Total Hepatic Blood Flow Research Articles

Intraoperative Blood Flow Measurements and Liver Allograft Function: Preliminary Results

Introduction Our previous studies showed a correlation of intraoperative renal allograft blood flow and immediate functions. A similar relation is not well established for liver transplantation. The aim of this study was to assess the relation between hepatic blood flow on revascularization and immediate liver graft function (IF). Methods Studies evaluating arterial and portal flow in newly transplanted livers were started in May 2004. Total hepatic artery and portal vein blood flow were assessed in 15 liver transplant recipients. Parenchymal flow was also recorded. Measurements were taken at 30 and 120 minutes after simultaneous arterial/portal reperfusion. Flow results were correlated with IF. Results Mean arterial blood flow (ABF) was 16.3 mL/min/100 g in both measurements. Portal flow was reduced from 168 to 127 mL/min/100 g from the first to the second measurement. Mean parenchymal flow (PF) did not alter over time (29.1 and 30.4 mL/min/100 g, respectively). Among recorded flow results we observed a significant correlation between PF with IF measured as: bile volume (R = 0.36 to 0.62; P < .05), serum AST (R = −0.4 to −0.68; P < .05), and ALT level (R = −0.2 to −0.71; P < .05), bilirubin level as well as INR (R = −0.39 to −0.61; P < .05) assayed daily for 14 days. Similar observations were made between ABF and INR, hiatal parenchymal flow, and ALT as well as INR. Conclusions These preliminary results suggest hepatic blood flow may be a reliable predictor of graft viability and function. Of the variables measured, portal blood flow seems to be the most valuable indicator of liver function.

New Measurement of Hepatic Blood Flow by Xenon CT System: An Animal Study with PGE1

A new Xenon computed tomography (CT) system was developed to measure both hepatic arterial and portal venous tissue blood flow (HATBF/PVTBF) non-invasively. Despite its clinical trial, the effect of prostaglandin E1 (PGE1) on hepatic hemodynamics is not well investigated. In a rabbit model, we evaluated the accuracy of this system by comparing it with the electromagnetic blood flowmeter (EMBF), the pharmacological effect of PGE1 on the fractional hepatic hemodynamics. Seven NZW-rabbits were used. Serial abdominal CT scan was obtained every min before and during the 4 min inhalation of the Xenon gas, followed by 5 min administration of oxygen air. From these images, HATBF and PVTBF were separately calculated with a special new imaging system. We also used EMBF during laparotomy, and directly measured the hepatic arterial and portal venous flow with or without PGE1 administration. Xenon CT showed HATBF of 18.4 +/- 4.5 (ml/min/100 g) and PVTBF of 69.4 +/- 15.0, was almost identical with those of EMBF (19.8 +/- 5.7 and 67.2 +/- 19.1, respectively). After PGE1 administration, Xenon CT showed 22.9 +/- 4.6 and 76.5 +/- 20.5, while those with EMBF were 21.0 +/- 6.5 and 84.7 +/- 21.6, respectively. There were significant correlations (P < 0.01) in total HTBF, HATBF, and PVTBF between results of Xenon CT and EMBF. Xenon CT with a newly developed imaging system enables us to measure the fractional hepatic tissue blood flow in rabbits, differentially and accurately. Venous administration of PGE1 increased total hepatic blood flow, mainly affecting the portal blood flow.

Characterisation and partial purification of Schistosoma mansoni egg-derived pro-angiogenic factor

Pathogenesis of Schistosoma mansoni infection is due to the accumulation of eggs in the liver and intestine of the host followed by granuloma formation and fibrosis at the site of egg embolism. Nevertheless, total hepatic blood flow and hepatic function appear to be maintained by neovascularisation of the periportal fibrotic tissue. Here we demonstrate that intact live eggs, excretory/secretory products of eggs and the extracts of homogenised eggs stimulate the proliferation and migration of endothelial cells. Formation of endothelial capillary-like outgrowths, as well as, the activation of p42/p44 mitogen-activated protein kinase signal transduction pathway was stimulated by egg extracts, whereas other stages of the schistosome life-cycle did not exhibit such activity. We have characterised and partially purified the pro-angiogenic factor. The active pro-angiogenic component was fast-acting, heat-stable, protease-resistant, weakly heparin-binding and a non-lipid. It could be extracted with acidified ethanol or a hot acetic acid solution and could be partially purified by reverse-phase HPLC. The S. mansoni egg-derived pro-angiogenic factor, described here, may directly contribute to vascular remodelling in the liver and illustrates how helminth parasites may modulate angiogenesis.

Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion

To assess the effects of low hepatosplanchnic blood flow on regional blood flow control and oxygenation. Three randomized, controlled animal experiments. Two university experimental research laboratories. Pigs of either gender. Isolated abdominal blood flow reduction: An extracorporeal shunt with reservoir and roller pump was inserted between proximal and distal aorta in 11 pigs. Abdominal aortic blood flow was reduced by 50% by activating the shunt. Mesenteric ischemia: In seven pigs, superior mesenteric arterial flow was reduced to 4 mL.kg.min for 4 hrs. Cardiac tamponade: In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 mL (moderate tamponade) and further to 30 mL.kg.min (severe tamponade) for 1 hr each. In each experimental condition, the same number of control animals was used. Abdominal blood flow reduction, acute mesenteric ischemia, and moderate tamponade resulted in a portal venous flow (QPV) reduction to 51 +/- 23%, 52 +/- 18%, and 61 +/- 25% (mean +/- sd) of baseline flow, respectively. During abdominal blood flow reduction, QPV and hepatic arterial flow (QHA) decreased proportionally, whereas in moderate tamponade and acute mesenteric ischemia QPV reduction was associated with an increase in QHA of 30 +/- 39% and 102 +/- 108%, respectively (p = .001 and .018). Prolonged mesenteric ischemia restored total hepatic blood flow (Qliver) completely. During all conditions, decreasing mesenteric oxygen consumption was partly prevented by increased mesenteric oxygen extraction (p < .001 for all conditions). In contrast, decreasing hepatic oxygen delivery was associated with increased oxygen extraction in tamponade (p = .009) but not in abdominal blood flow reduction. Blood flow redistribution can restore Qliver totally when mesenteric blood flow is reduced selectively, partially when cardiac output is reduced, and not at all during abdominal blood flow reduction. Since hepatic oxygen extraction does not increase in abdominal blood flow reduction, hepatic oxygenation is at risk in this condition.

The Banding of an Esophageal Varix

The proportion of patients with upper gastrointestinal bleeding (UGI) from esophageal varices varies among centres; however, in approximately 10% of all emergency patients with UGI bleeding, the source is identified as esophageal varices (1). Centres that have a special interest in liver disease may have a higher proportion of patients presenting with this problem. The significance of these lesions is highlighted by the high morbidity and mortality rates associated with the presence of acutely bleeding varices. Although varices from portal hypertension may develop within the stomach (ie, fundal), small intestine (duodenal, jejunal or ileal) or colon (classically rectal), the most common site is within the esophagus. The etiology of the varices is usually cirrhosis; however, any cause of portal hypertension (ie, portal vein thrombosis) can theoretically result in a similar vascular outcome. Overall, approximately 60% of patients with cirrhosis develop esophageal varices and 60% of these have a bleeding episode (2). The natural history of esophageal varices is dramatic in that up to one-third of patients may rebleed over the subsequent six weeks if untreated. The significance of this problem has therefore spawned numerous studies, and the optimal management of bleeding esophageal varices has been determined. The first step in the management of any UGI bleeding patient is resuscitation. As endoscopic therapy has become more widely available, the urgent call for the endoscopist tends be rapidly transmitted with alarming speed from the emergency room when an unstable patient arrives with hematemesis and/or melena. It should be clearly recognized that in the ‘ABCs’ of resuscitation, the ‘E’ for endoscopy actually comes after airway, breathing and circulation have been adequately managed. Most patients with UGI bleeding (approximately 80%) stabilize with intravenous fluid resuscitation. Access with two large-bore intravenous lines is preferable so that pharmacological agents and blood transfusions may be simultaneously administered. In the setting of esophageal variceal hemorrhage, the use of ancillary medications to improve outcomes (primarily by decreasing portal pressures) has been advocated. For many years, vasopressin (with or without nitroglycerin) was used at a dose of 0.4 units/min. Morbidity from the vasopressin occurs in 20% of patients if it is used in isolation; therefore, the addition of nitroglycerin has been instituted to decrease this risk. Another approach to avoid complications from vasopressin is to alter its underlying structure, so that a ‘slow-release’ vasopressin analogue results (glypressin). Glypressin has been associated with fewer side effects, but without improved efficacy. Unlike vasopressin, octreotide has no effect on systemic arterial pressure, cardiac index or pulse rate. Somatostatin and its longer-acting analogue octreotide are presently the primary pharmacological modality of therapy for UGI bleeding from esophageal varices. Somatostatin has a half-life of 2 min to 3 min, with a pharmacological half-life of 90 min. A bolus of 75 µg to 100 µg decreases splanchic blood flow by 25%, total hepatic blood flow by 25%, wedged hepatic vein pressure by 10% and measured varix pressure by approximately 35% (3-5). Somatostatin has been compared with vaso

