Liver Perfusion (liver + perfusion)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


Liver Perfusion in Sepsis, Septic Shock, and Multiorgan Failure

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 6 2008
Herbert Spapen
Abstract Sepsis causes significant alterations in the hepatic macro- and microcirculation. Diverging views exist on global hepatic blood flow during experimental sepsis because of the large variety in animal and sepsis models. Fluid-resuscitated clinical sepsis is characterized by ongoing liver ischemia due to a defective oxygen extraction despite enhanced perfusion. The effects of vasoactive agents on the hepatosplanchnic circulation are variable, mostly anecdotal, and depend on baseline perfusion, time of drug administration, and use of concomitant medication. Microvascular blood flow disturbances are thought to play a pivotal role in the development of sepsis-induced multiorgan failure. Redistribution of intrahepatic blood flow in concert with a complex interplay between sinusoidal endothelial cells, liver macrophages, and passing leukocytes lead to a decreased perfusion and blood flow velocity in the liver sinusoids. Activation and dysfunction of the endothelial cell barrier with subsequent invasion of neutrophils and formation of microthrombi further enhance liver tissue ischemia and damage. Substances that regulate (micro)vascular tone, such as nitric oxide, endothelin-1, and carbon monoxide, are highly active during sepsis. Possible interactions between these mediators are not well understood, and their therapeutic manipulation produces equivocal or disappointing results. Whether and how standard resuscitation therapy influences the hepatic microvascular response to sepsis is unknown. Indirect evidence supports the concept that improving the microcirculation may prevent or ameliorate sepsis-induced organ failure. Anat Rec, 291:714,720, 2008. © 2008 Wiley-Liss, Inc. [source]


Hepatic arterial buffer response in patients with advanced cirrhosis

HEPATOLOGY, Issue 3 2002
Veit Gülberg
Hepatic arterial buffer response (HABR) is considered an important compensatory mechanism to maintain perfusion of the liver by hepatic arterial vasodilation on reduction of portal venous perfusion. HABR has been suggested to be impaired in patients with advanced cirrhosis. In patients with hepatopetal portal flow, placement of a transjugular intrahepatic portosystemic shunt (TIPS) reduces portal venous liver perfusion. Accordingly, patients with severe cirrhosis should have impaired HABR after TIPS implantation. Therefore, the aim of this study was to investigate the effect of TIPS on HABR as reflected by changes in resistance index (RI) of the hepatic artery. A total of 366 patients with cirrhosis (Child-Pugh class A, 106; class B, 168; class C, 92) underwent duplex Doppler ultrasonographic examination with determination of RI and maximal flow velocity in the portal vein before and 1 month after TIPS placement. Portosystemic pressure gradient was determined before and after TIPS placement. In 29 patients with hepatofugal portal blood flow, RI was significantly lower than in 337 patients with hepatopetal flow (0.63 ± 0.02 vs. 0.69 ± 0.01; P < .001). TIPS induced a significant decrease of the RI in patients with hepatopetal flow (RI, 0.69 ± 0.01 before vs. 0.64 ± 0.01 after TIPS; P = .001) but not in patients with hepatofugal flow (RI, 0.63 ± 0.02 before vs. 0.63 ± 0.02 after TIPS; NS). This response was not dependent on the Child-Pugh class. In conclusion, our results suggest that some degree of HABR is preserved even in patients with advanced cirrhosis with significant portal hypertension. [source]


Portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2 -type receptors

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 1 2001
MaurÍcio R Loureiro-Silva
Abstract Background: We have shown that the portal hypertensive response to bradykinin in normal rats is mediated by B2 receptors. Methods: By using isolated and exsanguinated rat liver perfusion, we studied the portal hypertensive response to bradykinin or des-Arg9 -bradykinin (B1 agonist) in inflamed or cirrhotic rat livers. Livers were perfused with bovine serum albumin Krebs,Henseleit buffer (pH 7.4; 37°C) at a constant flow rate, in the absence or presence of des-Arg9[Leu8]-bradykinin or HOE 140 (B1 and B2 receptor antagonists, respectively). Bradykinin (140 nmol) or des-Arg9 -bradykinin was injected as a bolus via the afferent route to the liver. Results: Basal perfusion pressure in liver-cirrhotic rats was higher than in normal rats. In normal, inflamed, or liver-cirrhotic rats, the presence of the B1 antagonist did not change the portal hypertensive response to bradykinin, while the B2 antagonist abolished this response. A 140-nmol dose of des-Arg9 -bradykinin did not change the perfusion pressure; 700 nmol of this B1 agonist produced an insignificant perfusion pressure increase. The perfusion pressure increase induced by bradykinin in cirrhotic livers was lower than in normal livers. Conclusions: The portal hypertensive response to bradykinin in inflamed or cirrhotic rat livers is mediated by B2 receptors, but not B1 receptors, and there is a contracting hyporeactivity to bradykinin in cirrhotic rat livers. [source]


Median liver lobe of woodchuck as a model to study hepatic outflow obstruction: a pilot study

LIVER INTERNATIONAL, Issue 9 2008
Uta Dahmen
Abstract Background: Hepatic vein outflow obstruction represents an important clinical problem in living-liver transplantation. An animal model is required to study the influence of outflow obstruction on the intrahepatic regulation of liver perfusion and the subsequent effects on liver injury and recovery during liver regeneration. The size of woodchucks enables the use of standard clinical imaging procedures. Aim: This study aims at describing hepatic vascular and territorial anatomy of the woodchuck liver based on a virtual three-dimensional (3D) visualization of the hepatic vascular tree. Methods: Woodchucks (n=6) were subjected to an all-in-one computed tomography (CT) after contrasting the vascular and the biliary tree. CT-images were used for 3D-reconstruction of hepatic and portal veins and calculation of the corresponding portal and hepatic vein territories and their respective volume using hepavision (MeVisLab). A virtual resection was performed following the Cantlie-line and territories at risk were calculated. Results: The median lobe of the woodchuck liver has a similar vascular supply and drainage as the human liver with two portal (right and left median portal vein) and three hepatic veins (left, middle and right median hepatic vein). The corresponding portal and hepatic vein subterritories are of a similar relative size compared with the human liver. Virtual splitting of the median lobe of the woodchuck liver revealed areas at risk of focal outflow obstruction, as observed clinically. Conclusion: The median liver lobe of the woodchuck represents, to a small extent, the hepatic vascular anatomy of the human liver and is therefore a suitable potential model to correlate repeated imaging of impaired liver perfusion with histomorphological findings of liver damage and regeneration. [source]


Abdominal compartment syndrome after liver transplantation

LIVER TRANSPLANTATION, Issue 1 2005
Alexander E. Handschin
The abdominal compartment syndrome is a well-known complication after abdominal trauma and is increasingly recognized as a potential risk factor for renal failure and mortality after adult orthotopic liver transplantation (OLT). We present a case report of a young patient who presented with acute liver failure complicated by an acute pancreatitis. The patient developed an acute abdominal compartment syndrome after OLT. Transurethral measurement of intraabdominal pressure indicated an abdominal compartment syndrome associated with impaired abdominal vascular perfusion, including liver perfusion. Renal insufficiency was immediately reversed after decompressive bedside laparotomy. The abdominal compartment syndrome is a potential source of posttransplant renal insufficiency and liver necrosis in OLT. It remains, however, a rarely described complication after liver transplantation, despite the presence of significant factors that contribute to elevated intraabdominal pressure. (Liver Transpl 2005;11:98,100.) [source]


Influence of extracorporeal porcine liver perfusion on nonhuman primates: Minimizing hemolysis improves subsequent survival

