scholarly journals LIVER FUNCTION AS INFLUENCED BY ANESTHETICS AND NARCOTICS

1915 ◽  
Vol 21 (3) ◽  
pp. 203-212 ◽  
Author(s):  
G. H. Whipple ◽  
J. S. Speed
Keyword(s):  
Liver Injury ◽  
Liver Function ◽  
Functional Capacity ◽  
Liver Cells ◽  
Sufficient Evidence ◽  
Ether Anesthesia ◽  
Histological Changes ◽  
Histological Evidence ◽  
Passive Congestion

It has been established that specific liver poisons (chloroform, phosphorus) which cause histological changes in the liver cells, decrease the liver excretion of phenoltetrachlorphthalein. Also vascular disturbances (Eck fistula, passive congestion) with or without histological evidence may cause a fall in the output of phthalein through the liver. Sufficient evidence has been brought forward to show that the phenoltetrachlorphthalein excretion is a valuable index concerning the functional capacity of the liver. Ether anesthesia for a period of two hours usually causes a depression in the phthalein curve during the twenty-four hours following the anesthesia. Paraldehyde in doses sufficient to give anesthesia and stupor for a few hours will give adefinite fall in phthalein excretion. Chloral and urethane usually cause a decrease in phthalein output when given in considerable amounts. Alcohol causes a drop in the phthalein curve when given in large doses sufficient to cause stupor for a few hours. The drop in phenoltetrachlorphthalein excretion is demonstrated in the twenty-four hours following administration of the drug. A drop in the phthalein curve to two-thirds or one-half of normal indicates a definite liver injury and temporary impairment of function.

scholarly journals ECK FISTULA LIVER SUBNORMAL IN PRODUCING HEMOGLOBIN AND PLASMA PROTEINS ON DIETS RICH IN LIVER AND IRON

1945 ◽  
Vol 81 (2) ◽  
pp. 171-191 ◽  
Author(s):  
G. H. Whipple ◽  
F. S. Robscheit-Robbins ◽  
W. B. Hawkins
Keyword(s):  
Liver Injury ◽  
Hepatic Artery ◽  
Plasma Protein ◽  
Functional Capacity ◽  
Liver Dysfunction ◽  
Plasma Proteins ◽  
Lethal Dose ◽  
Standard Diet ◽  
Histological Changes ◽  
Hemoglobin Production

The Eck fistula shunts the portal blood around the liver which receives its blood only by way of the hepatic artery. There are slight gross and histological changes in the Eck fistula liver of the dog. There is evidence at times of some functional abnormalities of the liver due to the Eck fistula but the dog can tolerate this fistula for 1 to 8 years and appear normal. Chloroform is tolerated by the Eck fistula dog, which may take twice a lethal dose for the control dog without evidence of significant liver injury. Acacia given by vein is deposited in the Eck fistula liver and impairs further its functional capacity to contribute to hemoglobin production. The stress of anemia brings out the fact that the anemic Eck fistula animal cannot utilize standard diet factors and iron as efficiently as the anemic non-Eck control dog. The output of new hemoglobin in some instances may drop to one-fourth of normal. When hypoproteinemia alone or combined with anemia is produced in the Eck fistula dog, we observe at times very low production of plasma protein—seven a drop to one-tenth of normal. This interrelation of liver abnormality, liver dysfunction, and lessened plasma protein and hemoglobin production is significant. It is generally accepted that the liver is concerned with the production of several plasma proteins—fibrinogen, prothrombin, and albumin. The experiments above indicate that the liver is concerned directly or indirectly with the production of new hemoglobin. Our belief is that the liver contributes to the fabrication of hemoglobin by means of the mobile plasma proteins which to a large extent derive from the liver.

scholarly journals LIVER FUNCTION AS INFLUENCED BY THE DUCTLESS GLANDS

1914 ◽  
Vol 20 (3) ◽  
pp. 297-319
Author(s):  
G. H. Whipple ◽  
P. W. Christman
Keyword(s):  
Liver Function ◽  
Functional Capacity ◽  
Pancreatic Insufficiency ◽  
The Body ◽  
Fatal Poisoning ◽  
Histological Changes ◽  
Gland Tissue ◽  
Text Figure ◽  
Symptom Complex ◽  
Standard Solution

