巨大右半肝肿瘤切除术时的出血控制

巨大右半肝肿瘤切除过程中的出血量是决定手术能否成功的关键因素,控制手术过程中出血的技术也是右半肝切除术中的最重要的技术,有效控制术中出血的方法贯穿于整个手术过程中：良好的术前评估,术中于第一肝门处选择性阻断支配右半肝的入肝血流,于第二肝门处切断肝右静脉,于第三肝门处切断肝短静脉,在无血条件下用超声吸引刀切除预定的右半肝以及肝断面的处理等。此方法能有效控制手术过程中出血,保证左半肝血液供应,减轻肝脏缺血/再灌注损伤,减少术后肝功能不全的发生,保证了胃肠道血流的通畅,避免了黏膜屏障受损,全身血流动力学平稳,对其他脏器功能影响小,缩短了手术时间,极大地提高了手术的安全性。     

The absorption and metabolism in rats of small oral doses of dimethylnitrosamine. Implication for the possible hazard of dimethylnitrosamine in human food.

1. Groups of rats were given one dose of the carcinogen dimethylnitrosamine by gastric intubation. The dose was varied between 10mg/kg body wt. and 1 microgram/kg body wt. 2. The dose was rapidly absorbed. 3. The methylation of liver DNA resulting from the administration of this carcinogen was proportional to dose. This suggests that small doses are absorbed from the gut with no more loss than large doses. 4. As the dose was decreased there was a disproportionately greater decrease in the alkylation of kidney DNA, and when the dose was less than 40 microgram/kg body wt. the methylation of kidney DNA was no longer detectable. This possibly explains why small amounts of dimethylnitrosamine in the diet do not induce kidney tumours. 5. Comparison of the relative alkylation of liver DNA and kidney DNA resulting from an oral and from an intravenous dose of dimethylnitrosamine suggest that small amounts of dimethylnitrosamine absorbed into the portal blood from the gut are completely metabolized by the liver and do not enter the general circulation. 6. The implications of these results for the possible hazard of dimethylnitrosamine in human food is discussed.     

The effects of iodine level and source on iodine carry-over in eggs and body tissues of laying hens

In the presented study the effect of different iodine (I) levels and sources in hen feed on the iodine concentration of different tissues, blood serum, and eggs of laying hens was studied. For this purpose, two experiments were conducted with 30 laying hens each. In these experiments feed was enriched with KI and Ca(IO(3))(2), respectively, at 0 (Control), 0.25, 0.5, 2.5 and 5 mg I/kg feed, resulting a analysed iodine level from 0.44 to 4.20 mg/kg feed. After four weeks experimental feeding the iodine concentrations of thyroid glands, blood, meat, liver, abdominal fat and eggs were measured with inductively coupled plasma mass spectrometry. The experimental treatment did not affect hen performance. The iodine supplementation significantly increased the iodine concentration of eggs (144-1304?μg/kg), thyroid glands (3367-5975?μg/g), blood serum (16-67?μg/kg) and liver (13-43?μg/kg). Meat (about 14?μg I/kg) and abdominal fat (about 12?μg?I/kg) were not significantly affected by iodine treatment. Comparative regression analyses showed that at a similar iodine intake, the supply via KI resulted in significantly higher iodine deposition into eggs than Ca(IO(3))(2). Due to the high carry-over of iodine into eggs, eggs may considerably contribute to the iodine supply of the consumers.     

Survival of transfused cryopreserved granulocytic progenitor cells (CFU-C) in recipient circulation

We have studied the pattern of CFU-C disappearance from the peripheral blood of normal and total-body-irradiated dogs given cryopreserved cell suspensions from bone marrow, foetal liver and peripheal blood containing known numbers of CFU-C under an autologous and allogeneic donor-recipient relationship. Only a small fraction of infused donor CFU-C could be detected in the circulation of recipients at the end of the infusion. There was an exponential fall in circulating CFU-C, indicating random loss of infused CFU-C. The CFU-C disappearance pattern in each experimental group was reproducible. The mean half life of autologous blood derived CFU-C in the circulating blood of normal recipients was 8.2 min and the mean blood CFU-C turnover was calculated to be 9.3 X 10(5) CFU-C/kg per day.     