Hemodynamic study on liver cirrhosis: clinical application of CT perfusion imaging

目的 采用单层CT动态成像测定肝脏血流量,研究肝硬化程度与肝脏血流量动态变化的关系.方法对27例肝硬化患者及13例对照者选取同时含有肝脏、脾脏、主动脉和门静脉的层面进行单层CT动态增强扫描,绘制感兴趣区时间-密度曲线,计算肝脏血流量各参数.结果正常组肝动脉灌注量为(0.2823±0.0969)ml·min-1·ml-1,门静脉灌注量为(1.1788±0.4004)ml·min-1·ml-1,总肝血流量为(1.4563±0.4439)ml·min-1·ml-1,肝动脉灌注指数为(19.73±5.81)%.肝硬化程度不同时,肝动脉灌注量、门静脉灌注量、肝脏总血流量及肝动脉灌注指数变化间差异存在显著性意义.Child A、B级患者肝动脉灌注量[(0.1685±0.1068)ml·min-1·ml-1, (0.1921±0.0986)ml·min-1·ml-1]降低,而Child C 级患者肝动脉灌注量[(0.3072±0.1145)ml·min-1·ml-1]比Child A、B级患者增加,肝动脉灌注指数[(37.48±16.65)%]也增加.Child B、C级患者门静脉灌注量[(0.6331±0.2070)ml·min-1·ml-1, (0.5702±0.3562)ml·min-1·ml-1]及总肝血流量[(0.8252±0.2952)ml·min-1·ml-1, (0.8774±0.4118)ml·min-1·ml-1]下降.结论肝脏CT灌注成像可定量测定肝脏血流量参数,肝硬化时肝脏血流灌注的变化与疾病的严重程度相关。

Nature of Doppler perfusion index changes in patients with colorectal cancer liver metastases.

Occult hepatic metastases from colorectal cancer result in an increase of the ratio of arterial hepatic blood flow to total hepatic blood flow, described as the Doppler perfusion index. Whether this alteration is due to an increase in arterial blood flow or a decrease in portal venous inflow has not yet been unequivocally determined. The purpose of this study was to analyze changes in hepatic perfusion in patients with liver metastases from colorectal cancer by standardization of hemodynamic parameters to body surface area. Hemodynamic parameters (crosssectional area, blood flow, and congestive index) were measured for the common hepatic artery and portal vein with duplex color Doppler sonography in 20 patients with liver metastases and 20 healthy control subjects and evaluated relative to body surface area. No statistically significant differences in age, body surface area, cross-sectional area of the common hepatic artery, and congestion index of the common hepatic artery and portal vein were observed between control subjects and patients with liver metastases. Patients with liver metastases had significantly greater arterial hepatic blood flow and Doppler perfusion index and significantly smaller portal cross-sectional area portal blood flow as well as total liver blood flow (P <.001). This study supports the theory that the primary mechanism of alteration in liver perfusion is the reduction of portal inflow with subsequently increased arterial hepatic blood flow.

The effects of thoracic epidural anesthesia on hepatic perfusion and oxygenation in healthy pigs during general anesthesia and surgical stress.