When phenoltetrachlorphthalein is injected intravenously, it is eliminated from the body in the bile through the activity of the hepatic epithelium. The feces may be collected after purgation and the phthalein extracted and estimated against a standard solution. The estimation of phthalein can be done with accuracy in a suitable colorimeter and the elimination in normal dogs is quite constant. Given a definite liver injury by means of poisons (chloroform, phosphorus), the amount of phthalein excreted will be diminished and the fall in output will be proportional to the amount of injury. With an acute fatal poisoning the curve may fall to zero. Under certain conditions of vascular interference the liver phthalein may show a decreased output; in passive congestion of the liver and with the Eck fistula the liver output may fall considerably below normal. Known disturbances of the liver function due to parenchymatous injury or vascular disturbances are indicated by a fall in the phthalein. excretion curve. Conversely it may be claimed that a drop in phthalein excretion may indicate a decrease in the functional capacity of the liver even if there be no detectable histological changes. Adrenal insufficiency produced by extirpation of three fourths or more of the gland tissue will be associated with a drop in liver phthalein excretion. With hypertrophy of the adrenal fragment the excretion comes back to normal, but may fall again when more adrenal tissue is removed (text-figure 1). Pancreatic insufficiency causes a progressive fall in the phthalein excretion indicating a grave lowering of the functional capacity of the liver (text-figure 2). This fact has a direct bearing on the question of diabetes. Parathyroid insufficiency with tetany causes no decrease in phthalein output, but at times a rise above normal. This comes out best when the phthalein curve is low following pancreas extirpation. Parathyroid tetany may cause hyperactivity on the part of the liver cells. Thyroid insufficiency produces no change in the uniform curve of phthalein excretion. Hypophysis insufficiency shows an initial fall in the curve, followed by a return to normal and a final drop in the last few days before death. These experiments supply evidence to the effect that the liver is very much concerned in the derangement that follows the removal of the ductless glands. Hence it seems probable that this disturbance of the liver function may be an important factor in the general symptom complex of ductless gland insufficiency. In conclusion we wish to express our appreciation to Dr. S. J. Crowe and Dr. A. P. Jones for assistance rendered in performing some of the operations for gland removal.

Mass Spectrometry-based Label-free Quantitative Proteomic Analysis of CCl4-induced Acute Liver Injury in Mice Intervened by Total Glycosides from Ligustri Lucidi Fructus

2020 ◽  
Vol 17 ◽  
Author(s):  
Qian Lu ◽  
Hai-Zhu Xing ◽  
Nian-Yun Yang
Keyword(s):  
Insulin Resistance ◽  
Liver Injury ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Proteomic Analysis ◽  
Acute Liver Injury ◽  
Liver Cells ◽  
Differentially Expressed ◽  
Liver Protein ◽  
Differentially Expressed Proteins

Background: CCl4 acute liver injury (ALI) is a classical model for experimental research. However, there are few reports involved in the fundamental research of CCl4-induced ALI Ligustri Lucidi Fructus (LLF) are and its prescription have been used to treat hepatitis illness clinically. LLF and its active ingredients displayed anti-hepatitis effects, but the mechanism of function has not been fully clarified Objective: To investigate the proteomic analysis of CCl4-induced ALI, and examine the effects of active total glycosides (TG) from LLF on ALI of mice4, including histopathological survey and proteomic changes of liver tissues, and delineate the possible underlying mechanism. Methods: CCl4 was used to produce ALI mice model. The model mice were intragastrically administrated with TG and the liver his-topathological changes of mice were examined. At the end of test, mice liver samples were collected, after protein denaturation, re-duction, desalination and enzymatic hydrolysis, identification was carried out by nano LC-ESI-OrbiTrap MS/MS technology. The data was processed by Maxquant software. The differentially-expressed proteins were screened and identified, and their biological information was also analyzed based on GO and KEGG analysis. Key protein expression was validated by Western blot analysis Results: A total of 705 differentially-expressed proteins were identified during the normal, model and administration group. 9 signifi-cant differential proteins were focused based on analysis. Liver protein expression changes of CCl4-induced ALI mice were mainly involved in several important signal channels, namely FoxO signaling pathway, autophagy-animal, insulin signaling pathway. TG has anti-liver damnification effect in ALI mice, the mechanism of which is related to FoxO1 and autophagy pathways Conclusion: CCl4 inhibited expression of insulin-Like growth factor 1 (Igf1) and 3-phosphoinositide-dependent protein kinase 1 (Pdpk1) in liver cells and induced insulin resistance, thus interfered with mitochondrial autophagy and regeneration of liver cells and the metabolism of glucose and lipid, and caused hepatic necrosis in mice. TG resisted liver injury in mice. TG adjusted the expression level of key proteins Igf1 and Pdpk1 after liver injury and improved insulin resistance, thus promoted autophagy and resisted the liver damage

