The blood supply to the abdominal organs of the fetal guinea-pig

Guinea-pigs near term of pregnancy were anaesthetized with diazepam and sodium pentobarbitone. A fetus was exposed and the vitelline artery catheterized to measure blood pressure and heart rate or to render a reference sample of blood for the determination of organ blood flow by the microsphere technique. The radioactive microspheres were injected through a catheter in the right atrium. Mean arterial blood pressure was 4.0 kPa and heart rate was 261 beats min-1. The liver, spleen, pancreas and gut receive most of their blood supply from the same trunk as the vitelline artery. The sample from this vessel was also used to calculate blood flow to the adrenal glands, kidneys, urogenital tract, and placenta, assuming even mixing of microspheres and blood in the abdominal aorta. Umbilical blood flow, corrected to a fetal weight of 100 g, averaged 7.5 ml min-1. The adrenal glands, which are known to increase their cortisol secretion near term, had a very high rate of perfusion. If the microspheres were injected in the umbilical vein, almost all were trapped in the liver, confirming the absence of a ductus venosus in the guinea-pig fetus. Most of these microspheres were found in the quadrate lobe of the liver. Hepatic arterial blood flow was also unequally distributed, with more than two-thirds going to the right lobe of the liver. Although the distribution of portal venous blood flow is not known, it is evident that different areas of the liver are presented with blood of greatly varying oxygen saturation.     

Bacteremia in Experimental Tyzzer's Disease of Mice

Bacteremia was observed during the late stage of experimental Tyzzer's disease in mice. The number of organisms in the blood in mice treated with cortisone increased markedly in the infection with highly virulent organisms, whereas bacteremia was of low incidence and less severe in infections with low virulence organisms. The number of organisms in the blood stream was shown to increase linearly during the course of fatal infection attaining a maximum level of 10⁷ organisms per ml blood. The number of organisms in the blood was found to be closely related to the number in the liver when bacteremia was observed. In the peripheral blood, organisms were first detectable when the number of organisms in the liver gained a level of 10⁷ per g tissue, and the subsequent increase in the number of bacteria in the blood was approximately 3 times more rapid than in the liver. The organisms in the blood were comparable to those in the liver morphologically as well as in pathogenicity. Histopathological examination frequently revealed liberation of organisms from liver cells into sinusoids. There was no evidence of significant multiplication of the organisms in organs other than the liver.     

成人脂肪肝与体重指数和血脂水平的关系研究

目的:研究成人脂肪肝与体重指数(BMI)和血脂水平的关系。方法:选取2012年1月到2014年11月我社区成年人800例,检测所有入选者的体重和身高,并计算BMI,检测入选者的血脂水平和脂肪肝情况,应用Logistic回归分析来分析脂肪肝与BMI和血脂之间的关系。结果:共检测出脂肪肝376例,占47.0%,肥胖者532例,占66.5%;肥胖者伴随脂肪肝的发生率64.7%,显著高于非肥胖者脂肪肝的发生率11.9%,两者比较差异具有统计学意义(P0.05);脂肪肝者总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)显著高于非脂肪肝者,而高密度脂蛋白(HDL-C)显著低于非脂肪肝者,两者比较差异具有统计学意义(P0.05);Logistic回归分析显示:脂肪肝与BMI和血脂之间存在相关关系(P0.05)。结论:BMI和血脂水平与成人脂肪肝存在较大关系,应该注意控制体重,进而降低脂肪肝的发生率,改善脂肪肝的情况。     

Hepatic Damage Influences the Decay of Nitroxide Radicals in Mice—An In Vivo ESR Study

To determine the role of the liver in the elimination of free radicals from the body, the clearance rate (K) of nitroxide radicals (Tempol) at the hepatic domain was compared with that at the pelvic domain of live mice, using L-band ESR spectroscopy. The reduction of Ternpol in biopsy specimens (liver tissue and femoral muscle) and blood obtained from Tempol-treated mice was also monitored using X-band ESR spectroscopy. Results indicated that the reduction of nitroxide radicals was delayed in both the liver and peripheral tissues when the liver was damaged. The decrease in both blood supply and reductants in the damaged liver might be involved in delaying the reduction in the whole body, because the liver can reduce the radicals supplied via the blood from the peripheral tissues, and the reductants such as reduced glutathione in the peripheral tissues are supplied from the liver.     