Perioperative liver injury due to decreased perfusion may be an underlying mechanism behind the development of systemic inflammatory response syndrome. We designed this animal study to assess whether thoracic epidural anesthesia (TEA) impairs liver oxygenation due to induced hypotension. After ethical approval, 19 anesthetized and acutely instrumented pigs were randomly assigned to 3 groups (control and TEA alone versus TEA plus volume loading). Bupivacaine 0.5% 0.75 mL per segment was injected into the epidural space, aiming for a T5 to T12 block. After baseline values were obtained, measurements were repeated 60 and 120 min after epidural injection. TEA was associated with decreased mean arterial blood pressure but no change in total hepatic blood flow. Oxygen delivery to the liver and oxygen uptake remained unchanged. Liver tissue oxygen partial pressure did not decrease. The plasma indocyanine green disappearance rate remained stable. Volume loading before TEA did not relevantly affect total hepatic blood flow; it even decreased oxygen supply to the liver by hemodilution. We conclude that, despite decreased mean arterial blood pressure, TEA did not affect liver oxygenation. There was no clinically relevant effect of volume loading on total hepatic perfusion.

Impairment of hepatic microcirculation in fatty liver.

Fatty liver or hepatic steatosis, which is the result of the abnormal accumulation of triacylglycerol within the cytoplasm of hepatocytes, is a common histological finding in human liver biopsy specimens that is attributed to the effects of alcohol excess, obesity, diabetes, or drugs. There is a general consensus that fatty liver compromises hepatic microcirculation, the common exchange network upon which hepatic arterial and portal inflows converge, regardless of underlying etiology. A significant reduction in hepatic microcirculation has been observed in human fatty donor livers and in experimental models of hepatic steatosis. There is an inverse correlation between the degree of fat infiltration and both total hepatic blood flow and flow in microcirculation. Fatty accumulation in the cytoplasm of the hepatocytes is associated with an increase in the cell volume that reduces the size of the hepatic sinusoid space by 50% compared with a normal liver and may result in partial or complete obstruction of the hepatic sinusoid space. As a result of impaired hepatic microcirculation, the hepatocytes of the fatty liver have reduced tolerance against ischemia-reperfusion injury, which affects about 25% of the donors for liver transplantation because severe steatosis is associated with a high risk of primary nonfunction after liver transplantation.

Hepatic arterial buffer response: visualization by multiphasic high-resolution 3D magnetic resonance angiography

Hepatic arterial buffer response (HABR) is an intrinsic regulatory mechanism to maintain total hepatic blood flow when portal perfusion decreases [1]. This phenomenon has been shown under various experimental conditions and Doppler ultrasound studies have suggested persistence of HABR in cirrhotic patients with transjugular intrahepatic porto-systemic shunt [2].

Doppler ultrasonographic evaluation of hepatic blood flow in clinical sepsis

The aim of this study was to determine the hemodynamic response of the liver to sepsis by measuring hepatic blood flow. Thirty patients with sepsis were examined using Doppler ultrasonography and measurements of portal venous blood flow, hepatic arterial blood flow and total hepatic blood flow were recorded. Data were retrospectively reviewed and compared with findings for a control group of 12 healthy subjects. Significantly increased values of hepatic blood flow ( p < 0.01) and portal venous blood flow ( p < 0.001) were observed in patients during early sepsis (5 h). In contrast, hepatic arterial blood flow was not significantly different from controls. During late sepsis (24 h), no significant differences were observed between patients and healthy controls. Our results support the concept that hepatic blood flow is significantly increased in patients with early sepsis due to increased portal venous blood flow; however, during late sepsis, hepatic blood flow is similar to that in controls. (E-mail: kostis@magnet.gr)

Increased NAD(P)H fluorescence with decreased blood flow in the steatotic liver of the obese Zucker rat