scholarly journals A Preliminary Study on the Effect of Hydrogen Gas on Alleviating Early CCl4-Induced Chronic Liver Injury in Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1933
Author(s):  
Jianwei Wang ◽  
Quancheng Cheng ◽  
Jinyu Fang ◽  
Huiru Ding ◽  
Huaicun Liu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Liver Tissue ◽  
Uncoupling Protein ◽  
Liver Cells ◽  
Hydrogen Gas ◽  
Chronic Liver ◽  
Control Group ◽  
Protective Mechanism ◽  
Chronic Liver Injury ◽  
Ucp2 Expression

As a small-molecule reductant substance, hydrogen gas has an obvious antioxidant function. It can selectively neutralize hydroxyl radicals (•OH) and peroxynitrite (ONOO•) in cells, reducing oxidative stress damage. The purpose of this study was to investigate the effect of hydrogen gas (3%) on early chronic liver injury (CLI) induced by CCl4 and to preliminarily explore the protective mechanism of hydrogen gas on hepatocytes by observing the expression of uncoupling protein 2 (UCP2) in liver tissue. Here, 32 rats were divided into four groups: the control group, CCl4 group, H2 (hydrogen gas) group, and CCl4 + H2 group. The effect of hydrogen gas on early CLI was observed by serological tests, ELISA, hematoxylin and eosin staining, and oil red O staining. Immunohistochemical staining and Western blotting were used to observe the expression of UCP2 in liver tissues. We found that CCl4 can induce significant steatosis in hepatocytes. When the hydrogen gas was inhaled, hepatocyte steatosis was reduced, and the UCP2 expression level in liver tissue was increased. These results suggest that hydrogen gas might upregulate UCP2 expression levels, reduce the generation of intracellular oxygen free radicals, affect lipid metabolism in liver cells, and play a protective role in liver cells.

scholarly journals Spontaneous and experimental poisoning by nitroxinil at 34% in goats

2021 ◽  
Vol 41 ◽  
Author(s):  
João Ricardo C. Brito Junior ◽  
Karoline L. Soares ◽  
Yanca G.S. Soares ◽  
Flaviane N.L. Oliveira ◽  
Renato V. Alves ◽  
...  
Keyword(s):  
Liver Injury ◽  
Ambient Temperature ◽  
Acute Liver Injury ◽  
Clinical Signs ◽  
Abdominal Distension ◽  
High Ambient Temperature ◽  
Histological Changes ◽  
Physical Exercises ◽  
Vascular Congestion ◽  
High Doses

ABSTRACT: This study describes the epidemiological, clinical, and pathological aspects of spontaneous and experimental poisoning by nitroxinil at 34% concentration in goats. The outbreak occurred on a farm in the municipality of Prata, Paraíba state. Nitroxinil was administered to a herd of 120 goats, of which 18 presented with anorexia, vocalization, abdominal distension, weakness, staggering, and falls. Necropsy of three goats revealed that the main lesion was acute liver injury. Histologically the liver showed centrilobular necrosis associated with hemorrhage and hepatocyte degeneration. In the kidneys, tubular nephrosis with granular cylinder formations was observed. The lungs showed multifocal to coalescent areas of moderate interalveolar edema and vascular congestion. Experimental poisoning was carried out in two goats, with the same medication and doses administered on the farm. The experimental goats showed clinical signs and macroscopic and histological changes similar to the spontaneously poisoned goats. The diagnosis of nitroxinil poisoning was made based on epidemiological, clinical, and pathological data, and confirmed by experimental poisoning. The administration of nitroxinil in high doses, associated with high ambient temperature and physical exercises, can cause poisoning with high lethality in goats.