Altered functional and immunophenotypical properties of neutrophilic granulocytes in postpartum cows associated with fatty liver

The intention of the study was to analyze the relationship between liver triacyl glycerol content (liver TAG content) and immunophenotypical and functional properties of polymorphonuclear neutrophilic granulocytes (PMN) of dairy cows in the peripartum period. We investigated characteristics of bovine PMN from the blood and uterus of clinically healthy cows in the periparturient period. The numbers of circulating leukocytes and segmented granulocytes continuously increased until parturition and declined afterwards to starting values. This was independent of the liver TAG content and mainly affected neutrophils. The liver TAG content exceeded 40 mg/g liver, the reference value, in 12 of 19 cows in the first two weeks postpartum. Increased liver TAG content, > 40 mg/g, went in parallel with a reduced expression of function-associated surface molecules on blood neutrophils (e.g. CD11b/CD18 = CR3 and CD11c/CD18 = CR4). Moreover, in cows with high liver TAG levels the antibody-independent and -dependent cellular cytotoxicity (AICC, ADCC) of blood PMN was markedly reduced. PMN also were less capable of ROS generation after stimulation with Phorbol Myristate Acetate (PMA). In comparison with contemporarily harvested blood PMN, neutrophils recovered from the uterine lumen showed a decreased expression of 4/6 examined surface structures. Only the expression densities of CR3 molecules and those detected by mAb IL-A110 were enhanced on uterine PMN. The cytotoxic capacity and the ROS generation were significantly lower for uterine PMN than for blood PMN. The results suggest that increased liver TAG content in the first and second week after calving is associated with decreased functional capacities of PMN derived from blood and uterus. This may help to explain why cows who are too fat at calving (who therefore have an increased liver TAG content) have a higher incidence of infectious diseases such as endometritis     

Infectivity of hepatic strain Klebsiella pneumoniae in diabetic mice

Besides urinary tract infection (UTI) and pneumonia, increased severe liver abscesses caused by Klebsiella pneumoniae (KP), especially in diabetic patients, have been observed in infections acquired in hospitals. This indicates that different KP strains with higher virulence have emerged in recent years. Our goal was to investigate the infectivity of KP isolates in mice from liver abscess or UTI patients. Mice were injected with streptozotocin to induce diabetes. Male ICR mice were infected with KpU1 (UTI strain CG3 for survival experiment only) and KpL1 (liver abscess strain CG5) by tail-vein injection of 5 x 10(4) colony-forming units (CFU) bacterial suspension. The mice survival rates, cytokine level by enzyme-linked immunosorbent assay (ELISA), and bacterial presence in liver tissue by Giemsa stain were examined. The survival rates for the KpL1-infected animals were 28% and 0% in normal and diabetic groups, respectively, whereas, for the KpU1-infected mice, the rates were 100% and 75% during a 30-day observation. Nonsurviving KpL1-infected mice showed > 10(5) bacteria/ml blood and the bacteria appeared in the liver sinus area and inside liver cells. The KpL1-infected mice showed a tendency to increase the blood interleukin 1beta (IL-1beta) level in both nondiabetic and diabetic groups, whereas the tumor necrosis factor-alpha (TNF-alpha) level was significantly decreased in the KpL1-infected diabetic mice (P = 0.002). In conclusion, the KP strain from liver abscess showed a greater virulence in mice than the KP from UTI and was more virulent in diabetic than in nondiabetic mice. The infection with KP from liver abscess significantly decreased the blood TNF-alpha level in diabetes mellitus (DM) mice and the blood IL-1beta level tended to increase in both infected nondiabetic and diabetic groups. High blood bacterial count and appearance of bacteria in liver sinus and cells usually contribute to death of the animals.     

Early ontogeny of monocytes and macrophages in the pig

Prenatal development of cord blood monocytes and tissue macrophages was studied in pig foetuses by immunophenotyping and functional assays. The function of peripheral blood monocytes was compared in germ-free and conventional piglets. First macrophages were identified by electron microscopy in foetal liver on the 25th day of gestation. Monoclonal antibodies against porcine CD45 and SWC3 antigens were used for flow cytometric identification of myelomonocytic cells in cell suspensions prepared from the yolk sac, foetal liver, spleen and cord blood. Leukocytes expressing the common myelomonocytic antigen SWC3 were found in all organs studied since the earliest stages of development. Opsonized zymosan ingestion assay was used to determine the phagocytic capacity of foetal mononuclear phagocytes isolated from cord blood, liver and spleen. In the foetal liver, avid phagocytosis of apoptic cells had been found to occur before cells were able to ingest zymosan in vitro. The first cells capable of ingesting zymosan particles were found on the 40th day of gestation in umbilical blood and 17 days later in foetal spleen and liver. Their relative proportion increased with age. Cord blood monocytes and peripheral blood monocytes in germ-free piglets had low oxidatory burst activity as shown by iodonitrophenyl tetrazolium reduction assay. A remarkable increase of oxidatory burst activity was observed in conventional piglets, probably due to activation of immune mechanisms by the microflora colonizing gastrointestinal tract.     