Comparing functional metabolic effects of marginal and sufficient selenium supply in sheep

This study was performed to characterise key data of long-term ovine Se metabolism and to work out the best biomarker of Se status. An upgrade from marginal (<0.05 mg Se/kg diet, ‘Se?’) to sufficient (0.2 mg Se/kg diet, ‘Se+’) nutritional Se supply using sodium selenite was monitered biweekly by analysing Se concentration, glutathione peroxidase (Gpx) activity and routine biochemistry in blood/serum over 2 years. Se, Cu, Zn, cytosolic Gpx and thioredoxin reductase (TrxR) activity were measured in the liver (biopsies/post-mortem). Se, Gpx, TrxR, glutathione-S-transferase-alpha (aGST) and iodothyronine deiodinase (Dio1) were analysed in the kidney, heart muscle and thyroid. Relative mRNA expression of hepatic aGST1 and Gpx1 was determined.Improvement of Se supply strongly increased serum and liver Se concentration within 10 and 20 days, respectively followed by a plateau. Whereas the achievement of a maximum whole blood Gpx activity was reached after 3 months, serum Gpx3 activity increased with high variations. Hepatic Gpx activity reached a maximum during days 100–200, decreasing thereafter. Distinct group differences in Se and cytosolic Gpx activity were evident in all organs (except Se in kidney). TrxR and Dio1 activity was affected only in the liver. The Se? sheep showed an ongoing decrease in serum Se concentration within 2 years, whereas liver Se remained almost unaffected. High relative Gpx1 mRNA expression in the Se+ group was consensual to high hepatic Gpx activity. Relative mRNA expression of hepatic aGST1 was higher in the Se? sheep. Clinical signs and abnormalities in routine biochemistry were absent.In summary, the best biomarker of Se deprivation and nutritional Se upgrade, respectively was Se in serum. Moreover, hepatic Se concentrations reliably reflected the upgrade of Se supply within days. Whole blood Gpx reacts slowly depending on newly formed erythrocytes restricting its diagnostic use. Vital organs are affected by Se deficiency due to a decrease of cytosolic Gpx activity attenuating the antioxidative system. Cellular up-regulation of aGST1 mRNA expression in the Se? group is assumed to partially compensate for the decreased antioxidant defence due to a loss in Gpx activity. This sheep model appears advantageous for long-term studies on sub-clinical metabolic effects in experimental modifiable nutritional Se supply.     

Untersuchungen über den Eiweißbedarf der Mastente unter Berücksichtigung einer Lysin-, Methionin- und Vitamin-B-Ergänzung des Mastfutters: (Kurze Originalmitteilung)

In the presented study the effect of different iodine (I) levels and sources in hen feed on the iodine concentration of different tissues, blood serum, and eggs of laying hens was studied. For this purpose, two experiments were conducted with 30 laying hens each. In these experiments feed was enriched with KI and Ca(IO₃)₂, respectively, at 0 (Control), 0.25, 0.5, 2.5 and 5 mg I/kg feed, resulting a analysed iodine level from 0.44 to 4.20 mg/kg feed. After four weeks experimental feeding the iodine concentrations of thyroid glands, blood, meat, liver, abdominal fat and eggs were measured with inductively coupled plasma mass spectrometry. The experimental treatment did not affect hen performance. The iodine supplementation significantly increased the iodine concentration of eggs (144–1304 μg/kg), thyroid glands (3367–5975 μg/g), blood serum (16–67 μg/kg) and liver (13–43 μg/kg). Meat (about 14 μg I/kg) and abdominal fat (about 12 μg I/kg) were not significantly affected by iodine treatment. Comparative regression analyses showed that at a similar iodine intake, the supply via KI resulted in significantly higher iodine deposition into eggs than Ca(IO₃)₂. Due to the high carry-over of iodine into eggs, eggs may considerably contribute to the iodine supply of the consumers.     

