPHT canine models were made by coarctating a half main portal vein with silk line chronic embolization. Two weeks later, the canine models were assigned to hemorrhagic shock by femoral artery venesection quickly. They were divided into two groups: large volume infusion group (n=6) and small volume infusion group (n=6). Hemodynamics indexes of PHT canines after HS were monitored continuously. We also examined the effect of different infusion volume on hemodynamics.

RESULTSPHT canines showed a series of hemodynamics changes in hemorrhagic shock stage, which aggravated hemodynamics disorder in PHT. After quick infusion, MAP, IVCP, PVP, PVPG, PVBF, HABF, and HBF increased significantly. These indexes in large volume infusion group were higher than those in small volume infusion group. PVR, SVR, HAR decreased significantly. PVP, PVPG, PVBF, HABF, and HBF showed a rebound increase above baseline values in large volume infusion group. The changes of PVP, PVPG, PVBF, HABF, and HBF were parallel with MAP and IVCP and without rebound increase in small volume infusion group. In large volume infusion group PVPG increased earlier and more significant than PVP and exceeded baseline by 13% (2.58 0.37) kPa, so the danger of rebleeding rose greatly. In small volume infusion group PVPG was over 22% (1.67 0.27) kPa lower than baseline, which infers that the danger of rebleeding reduced greatly. SVR and HAR were lower in large volume infusion group. PVP, PVPG, PVBF, HABF, and HBF showed a positive correlation with accumulated vein infusion volume. PVR showed a positive correlation with accumulated vein infusion volume in small volume infusion group. HAR showed a negative correlation with accumulated vein infusion volume in large volume infusion group.

CONCLUSIONSPHT canines after HS show a rebound increase of PVP, PVPG, PVBF, HABF, and HBF above baseline values in large volume infusion group. In small volume infusion group, however, no rebound increase is noticed. Large volume infusion may cause PVP, PVPG, PVBF, HABF, and HBF increase higher than small volume infusion.

Animals ; Dogs ; Hemodynamics ; Hypertension, Portal ; etiology ; physiopathology ; Portal Vein ; physiopathology ; Shock, Hemorrhagic ; complications

Hemodynamics ; Humans ; Hypertension, Portal ; etiology ; physiopathology ; surgery ; Liver Cirrhosis ; complications ; physiopathology ; surgery ; Liver Transplantation ; Postoperative Period

Humans ; Hypertension, Portal ; physiopathology ; surgery ; Liver ; physiopathology ; Liver Cirrhosis ; complications ; Liver Transplantation ; Portasystemic Shunt, Transjugular Intrahepatic

Esophageal and Gastric Varices ; etiology ; therapy ; Hemodynamics ; Humans ; Hypertension, Portal ; complications ; therapy ; Liver Cirrhosis ; complications ; therapy ; Portal Vein ; physiopathology

INTRODUCTIONHepatic venous pressure gradient (HVPG) measurement is recommended for prognostic and therapeutic indications in centres with adequate resources and expertise. Our study aimed to evaluate the quality of HVPG measurements at our centre before and after introduction of a standardised protocol, and the clinical relevance of the HVPG to variceal bleeding in cirrhotics.

METHODSHVPG measurements performed at Singapore General Hospital from 2005-2013 were retrospectively reviewed. Criteria for quality HVPG readings were triplicate readings, absence of negative pressure values and variability of ≤ 2 mmHg. The rate of variceal bleeding was compared in cirrhotics who achieved a HVPG response to pharmacotherapy (reduction of the HVPG to < 12 mmHg or by ≥ 20% of baseline) and those who did not.

RESULTS126 HVPG measurements were performed in 105 patients (mean age 54.7 ± 11.4 years; 55.2% men). 80% had liver cirrhosis and 20% had non-cirrhotic portal hypertension (NCPH). The mean overall HVPG was 13.5 ± 7.2 mmHg, with a significant difference between the cirrhosis and NCPH groups (p < 0.001). The proportion of quality readings significantly improved after the protocol was introduced. HVPG response was achieved in 28 (33.3%, n = 84) cirrhotics. Nine had variceal bleeding over a median follow-up of 29 months. The rate of variceal bleeding was significantly lower in HVPG responders compared to nonresponders (p = 0.025).

CONCLUSIONThe quality of HVPG measurements in our centre improved after the introduction of a standardised protocol. A HVPG response can prognosticate the risk of variceal bleeding in cirrhotics.