The steatotic liver is characterized by deranged intrahepatic microvasculature that is believed to predispose it to ischemia-reperfusion injury. The aim of this study was to investigate the distorted hepatic hemodynamics and its impact on the redox status of the steatotic liver. Hepatic hemodynamic parameters, hepatic microcirculatory perfusion (HMP), and in vivo reduced nicotinamide adenine dinucleotide (phosphate) [NAD(P)H] autofluorescence, which reflects the mitochondrial redox status and tissue oxygen levels, were measured in obese ( n = 7) and lean Zucker rats ( n = 7). Portal venous and total hepatic blood flow per unit of liver weight were found to exhibit a 37.9% and 35.9% reduction, respectively, in the steatotic liver compared to the nonsteatotic liver of the lean group ( P < 0.0001) as was HMP (obese, 96.1 ± 18.1 PU; lean, 143.8 ± 12.0 PU, P < 0.05) that showed a 33.2% decrease in the former. Hepatic arterial resistance, however, was 38.7% lower in the obese rat (83.1 ± 9.1 mmHg · ml −1 · min) than in the lean rat (135.5 ± 15.8 mmHg · ml −1 · min) ( P < 0.05). NAD(P)H fluorescence intensity was significantly elevated in the steatotic liver (0.16 ± 0.001 aU) compared with the lean one (0.14 ± 0.007 aU) ( P = 0.014). Our results suggest that, in response to a reduced portal venous blood flow, there is a significant decrease in hepatic arterial resistance that, nevertheless, cannot completely compensate for the drop in overall hepatic perfusion and oxygenation of the microvascular bed in the steatotic liver of the obese Zucker rat.

Oxygen-15 positron-emission tomography for predicting selective delivery of a chemotherapeutic agent to hepatic cancers during angiotensin II-induced hypertension

Selective drug delivery is important for successful chemotherapy. In patients with hepatic cancer, we used (15)O-carbon dioxide (steady-state) and (15)O-water (dynamic) positron emission tomography (PET) to evaluate changes in blood flow induced by angiotensin (AT) II in the liver parenchyma, hepatic tumors, and spleen. The study group comprised 13 patients, 6 with hepatic metastasis and 7 with hepatocellular carcinoma. PET was performed before and during AT II administration to induce hypertension. Steady-state PET images showed a preferential increase in blood flow to hepatic tumor compared with liver parenchyma during hypertension. In dynamic PET, tumor blood flow was maintained during induced hypertension while hepatic arterial blood flow, portal blood flow, total hepatic blood flow, and splenic blood flow decreased to 71.4% (not significant), 65% (P<0.01), 67.2% (P<0.001), and 72.3% (P<0.01) of the respective baseline values. AT II-induced hypertension produced a relative increase in tumor blood flow. Oxygen-15 PET should be useful for predicting preferential drug delivery to hepatic cancers.

Effects of carbon dioxide pneumoperitoneum on hemodynamics in cirrhotic rats.

The aim of our study was to investigate the effect of carbon dioxide pneumoperitoneum on systemic and splanchnic hemodynamics in cirrhotic rats. Sprague-Dawley rats (n = 80) were used in this study. Liver cirrhosis was induced by thioacetamide administration intraperitoneally (200 mg/kg body weight, twice a week for 16 weeks). The radioactive microsphere method was used to measure systemic and regional hemodynamic parameters before, 1 h after the start, and 1 h after the release of pneumoperitoneum. Splanchnic blood flow and cardiac index were significantly depressed during pneumoperitoneum in liver cirrhosis and control groups, but no significant differences were seen between the two groups. In both groups, portal venous inflow decreased and hepatic arterial blood flow increased significantly during pneumoperitoneum. However, during pneumoperitoneum, total hepatic blood flow as a percentage of its value before pneumoperitoneum was lower in cirrhotic rats (71.0%) than in control rats (91.9%) (p <0.05, Mann-Whitney U-test). Carbon dioxide pneumoperitoneum markedly decreases total hepatic blood flow in cirrhotic rats due to the impaired hepatic arterial buffer response. Liver function should be carefully controlled in cirrhotic patients after laparoscopic surgery with pneumoperitoneum.

Hepatic arterial blood flow in large hepatocellular carcinoma with or without portal vein thrombosis: assessment by transcutaneous duplex Doppler sonography.