Carbohydrate metabolism in temporal and persistent hypoglycemic chickens induced by insulin infusion

In order to elucidate the regulatory mechanism of blood glucose concentrations specific to chickens, carbohydrate metabolism in the liver, muscle and kidney and metabolite concentrations in the blood were investigated in chickens with acute and persistent hypoglycemia. Acute and persistent hypoglycemia were experimentally induced by a single injection of insulin (8 U/kg BW) or by continuous infusion of insulin (22.5 U/kg BW/day) for 4 days. Non-esterified fatty acid (NEFA) concentration in plasma and D-3-hydroxybutyrate (3HB) concentrations in liver and muscle increased in the acute hypoglycemia. Plasma NEFA concentration and 3HB concentration in the blood and liver were not changed at day 3 of persistent hypoglycemia, while 3HB concentration in the muscle was decreased. Phosphofructokinase (PFK) activity in the liver tended to increase but PFK and pyruvate kinase (PK) activities were unchanged in acute hypoglycemia. In persistent hypoglycemia, increase of hepatic PFK activity at day 1 in which it was reversed at day 3, and a small increase of muscle PK activity were observed, while PK and phosphoenolpyruvate carboxykinase (PEPCK) activities in the liver and kidney were not significantly changed. These results show that in the persistent hypoglycemic chickens, hepatic glycolysis transiently increases, which is followed by a small decrease, while glycolysis in muscles and gluconeogenesis in the liver and kidney are not significantly changed.     

Tissue oxygen monitoring in rodent models of shock

Tissue Po(2) (tPo(2)) reflects the balance between local O(2) supply and demand and, thus, could be a useful monitoring modality. However, the consistency and amplitude of the tPo(2) response in different organs during different cardiorespiratory insults is unknown. Therefore, we investigated the effects of endotoxemia, hemorrhage, and hypoxemia on tPo(2) measured in deep and peripheral organ beds. We compared arterial pressure, blood gas and lactate levels, descending aortic and renal blood flow, and tPo(2) in skeletal muscle, bladder epithelium, liver, and renal cortex during 1) LPS infusion (10 mg/kg), 2) sequential removal of 10% of circulating blood volume, and 3) reductions in inspired O(2) concentration in an anesthetized Wistar rat model with values measured in sham-operated animals. Different patterns were seen in each of the shock states, with condition-specific variations in the degree of acidemia, lactatemia, and tissue O(2) responses between organs. Endotoxemia resulted in a rise in bladder tPo(2) and an early fall in liver tPo(2) but no significant change in muscle and renal cortical tPo(2). Progressive hemorrhage, however, produced proportional declines in liver, muscle, and bladder tPo(2), but renal cortical tPo(2) was maintained until profound blood loss had occurred. By contrast, progressive hypoxemia resulted in proportional decreases in tPo(2) in all organ beds. This study highlights the heterogeneity of responses in different organ beds during different shock states that are likely related to local changes in O(2) supply and utilization. Whole body monitoring is not generally reflective of these changes.     

Cortisol induces perinatal hepatic gluconeogenesis in the lamb.

To examine the influence of a prenatal increase in plasma cortisol concentration on perinatal initiation of hepatic gluconeogenesis, we infused cortisol into seven fetal sheep at 137-140 days gestation. 14C-Lactate provided tracer substrate for estimation of gluconeogenesis. We measured hepatic blood flow using radionuclide-labeled microspheres. After delivery, fetal arterial blood glucose concentration (1.33 +/- 0.4 mmol/l) increased transiently, but returned to fetal levels within 1 h after delivery. Substantial hepatic gluconeogenesis was induced in the fetus after cortisol infusion, averaging 23.4 +/- 12.2 mumol/min/100 g liver (7.8 +/- 4.4 mumol/min/kg fetal weight). Fetal hepatic glucose output was 44.4 +/- 17.7 mumol/min/100 g liver. Hepatic glucose output did not change after delivery; estimated gluconeogenesis decreased immediately, then increased by 6 h after delivery. Lactate supply to the liver fell substantially, from 1.1 +/- 0.4 mmol/min/100 g in the fetus to 0.24 +/- 0.09 at 1 h after delivery. Lactate flux across the liver decreased from 75.3 +/- 23 mumol/min/100 g in the fetus to 20.2 +/- 15.7 at 1 h after delivery. Hepatic lactate flux was significantly related to gluconeogenesis (r = 0.734, P = 0.0001). We conclude that cortisol induces substantial hepatic gluconeogenesis in fetal sheep near term. After delivery, there appears to be a transient decline in gluconeogenesis from lactate, which may be secondary to limited hepatic oxygen and substrate supply. Onset of gluconeogenesis in the fetus fails to sustain increases in either fetal or postnatal blood glucose concentrations.     