Esophageal and Gastric Varices ; complications ; physiopathology ; Female ; Follow-Up Studies ; Gastrointestinal Hemorrhage ; etiology ; physiopathology ; prevention & control ; Humans ; Hypertension, Portal ; complications ; physiopathology ; Liver Cirrhosis ; complications ; physiopathology ; Male ; Middle Aged ; Portal Pressure ; physiology ; Prognosis ; Retrospective Studies

Portal hypertension is a severe consequence of chronic liver diseases and is responsible for the main clinical complications of liver cirrhosis. Hepatic venous pressure gradient (HVPG) measurement is the best available method to evaluate the presence and severity of portal hypertension. Clinically significant portal hypertension is defined as an increase in HVPG to >10 mmHg. In this condition, the complications of portal hypertension might begin to appear. HVPG measurement is increasingly used in the clinical fields, and the HVPG is a robust surrogate marker in many clinical applications such as diagnosis, risk stratification, identification of patients with hepatocellular carcinoma who are candidates for liver resection, monitoring of the efficacy of medical treatment, and assessment of progression of portal hypertension. Patients who had a reduction in HVPG of > or =20% or to < or =12 mmHg in response to drug therapy are defined as responders. Responders have a markedly decreased risk of bleeding/rebleeding, ascites, and spontaneous bacterial peritonitis, which results in improved survival. This review provides clinical use of HVPG measurement in the field of liver disease.
Chronic Disease ; Hemodynamics ; Hemorrhage/etiology ; Hepatic Veins/physiology ; Humans ; Hypertension, Portal/complications ; Liver Cirrhosis/diagnosis ; Liver Diseases/complications/*physiopathology ; Portal Pressure

The lymphatic system is part of the circulatory system and plays a key role in normal vascular function. Its failure plays a crucial role in the development and maintenance of various diseases including liver diseases. Lymphangiogenesis (the growth of lymphatic vessels) and changes in the properties of lymphatic vessels are associated with pathogenesis of tumor metastases, ascites formation, liver fibrosis/cirrhosis and portal hypertension. Despite its significant role in liver diseases and its importance as a potential therapeutic target for those diseases, the lymphatic vascular system of the liver is poorly understood. Therefore, how the lymphatic vascular system in general and lymphangiogenesis in particular are mechanistically related to the pathogenesis and maintenance of liver diseases are largely unknown. This article summarizes: 1) the lymphatic vascular system; 2) its role in liver tumors, liver fibrosis/cirrhosis and portal hypertension; and 3) its role in ascites formation.
Ascites/*etiology ; Humans ; Hypertension, Portal/complications/pathology ; Liver Cirrhosis/complications/pathology ; Liver Diseases/complications/*pathology ; Liver Neoplasms/complications/pathology ; Lymphangiogenesis ; Lymphatic Vessels/metabolism/physiopathology

OBJECTIVETo investigate the relationship between perioperative free portal pressure (FPP) after devascularization or spleno-renal shunt operation added devascularization and rebleeding or encephalopathy in patients with portal hypertension, and evaluate the relationship between dynamic changes of FPP and surgical approaches.

METHODSThe clinical data of 170 patients with portal hypertension receiving devascularization or devascularization with spleno-renal shunt operation (combination group) from January 2001 to December 2007 were retrospectively analyzed. All patients were divided into three groups: low pressure group [L group, after devascularization FPP 22 mm Hg, n = 60) and combination group (C group, n = 47). There was no significant difference in preoperative Child-Pugh score and pre-operation FPP (P > 0.05) among the three groups. Perioperative FPP, morbidity of rebleeding and encephalopathy were compared with each other.

RESULTSThe values of postoperative FPP were (27.1 +/- 1.9) mm Hg, (20.8 +/- 1.8) mm Hg and (21.5 +/- 2.2) mm Hg among the H group, L group and C group respectively. The rebleeding rates were 21.7%, 4.6% and 4.5% among the three groups respectively. All the values in H group were higher than those in L group and C group remarkably. The encephalopathy rate in C group (10.4%) was higher than that in L group (7.0%) or H group (3.3%), but there were no statistical significance (P > 0.05).

CONCLUSIONSFPP after splenectomy and devascularization may be a basis of choice of surgical approaches in portal hypertension. The spleno-renal shunt operation should be performed in the patients when FPP is over 22 mm Hg after devascularization.