Transhepatic absorption and biliary excretion of insulin

The application of insulin to the liver in rats is followed by an increase of the insulin concentration in the bile. The pathway of insulin from the liver surface to the bile may include a secretory process by the hepatic cells, or it may bypass the hepatic cells, using direct anatomical pathways from blood and lymph to bile. The concentration of insulin in arterial and venous blood, in lymph, and in bile was measured following application of insulin to the liver surface and following peritoneal or intravenous administration. The results confirm that insulin is absorbed from the surface of the liver, but the glucose modulating effect was less effective than after intravenous administration. The insulin concentration in bile was increased after insulin administration by all routes, with the highest and most prolonged increases found after intraperitoneal administration. The results suggest that following transhepatic and intravenous administration, insulin reaches the bile without passing through the liver cells.     

Blood flow to the placenta and lower body in the growth-retarded guinea pig fetus

Blood flow to the placenta and lower body of control and growth retarded (IUGR) guinea pig fetuses was measured between 60-64 days of pregnancy by the microsphere technique. Further information about the hepatic blood supply and its interlobular distribution was obtained by injecting microspheres into the umbilical vein and a branch of the portal vein. Liver weight was reduced by 60% in IUGR fetuses from 5.0 +/- 0.2 to 2.0 +/- 0.1 g, compared to a decrease in body weight of 50% from 91.6 +/- 3.0 to 45.4 +/- 2.6 g. In addition, there was a proportionately greater reduction in the size of the right liver lobe. Umbilical blood flow was 10.8 +/- 1.0 ml min-1 in control fetuses and 4.9 +/- 1.2 ml.min-1 in IUGR fetuses, whilst blood flow in the portal vein was reduced from 1.4 +/- 0.1 to 0.8 +/- 0.3 ml min-1 and that in the hepatic artery from 0.6 +/- 0.1 to 0.3 +/- 0.1 ml.min-1. Since ductus venosus flow was absent or negligible, the umbilical venous return accounted for greater than 80% of the hepatic blood supply in both control and IUGR fetuses. Blood flows were, however, unequally distributed between the liver lobes. The right lobe was supplied mainly by the portal vein in IUGR fetuses as well as the controls, and received less than 6% of the umbilical venous return. No significant change occurred in total liver perfusion, which was 2.8 +/- 0.2 ml min-1 per g in control fetuses and 2.6 +/- 0.4 ml min-1 per g in IUGR fetuses. It is therefore suggested that a high rate of liver metabolism is maintained in IUGR, but by a smaller tissue mass, and that the rate of umbilical blood flow may be one factor determining the size of the liver. The relatively greater reduction in size of the right lobe in IUGR is probably the result of poor oxygenation of the portal venous blood.     

Effects of luteolin on arylamine N-acetyltransferase activity in rat blood and liver.

In this study we investigated inhibition of Arylamine N-acetyltransferase (NAT) activity in rat blood and liver tissue cytosols by luteolin. Using high-performance liquid chromatography, NAT activity for acetylation of 2-aminofluorene and remaining unacetylated 2-aminofluorene were examined. The NAT activity in rat blood and liver tissue was inhibited by luteolin in a dose-dependent manner: higher concentrations of luteolin in the reaction resulted in greater inhibition of NAT activities in both examined tissues. The data also indicated that luteolin decreased apparent Km and Vmax of NAT enzymes from rat blood and liver tissue cytosols. This report is the first demonstration that luteolin can affect rat blood and liver tissue NAT activity.     

原位肝移植术后急性肺损伤的相关因素的临床分析

目的：探讨肝移植后急性肺损伤（ALI）的相关因素,为肝移植术后ALI的预防和治疗提供参考。方法：回顾性分析了2005年1月-2010年10月在我院行肝移植术的98例患者的临床资料,对术后并发ALI的相关因素进行分析。结果：98例行肝移植术后发生ALI12例,发生率为12．24％。单因素分析显示年龄、术前血清TBIL、术中失血量、术中尿量和术后血BUN对ALI的发生有显著影响（P〈0．05）。多因素Logistic回归法分析表明,术中失血量、术前TBIL、年龄为术后并发ALI的危险因素。结论：术中失血量、术前TBIL、年龄为术后并发ALI的危险因素,对上述因素加以重点评估和合理控制,可以控制肝移植术后ALI的发生。     