Effects of volume and rate of blood loss on indicators of auto-hemodilution

The results of synchronous monitoring of blood impedance versus body impedance in dog experiments showed that the speed of physiological hemodilution related to blood loss up to 30 ml/kg is poorly dependent on the rate of blood loss (0.4-1.0 ml/kg/min) and averages 0.186 +/- 0.02 ml/min/kg. Termination of blood loss is followed by marked reduction in the rate of auto-hemodilution. In bloodletting the studies revealed a linear dependence between the volume of blood loss up to 30 ml/kg and tissue fluid volume entering the blood stream. In blood loss intestinal absorption of fluid does not block the fluid introduction from the interstice. When associated, both these flows increase volume of fluid filling vascular bed and promote stable recovery of the baseline circulating blood volume.     

Biochemical response to cadmium

The effect of daily oral administration of ethanol (2.5, 5, or 10% in drinking water for 8 wk), lead (10 mg/kg, po, once daily for 8 wk), or their combination on tissue trace-metal concentration and hematopoietic and hepatic biochemical indices was investigated in male rats. Ethanol (10%) ingestion enhanced the hepatic lipid peroxidation and decreased the calcium and magnesium content of blood and liver. Coexposure to lead and ethanol (5 and 10%) produced a more pronounced elevation of blood zinc protoporphyrin (ZPP) and hepatic lipid peroxidation. Combined lead-ethanol exposure also lowered the concentration of blood and hepatic magnesium and calcium and increased the amount of lead in the blood, liver, and brain compared to a group treated with lead alone. The results suggest that chronic alcohol ingestion results in calcium and magnesium loss. However, coexposure to lead and ethanol could result in more serious depletion of calcium and magnesium, and this could be the cause of suspected synergism between alcohol consumption and lead poisoning.     

RETRACTED ARTICLE: Effect of preischemic treatment with fenofibrate,a peroxisome proliferator-activated receptor-α ligand,on hepatic ischemia–reperfusion injury in rats

Liver ischemia/reperfusion (I/R) injury is a serious clinical problem. The reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-α) are important mediators in liver I/R injury. This study was designed to investigate the effect of preischemic treatment with fenofibrate (Peroxisome proliferator-activated receptor- α agonist) on the oxidative stress and inflammatory response to hepatic I/R injury in rats. Hepatic I/R was induced by clamping the blood supply of the left lateral and median lobes of the liver for 60 min, followed by reperfusion for 4 h. Each animal group was pretreated with a single dose of fenofibrate (50 mg/kg body weight) intraperitoneally 1 h before ischemia. At the end of reperfusion, blood samples and liver tissues were obtained to assess serum alanine aminotransferase (ALT), TNF-α, hepatic malondialdehyde (MDA) and superoxide dismutase activity (SOD). Liver specimens were obtained and processed for light and electron microscopic study. Hepatic I/R induced a significant elevation of serum ALT and TNF-α with significant elevation of hepatic MDA and reduction of SOD activity. Histopathological examination revealed hepatic inflammation, necrosis and apoptosis. Preischemic treatment with fenofibrate at a dose of 50 mg/kg significantly attenuated the biochemical and structural alterations of I/R-induced liver injury.     