Adult ; Aged ; Female ; Gastrointestinal Hemorrhage ; etiology ; Hepatic Encephalopathy ; etiology ; Humans ; Hypertension, Portal ; physiopathology ; surgery ; Male ; Middle Aged ; Monitoring, Intraoperative ; Portal Pressure ; physiology ; Postoperative Complications ; etiology ; Retrospective Studies

It was reported that pancreatic arteries constricted during the early phase of bile salt-induced acute pancreatitis (AP), leading to pancreatic microcirculatory disturbance. We conducted this experiment to verify whether the above-mentioned finding was true. AP was induced with intraductal injection of taurodeoxyholate. Small pancreatic artery pressure in dogs was recorded. Functional capillaries were counted and calibrated by multiplying wet weight of pancreas. Pancreatic perfusion was measured with Laser Doppler flowmeter. Pancreatic arterioles of rats dilated during the initial 20 min of AP, and pancreatic arterial pressure declined during the early phase of AP in dogs (from 104.5 +/- 4.8 mmHg to 54.6 +/- 5.6 mmHg). The hematocrit of blood from inferior vena cava was significantly lower than that of portal vein at 5 min after pancreatitis induction. The "true" pancreatic functional capillary density increased. The early pancreatic microcirculatory disturbance coincided with a marked increase of portal vein pressure (PVP) as high as 9.18 +/- 0.78 mmHg. Reduction of PVP to baseline level was followed by a marked increase of pancreatic perfusion (by 1.4-fold). Arterial dilatation, but not constriction, occurred during the early phase of bile salt-induced AP. The pancreatic microcirculatory disturbance was due to a marked rise in PVP that greatly reduced the pressure difference in the pancreatic blood vessels and increased plasma extravasation which led. to local hemoconcentration.
Animals ; Bile Acids and Salts ; adverse effects ; Hypertension, Portal ; complications ; Male ; Microcirculation ; drug effects ; physiology ; Pancreas ; blood supply ; Pancreatitis ; etiology ; physiopathology ; Portal Pressure ; Portal Vein ; physiopathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate the predictive value of portal vein flow rate preoperative for portal vein thrombosis (PVT) after periesophagastric devascularization in hepatitis B cirrhosis-related portal hypertension.

METHODSFrom January 2007 to July 2008, 45 patients with portal hypertension caused by hepatitis B cirrhosis were performed splenectomy with peri-esophagogastric devascularization in the same medical group in West China Hospital of Sichuan University. The portal vein flow rate and the diameter of portal vein were measured with doppler sonography respectively before and after the operation. At the same time, the level of PT and PLT were detected. The weight of spleens were measured after operation.

RESULTSThirteen cases suffered from PVT postoperatively. Portal vein flow rate was significantly lower in patients with PVT postoperation than that in patients without PVT (P < 0.01). In patients with PVT (n = 13) postoperation, the preoperative portal vein flow rate was (19.5 +/- 5.3) cm/s. Among the 13 cases, there were 12 cases whose flow rate were lower than 25 cm/s, and 1 case whose flow rate was 32. 3 cm/s; In patients without PVT (n = 32), the preoperative portal vein flow rate was (9.6 +/- 8.0) cm/s. In patients with lower rate (n = 17), the incidence rate of PVT was 70.6%; in patients with higher rate (n = 28), the incidence rate of PVT was 3.6%. The incidence rate of PVT in patients with lower rate was significantly lower than patients with higher rate (P < 0.01). The diameter of portal vein in patients with PVT was significantly wider than patients without PVT. The diameter of portal vein was negative correlative with the portal vein flow rate. The value 25 cm/s was of diagnostic efficiency, the sensitivity was 92.3%, and specificity was 70.6%.

CONCLUSIONSThe portal vein flow rate preoperative can be used as an early predictor of portal vein thrombosis after periesophagastric devascularization in hepatitis B cirrhosis-related portal hypertension to give a guide to clinical work.

Adult ; Aged ; Blood Flow Velocity ; Female ; Humans ; Hypertension, Portal ; etiology ; physiopathology ; surgery ; Liver Cirrhosis ; complications ; Male ; Middle Aged ; Portal Vein ; diagnostic imaging ; physiopathology ; Postoperative Complications ; diagnosis ; etiology ; Preoperative Care ; Risk Factors ; Splenectomy ; Ultrasonography ; Venous Thrombosis ; diagnosis ; etiology