Liver cell myosin: isolation and properties

We have purified myosin from isolated rabbit liver cells that had been previously shown to be well separated from blood vessels and connective tissue (Okamoto, Y. et al. (1983) J. Biochem. 94, 645-653). It comprises a 200-kDa heavy chain and light chains of 24-kDa, 22-kDa, and 17-kDa. In the light chain composition and in the mobility in PPi-PAGE, liver cell myosin differs from the myosin in liver blood vessels. The light chains of liver cell myosin were phosphorylated by myosin light-chain kinase from chicken gizzard and the Mg2+-ATPase activity of phosphorylated myosin was activated 10-fold by F-actin.     

Identification of transferrin as the principal plutonium-binding protein in the blood serum and liver cytosol of rats: immunological and chromatographic studies

An analysis of 239Pu-labelled protein complexes in serum and liver cytosol fractions prepared from rats injected intravenously with 239Pu-citrate indicated that among the possible metal-binding proteins, ferritin, transferrin and metallothionein, 239Pu was bound almost exclusively to transferrin. The method employed for the quantitative determination of 239Pu-transferrin was chromatography on immobilized rabbit anti-rat apo-transferrin. There was no evidence that transferrins from serum and liver cytosol are serologically different. The residual blood content of perfused and non-perfused liver was measured using 51Cr-labelled red blood cells and the amounts of blood-derived 239Pu and 239Pu-transferrin in the liver cytosol were calculated. The results are discussed with respect to the possible role of transferrin in the uptake of Pu into cells.     

The in vivo disposition of aflatoxin B1 in rat liver

The disposition of a non-toxic i.p. dose of [3H]-aflatoxin B1 (0.70 micrograms/kg) in the blood, plasma, and liver was studied in male Wistar rats. Uptake into the blood, plasma, and liver was biphasic; there was an initial rapid rise (0-2 hr) followed by a second phase (2-12 hr) of a gradual increase. Most of the radioactivity in the blood was bound noncovalently to albumin. Distribution of radioactivity in the subcellular fractions of liver showed that the microsomes exhibited the highest labeling which increased over the time course; labeling of the cytosol reached a maximum at 2 hr then decreased to a new steady state, whereas the mitochondria and nuclei reached a plateau. When the content of aflatoxin B1 in the nuclear subfractions was examined, greater than 92% of the total radioactivity was found in the deoxyribonucleoprotein fraction, and 84% of this was bound noncovalently. These results suggest that aflatoxin B1 is transported from the site of injection through the blood to the liver and its subcellular and subnuclear fractions primarily in a noncovalent form.     

Serum IGF-1 levels correlate negatively to liver damage in diabetic rats

Abstract

Diabetes and insulin resistance frequently cause liver damage. Diabetes also causes reduction in liver and blood IGF-1 levels. We investigated the relation between liver damage and IGF-1 levels in diabetic rats. Fourteen Wistar albino rats were divided into control and diabetic groups. Diabetes was induced by streptozotocin. Rats were sacrificed for biochemical and histologic examinations 2 weeks after streptozotocin injection. Serum and liver IGF-1 levels were decreased, liver malondialdehyde (MDA) levels were increased, glutathione peroxidase (GPx) enzymes activities were decreased and serum alanine aminotransferase (ALT) levels were increased in diabetic group. Microscopic examination of liver revealed that normal tissue organization was disrupted in streptozotocin-induced diabetic rats. There was a strongly positive correlation between blood glucose levels and liver injury, and blood and liver IGF-1 levels. There was a strongly negative correlation between blood IGF-1 levels and hepatic injury. Our results suggest that reduction of blood IGF-1 levels correlates with hepatic injury and circulating IGF-1 levels may have predictive value for determining hepatic damage that results from diabetes. In addition, circulating IGF-1 levels are correlated with glutathione levels and the oxidative stress status of diabetic rat liver.     

Transfer of nitric oxide from the liver to erythrocytes--an ESR study using nitroglycerin-treated mice

Nitric oxide (NO) formation in the liver and blood of the mouse following intraperitoneal treatment with nitroglycerin (glycerol trinitrate, GTN) was determined using electron spin resonance (ESR) spectroscopy. ESR signals of heme-NO complexes were detected at maximum levels within 5 min in the liver, but increased to a maximum level about 15-30 min later in the blood. GTN is not metabolized to release NO in vitro in the blood of the mouse. The hepatic microsomes which showed the heme-NO complexes ESR signals were incubated with mouse erythrocytes, with the result that a hemoglobin-NO signal was obtained from the erythrocytes. The activities of microsomal cytochrome P-450, the hepatic level of glutathione, and the reduction rate of nitroxide radicals in the in vivo liver, measured using L-band ESR spectroscopy, were temporarily decreased following GTN administration. In conclusion, NO in the liver could be scavenged by circulating erythrocytes, which might minimize NO-induced liver damage.     