纳米氧化锌经口染毒对C57BL/6J小鼠外周脏器的影响*

目的:探讨纳米氧化锌经口染毒60 d对C57BL/6J小鼠多种外周脏器的损伤作用。方法:20只雄性C57BL/6J小鼠随机分为对照组和实验组,每组10只,实验组将纳米氧化锌溶液以20 mg/kg体重的剂量连续灌胃染毒60 d,对照组给予相应量的生理盐水;小鼠每周称重一次,染毒结束后,眼球取血,检测血糖、血脂、肝功能和肾功能相关指标,以及血清中炎症因子PAF、IL-6和TNF-α含量;取心脏、肝脏、脾脏、肺、肾脏和小肠组织制备病理切片,HE染色后,观察组织形态学变化。结果:实验组和对照组之间的体重无显著性差异;与正常对照组比较,实验组大鼠血中白蛋白(ALB)、白蛋白/球蛋白比值(A/G)、碱性磷酸酶(ALP)、谷草/谷丙转氨酶比值(S/L)、尿酸(UA)和尿素氮(BUN)含量明显升高(P＜0.05或 P＜0.01);两组间血清中炎症因子含量无显著差异。病理学检查发现,实验组心肌中部分区域出现浊肿,肝脏出现轻度炎性病变(灶性或小灶性坏死),脾脏色素沉着减少,肺部出现轻或中度间质性炎症,肾脏和小肠未见明显病理改变。结论:纳米氧化锌经口染毒60 d未引起C57BL/6J小鼠血液系统炎症,但可诱导心脏、肝脏、脾脏和肺脏出现轻度的病理变化,并导致肝脏和肾脏的功能异常。     

Contribution of intestine and kidney to glucose fluxes in different nutritional states in rat

The liver is considered the main contributor of endogenous glucose production (EGP) in the postabsorptive (PA) state in mammals. However, it has been shown that the kidney, in PA and fasting states, and the intestine, in insulinopenia states, could make significant contributions to EGP. Using glucose tracer dilution combined to a vessel ligaturing approach, we studied the respective role of these organs in glucose turnover under various nutritional conditions in the rat (Rattus norvegicus). Both organs constitute key sites of glucose disposal in all situations in the non-moving rat. The kidney makes a small (12%) contribution to EGP in the PA state (9.6+/-1.3 micromol/kg min, means+/-SEM, n=5), which is dramatically increased (p<0.01) in 24 h-fasting (18.8+/-1.0 micromol/kg min) or streptozotocin diabetes (48+/-3 micromol/kg min). The small intestine contributes to EGP via two ways: a direct glucose contribution that may only take place in fasting and diabetes; an indirect contribution via the supply of alanine and lactate to liver gluconeogenesis that may account for up to 5 micromol/kg min in both PA and fasted states in the rat. These data emphasize the coordinate interactions among the three gluconeogenic organs in glucose homeostasis when nutritional conditions are changing.     

The effects of dietary sulfur on selenium utilization by the rat

The antagonistic effects of S on Se utilization were studied by measurement of tissue Se concentrations and glutathione peroxidase (GSHpx, E.C.1.11.1.9) activities in rats offered Torula yeast-based diets supplemented with sodium sulfate to provide 1.5, 3, or 5 g S/kg diet. Increasing sulfur concentrations in the diet caused small but significant decreases in GSHpx activity of liver, spleen, heart, lung small intestine, and skeletal muscle. Also significantly decreased were Se concentrations in liver and hair. Dietary sulfur content had no significant effect on body weight gain of the rats. With an adequate supply of Se in the diet, there are probably no major deleterious effects of dietary S on Se metabolism in the rat.     

Der Einfluß endogener Faktoren auf den Asche-, Kalzium-, Magnesium-, Kalium-, Natrium-, Phosphor-, Zink-, Eisen-, Kupfer- und Mangangehalt der Schweineborste

The objective of the present study was to investigate physiological effects of a marginal copper and iron supply on pigs. Therefore an experiment was conducted with 4 × 12 growing pigs of the crossbreed Pietrain × Deutsche Landrasse. The animals were fed for a period of 119 days with a diet poor of copper (1.5 mg Cu/kg diet) and/or poor of iron (35 mg Fe/kg diet). Control animals were supplied adequately with copper (4.8 mg Cu/kg diet) and iron (85 mg Fe/kg diet). The diet was given according to weight. After reaching an average weight of 102.6 ± 3.5 kg the animals were slaughtered. Due to the activity of the coerulplasmin and katalase enzyme and the haematological parameters, the supply of copper and iron could be classified as marginal. There was no interaction between copper deficiency and iron metabolism. The protein metabolism was unchanged. Low copper intake reduced the copper concentrations in serum, liver, muscle and backfat, and low iron intake reduced the iron concentration in serum, liver and muscle. Marginal copper and iron supply had no relevant effect on either food intake and growth performance or carcass characteristics and meat quality.     