LIVER TRANSPLANTATION, Issue 7 2001
Ryuta Nishitai MD
The aim of this study is to detect and analyze risk factors of direct cross-circulation between porcine liver and nonhuman primates before a clinical application of extracorporeal liver perfusion (ECLP) as a liver-assist method. Porcine livers were perfused with baboon blood in an ECLP system. Six healthy baboons were directly connected to the ECLP system with continuous prostaglandin E1 administration. Cross-circulation was terminated in the following circumstances: (1) hepatic arterial or portal perfusion pressures elevated to 200 or 60 mm Hg, respectively; (2) massive exudative bleeding from the graft surface; or (3) bile output decreased to less than 5 ,L/h/g of liver weight. In case 1, cross-circulation was continued for 10 hours. Severe macroscopic hemolysis occurred, and serum hemoglobin (s-Hb) concentration reached a peak of 47 mg/dL. The baboon died of acute renal failure 2 days later. Histological study of the perfused porcine liver showed marked microthrombi formation. In 3 of the later 5 cases, cross-circulation was discontinued when mild macroscopic hemolysis was observed. The duration of the 5 cross-circulations was maximally 6 hours (mean, 4.4 ± 1.2 [SD] hours). Mean s-Hb concentration in the 5 cases was elevated to 14.8 ± 5.8 mg/dL at the end of cross-circulation and decreased to the baseline level within 24 hours. These 5 baboons survived without organ dysfunction or immunologic disturbance. When severe hemolysis is avoided, direct cross-circulation using the ECLP system can be achieved without serious complications in nonhuman primates. [source]


Prospective Evaluation of Intraoperative Hemodynamics in Liver Transplantation with Whole, Partial and DCD Grafts

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2010
M. Sainz-Barriga
The interaction of systemic hemodynamics with hepatic flows at the time of liver transplantation (LT) has not been studied in a prospective uniform way for different types of grafts. We prospectively evaluated intraoperative hemodynamics of 103 whole and partial LT. Liver graft hemodynamics were measured using the ultrasound transit time method to obtain portal (PVF) and arterial (HAF) hepatic flow. Measurements were recorded on the native liver, the portocaval shunt, following reperfusion and after biliary anastomosis. After LT HAF and PVF do not immediately return to normal values. Increased PVF was observed after graft implantation. Living donor LT showed the highest compliance to portal hyperperfusion. The amount of liver perfusion seemed to be related to the quality of the graft. A positive correlation for HAF, PVF and total hepatic blood flow with cardiac output was found (p = 0.001). Portal hypertension, macrosteatosis >30%, warm ischemia time and cardiac output, independently influence the hepatic flows. These results highlight the role of systemic hemodynamic management in LT to optimize hepatic perfusion, particularly in LDLT and split LT, where the highest flows were registered. [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]


Disposition of isosteviol in the rat isolated perfused liver

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2010
Hongping Jin
Summary 1. The aim of the present study was to investigate the mechanisms involved in the clearance of isosteviol using the rat isolated perfused liver. 2. Six livers from male Sprague-Dawley rats were perfused with 15.7 ,mol isosteviol in a recirculating system. Perfusate and bile samples were collected for 60 min and the liver was collected at the end of the perfusion. All samples collected were incubated with ,-glucuronidase. Isosteviol,glucuronide was determined as equivalent isosteviol. Isosteviol concentrations were determined using a previously developed liquid chromatography,tandem mass spectrometry method. The final isosteviol liver/perfusate (L/P), bile/liver (B/L) and isosteviol-glucuronide in bile/liver (BG/LG) ratios were determined. 3. Isosteviol has a high clearance (21.4 ± 4.8 mL/min) from the perfusate, with a short half-life (13 ± 4 min). ,-Glucuronidase incubation revealed that isosteviol is conjugated in the liver and excreted into the bile. There was no isosteviol-glucuronide detected in perfusate samples. The total recovery of the rat isolated perfused liver system is 74 ± 14% and glucuronidated isosteviol accounted for 23 ± 4% of the administered dose. 4. In conclusion, we are the first to characterize the metabolism of isosteviol using rat isolated liver perfusion. Our results strongly suggest that the liver is the main organ of isosteviol elimination and that isosteviol is glucuronidated in the liver before it is excreted into the bile. [source]