Liver chalones]

Administration of a liver extract and the blood serum of adult intact mice and also of the blood serum of practically healthy persons to CBA X C57B1 hybrid mice produced a sharp depression of the mitotic activity of hepatocytes in the regenerating liver after its partial removal. The extract of the regenerating liver and the blood serum of the animals with the regenerating liver failed to depress mitoses in hepatocytes. The blood serum of man with the postnecrotic active cirrhosis of the liver not only failed to depress mitoses in the hepatocytes, but even caused an increase in their count. It is supposed that there was a reduction of the chalone concentration in the cirrhotic liver.     

Fluorescence microscopical and chemical characterization of the adrenergic innervation in mammalian liver tissue

Liver tissue from 12 different mammalian species was studied with a fluorescence histochemical technique for the cellular localization of amines (Falck-Hillarp technique) and with a chemical method for the determination of norepinephrine (HPLC-technique). Adrenergic nerve plexus were found in interlobular blood vessels derived from the portal vein and hepatic artery. Varicose adrenergic nerve fibres were, generally, seen to branch from the fibres around the blood vessels and to enter the liver parenchyma, where they formed a randomly distributed intralobular network. The density of these intralobular fibres showed marked species variation. Human liver and liver from the rhesus monkey, baboon, cynomolgus monkey and guinea pig showed a high density of parenchymal adrenergic nerves. Rabbit, cat, pig, cow and horse liver formed an intermediate group, having fewer varicose adrenergic nerve fibres but an unequivocal distribution of these nerves to the liver parenchyma. In rat and mouse liver no parenchymal innervation could be demonstrated. The density of the parenchymal innervation generally correlated with the concentration of norepinephrine in the liver tissue.     

Limitation in glucose penetration from the liver into blood and other metabolic symptoms of ethanol withdrawal in rats

Studies were undertaken to determine whether the distribution of glycolytic intermediates between the blood and liver in rats would be changed upon ethanol consumption and after its withdrawal. More drastic impairment of energy metabolism appeared to occur after ethanol withdrawal than upon chronic ethanol ingestion. The major metabolic manifestations of withdrawal were severe hypoglycemia, hyperlactatemia and dramatic hypopyruvatemia. The liver/blood gradient of glucose attained a value of 4.2 after ethanol withdrawal, suggesting that glucose penetration from the liver into circulation became limited. Besides, glycogen was accumulated in the liver of withdrawn animals despite the severe hypoglycemia.     

Involvement of the liver in the regulation of tryptophan availability. Possible role in the responses of liver and brain to starvation

The concentrations of free and total (free plus albumin bound) tryptophan were measured in plasma of blood taken from the portal vein, hepatic vein and abdominal aorta of male rats, fed, and starved for one and three days. Liver and brain tryptophan concentrations were measured in similar groups of rats.On starvation, there was an increase in arterial plasma free tryptophan concentration which took place peripherally and was paralleled by an increase in brain tryptophan. In both the fed and starved rats, the portal vein concentrations of free tryptophan were high and as the blood flowed through the liver they were reduced to relatively low levels not directly related to the arterial values. All these changes were due to alterations in degree of binding of tryptophan to plasma albumin.The measurements of plasma total tryptophan concentrations showed that postabsorptively and during starvation there was a net uptake of tryptophan by the peripheral tissues (which included brain), but no overall fall in plasma concentration. At the same time, there was a net release from the liver, and to a lesser extent from the portal-drained tissues. The released tryptophan largely entered the albumin bound plasma pool. Accompanying the hepatic output was a fall in tryptophan concentration in the liver which was apparently caused by altered cell membrane transport.The results suggest (1) that the liver protects the brain from the high free tryptophan level in portal blood, (2) that the availability of tryptophan to the brain is maintained postabsorptively and during starvation by hepatic output into the albumin bound pool and (3) that this release of tryptophan from the liver and the fall in intracellular tryptophan concentration are initiated by altered membrane transport. The pattern of changes is consistent with a role for tryptophan in the mediation of changes in liver protein synthesis and gluconeogenesis and cerebral serotonin turnover on starvation.