As liver cirrhosis progresses, the portal venous blood (PVBF) flow decreases, accompanied by an increase in hepatic arterial blood flow. Large hepatocellular carcinoma is a hypervascular tumour with a rapid growth, which seems to require an increase of the tumoral arterial blood flow. Furthermore, hepatocellular carcinoma is frequently associated with portal vein thrombosis, which subsequently impedes portal blood supply. The purpose of our study was to estimate alterations in the hepatic arterial blood flow in large hepatocellular carcinomas occurring in liver cirrhosis, in comparison with liver cirrhosis and controls. Liver blood flow measurements were determined by duplex Doppler sonography in 47 patients with large hepatocellular carcinomas (13 with portal vein thrombosis and 34 without this thrombosis), 42 liver cirrhosis patients and 30 controls. The Doppler perfusion index was calculated as the ratio of hepatic arterial blood flow to total hepatic blood flow. The patients with liver cirrhosis had a significant increase of hepatic arterial blood flow as compared to controls (P < 0.001), accompanied by a significant reduction in PVBF (P < 0.005). As a result, the Doppler perfusion index was increased in patients with liver cirrhosis as compared to controls (P < 0.001). The hepatic arterial blood flow was increased in patients with hepatocellular carcinoma but without portal vein thrombosis as compared to the cirrhotic patients (P < 0.001), with a significant reduction of PVBF (P < 0.001). Hepatic arterial blood flow was also increased in patients with both hepatocellular carcinoma and portal vein thrombosis as compared to the patients without this thrombosis (P < 0.001). These results suggest that in large hepatocellular carcinomas there is a decreased PVBF, accompanied by an increased hepatic arterial blood flow. The hepatic arterial buffer response seems to be active in hepatocellular carcinomas and maintains liver perfusion to adequate levels.

Is it feasible to monitor total hepatic blood flow by use of transesophageal echography? A validation in patients

Is it feasible to monitor total hepatic blood flow by use of transesophageal echography? A validation in patients

The effects of vasoactive drugs on hepatic blood flow changes induced by CO2 laparoscopy: an animal study.

Laparoscopic surgery is associated with systemic and splanchnic hemodynamic alterations. Recent data suggest that small-dose dobutamine may attenuate the reduction in splanchnic blood flow associated with increments in intraabdominal pressure. We conducted this study to analyze the effects of dopamine and dobutamine on the hepatic circulation in this setting. Twenty-one pigs were anesthetized and mechanically ventilated. A flow-directed pulmonary artery and carotid artery catheters were inserted. Perivascular flow probes were placed around the main hepatic artery and the portal vein. CO2 was insufflated into the peritoneal cavity to reach an intraabdominal pressure of 15 mm Hg. After 60 min, animals received dopamine (5 microg x kg(-1) x min(-1); n = 8), dobutamine (5 microg x kg(-1) x min(-1); n = 8), or saline (n = 5) for 30 min. Pneumoperitoneum induced significant increases in heart rate, mean arterial pressure, and systemic vascular resistance, with decreases in cardiac output and hepatic artery and portal vein blood flows. Dobutamine infusion, in contrast to dopamine, corrected, at least in part, cardiac output, systemic vascular resistance, and hepatic artery blood flow alterations, but neither drug restored total hepatic blood flow. Hepatic blood flow decreases during laparoscopic surgery. A small-dose infusion of neither dobutamine nor dopamine corrects the total hepatic blood flow impairment, but the former is able to restore the hepatic arterial blood supply in an animal model mimicking this condition.

Alterations in hemodynamics and hepatic and splanchnic circulation during laparoscopy in rats.