Roentgen anatomy of the arteries of the gallbladder (according to intravital angiography)]

Examiniation of 163 series of coeliacograms and 10 series of angiograms of the superior mesentery artery has established thatby a conventional method the gallbladder artery is revealed in 79.1% of observations. The gall-bladder is blood supplied by a solitary or a double artery , or by numerous small vessels (scattered type of blood supply). Distinctive features of the gall-bladder arteries are:the site of their origination, the type of branching, irregular sinous course and false enlargements of the lumen as well as the disposition of arteries and their branches coinciding withthe topographs of the bladder determined in the parenchymatous phase. The main causes preventing determination of the gall-bladder arteries are both insufficiently contrast angiograms andpoor accumulation of the contrast substance in the bladder wall. Superposition of theshade of the enlarged liver is one of the obstacles in determinating the gall-bladder arteries. The author's experience show that the sourses of the gall baldder blood supply can be revealedin most cases in ordinary coeliacograms.     

Effect of crude sulphated polysaccharide from brown algae against acetaminophen-induced toxicity in rats

This study was conducted to examine the protective role of crude polysaccharide from brown seaweed Sargassum polycystum against acetaminophen-induced abnormality in blood glucose, serum albumin/globulin ratio, and liver glycogen, lactate, and pyruvate. Liver and renal tissue histology was performed to confirm the efficacy of Sargassum polysaccharide. A toxic dose of acetaminophen (800 mg/kg body weight intraperitoneally) induced severe abnormality in all basic parameters with apparent toxicity in liver (enlargement of hepatocytes, loss of cytoplasmic content with disruption in the hepatic plates and sinusoidal dilation) and renal tissue (glomerular damage with congestion of tubules). The isolated liver cells were stained with acridine orange and examined under fluorescence microscope, which revealed that the acetaminophen induced significant damage. In contrast, the rats pretreated with Sargassum polysaccharide (200 mg/kg body weight) daily for 3 weeks did not show liver and renal tissue with these severe aberrations induced by acetaminophen. Histology results were also consistent with analyzed basic biochemical parameters, which confirmed the effectiveness of the crude polysaccharide against acetaminophen-induced abnormality in rats.     

Fibrin glue eliminates the need for packing after complex liver injuries.

Hemostasis after traumatic liver injury can be extremely difficult to obtain, particularly in coagulopathic patients who have suffered extensive liver damage. We determined the ability of a fibrin glue preparation (FG) to terminate ongoing bleeding using a new, clinically relevant porcine model of complex hepatic injury. Anesthetized swine (n = 6, 18 to 19 kg) received an external blast to the right upper abdomen and were immediately anticoagulated with intravenous heparin (200 u/kg). Uncontrolled hemorrhage from blast continued from time of injury (t = 0 minutes) to t = 15 minutes. Lactated Ringer's solution was infused to keep mean arterial pressure (MAP) > 80 mm Hg until the end of experiment (t = 90 minutes). Animals underwent routine surgical techniques to control bleeding, and FG was employed in the event these measures failed. Estimated blood loss and fluid resuscitation volume were measured. Serial MAP, arterial base excess, and temperature were recorded. Animals were severely injured with significant blood loss prior to laparotomy (26 +/- 6 cc/kg) and during routine surgical efforts to arrest hemorrhage (11 +/- 2 cc/kg). Bleeding could not be controlled with standard techniques in any animal. FG rapidly controlled hemorrhage and eliminated the need for packing. Re-bleeding was noted in only one animal (portal vein injury). FG can control severe hepatic hemorrhage when surgical techniques fail. Further work in the clinical arena is warranted to determine the potential benefits of FG in arresting hemorrhage in hemodynamically unstable coagulopathic patients with complex hepatic injuries.     

Hydrodynamics of arterial branching--the effect of arterial branching on distal blood supply

A study was conducted to investigate the hydrodynamics of branching flow in relation to the blood supply to the basal part of the brain. A series of measurements of the branching loss-coefficients under laminar steady flow were conducted using model branches with various geometries, and the effect of branching on blood supply to distal areas was described using a lumped-parameter model of the vascular structure. It was revealed that in the blood circulation, branching loss is important where a small artery divides off with a large branching angle from a large trunk. It was also indicated that the effect of such branching on the distal blood supply might become more significant when the peripheral resistance is reduced, thereby increasing the blood velocity in the trunk.