There is growing evidence that a pneumoperitoneum with increased intraabdominal pressure exerts adverse cardiovascular and splanchnic circulatory effects, whereby portal blood flow, in particular, is disturbed. Cardiovascular hemodynamics and the blood flow of hollow viscus and solid organs were evaluated in rats undergoing laparotomy, followed by diagnostic carbon dioxide (CO2) laparoscopy with an intraabdominal pressure of either 4 or 10 mmHg and rapid desufflation of the abdominal cavity. The method we employed used g-labeled microspheres and conventional hemodynamic measurements. During CO2 laparoscopy, cardiac output and mean arterial pressure were significantly reduced to between 20.5% and 25% and 14.8% and 18% respectively. After rapid desufflation, cardiovascular hemodynamics normalized to baseline values. During laparoscopy, blood flow in the hollow viscus organs was less disturbed than that in the solid organs. Although small and large bowel blood flow was reduced significantly (26.6% and 23.9%, respectively), gastric blood flow remained unchanged. The decreases in the liver, spleen, pancreas, and kidney circulation were 29-37.2%, 37.6-64.6%, 51.2-57.5%, and 34.8-40.6%, respectively. Total hepatic blood flow was influenced predominantly by portal blood flow, which was particularly decreased; hepatic arterial flow remained stable. Severe alterations in cardiovascular hemodynamics, and to hepatic and splanchnic circulation occur rapidly during CO2 laparoscopy. It can be presumed that both increased intraabdominal pressure and hypercapnia are the main factors underlying these disturbances.

Splanchnic and systemic hemodynamic effects of sustained euglycemic hyperinsulinemia in rats.

Insulin, in addition to its metabolic function, was found to induce skeletal muscle vasodilatation after acute administration. The vasoactive effects of sustained euglycemic hyperinsulinemia, especially in the splanchnic circulation, are less well known. The aim of this study was to evaluate the systemic and splanchnic hemodynamic effects of sustained euglycemic hyperinsulinemia. Hyperinsulinemia was induced by a sustained-release insulin implant in the scurf area of male rats (release rate -1 U/day). Beginning on the 3rd day, the study group was fed a glucose-rich diet. Hemodynamic studies were performed on the 5th day using the radioactive microsphere technique. Serum insulin was measured by radioimmunoassay. At the time of the hemodynamic measurements, plasma insulin level was higher in the insulin-treated (n=8) compared to control rats (n=8) (23.6 +/- 4.7 vs. 13.2+/-3.9 microu/mL, respectively; p<0.001). Plasma glucose level of the two groups was similar (5.43 +/- 1.07 vs. 5.83 +/- 1.44 mmol/L, respectively). Abdominal skeletal muscle blood flow was higher in the insulin-treated group (0.11 +/- 0.05 vs. 0.05 +/- 0.04 mL x min(-1) x g(-1), respectively; p<0.02). No significant changes were observed in cardiac output and renal blood flow. In the splanchnic circulation: stomach, pancreatic, intestinal, splenic, hepatic arterial and total hepatic blood flow were also not significantly different. In summary, short-term, sustained euglycemic hyperinsulinemia in rats increased blood flow to skeletal muscle but had no hemodynamic effects on cardiac output or splanchnic circulation.

Hepatic Indocyanine Green Uptake and Excretion in a Rabbit Model of Steatosis

Transplantation of a fatty liver is associated with a higher incidence of primary non-function of the graft. Indocyanine green (ICG) has been used for assessing hepatic dysfunction but not for quantifying liver steatosis. New Zealand white rabbits were fed a normal diet (group A) or a high-cholesterol (2%) diet for 4, 8, and 12 weeks in groups B, C, and D, respectively. Laparotomy was performed for liver exposure. Hepatic artery, portal vein, and total blood flow, hepatic microcirculation, portal pressure, liver function parameters, and blood cholesterol levels were measured. The hepatic ICG concentration was measured using near-infrared spectroscopy, and its uptake and excretion rates were calculated. The severity of steatosis was assessed from liver biopsy specimens by a semiquantitative grading system. Cholesterol feeding resulted in mild steatosis after 4 weeks and in moderate steatosis after 8 and 12 weeks. Mild steatosis was associated with insignificant changes in haemodynamic parameters, liver function, and ICG handling as compared with controls. Moderate steatosis caused a significant reduction in portal and total hepatic blood flow and microcirculation with a significant increase in hepatic artery flow and portal pressure. These haemodynamic changes were associated with a significant alteration in liver function tests. With moderate steatosis, ICG uptake and excretion were significantly reduced. The ICG uptake rate significantly correlated with total blood flow and microcirculation. The ICG excretion rate significantly correlated with the changes in bilirubin, liver enzymes, and albumin. Direct ICG quantification by near-infrared spectroscopy could be used to assess the severity of hepatic steatosis by reflecting impaired parenchymal perfusion and liver dysfunction.