scholarly journals Vitamin A Supplementation Alleviates Extrahepatic Cholestasis Liver Injury through Nrf2 Activation

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Guiyang Wang ◽  
Peng Xiu ◽  
Fu Li ◽  
Cheng Xin ◽  
Kewei Li
Keyword(s):  
Bile Duct ◽  
Liver Injury ◽  
Liver Function ◽  
Vitamin A ◽  
Western Blotting ◽  
Bile Duct Ligation ◽  
Retinyl Palmitate ◽  
Binding Activity ◽  
Extrahepatic Cholestasis ◽  
Duct Ligation

Aim. To investigate the role of vitamin A in liver damage induced by bile duct ligation (BDL) in rats.Methods. Thirty male Wistar rats were randomly divided into three groups: SHAM group, BDL group, and BDL + VitA group . The concentrations of retinol and retinyl palmitate in the liver were analyzed using HPLC, and liver function was evaluated by the level of TBIL, ALT, AST, and ALP in serum. Hepatic oxidative status was estimated by measuring T-SOD, CAT, GSH, MDA, and AOPP. Nrf2 expression was assessed using immunohistochemistry and western blotting, and EMSA was performed to determine Nrf2 DNA-binding activity. The expression of the downstream factors such as Ho1 and Nqo1 was also examined using immunohistochemistry and western blotting assays.Results. Vitamin A treatment restored levels of retinoids in liver, improved liver function, alleviated oxidative stress, and facilitated the translocation of Nrf2 to the nucleus in the experimental obstructive jaundice. Vitamin A was also found to increase the expression of Nrf2 downstream proteins such as Ho1 and Nqo1.Conclusion. Vitamin A was here found to ameliorate cholestatic liver injury. This effect may be related to the activation of Nrf2/ARE pathway in bile duct ligation rats.

Adiponectin alleviates nonalcoholic fatty liver injury via regulating oxidative stress in liver cells

2020 ◽  
Author(s):  
Wenwen Ma ◽  
Shanshan Zhang ◽  
Yi Li ◽  
Tansheng Chen ◽  
Qin Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Fatty Liver ◽  
Liver Cells ◽  
Nonalcoholic Fatty Liver

scholarly journals Prophylactic Therapy of Silymarin (Milk Thistle) on Antituberculosis Drug-Induced Liver Injury: A Meta-Analysis of Randomized Controlled Trials

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Lina Tao ◽  
Xiaoyu Qu ◽  
Yue Zhang ◽  
Yanqing Song ◽  
Si-xi Zhang
Keyword(s):  
Liver Injury ◽  
Liver Function ◽  
Randomized Controlled Trials ◽  
Controlled Trials ◽  
Cochrane Central Register ◽  
Prophylactic Therapy ◽  
Antituberculosis Drug ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Randomized Controlled

Background. Prophylactic therapy with silymarin to prevent the development of antituberculosis drug-induced liver injury (anti-TB DILI) has been under debate. We aimed to evaluate the effect of silymarin in the prevention of anti-TB DILI. Methods. We searched MEDLINE, PubMed, Embase, and Cochrane Central Register of Controlled Trials (CENTRAL) up to 30th November 2018. Randomized controlled trials (RCTs) that compared silymarin and placebo to prevent anti-TB DILI were included. All statistical analyses were conducted using STATA 12.0 software. Standardized mean difference (SMD) and risk ratio (RR) with 95% confidence intervals (CIs) were used to evaluate the effect of silymarin. The quality of included studies was assessed according to Cochrane handbook. Funnel plots and Egger’s tests were carried out to evaluate publication bias. Sensitivity analysis was conducted to assess the influence of each study. Results. A total of 1198 patients from five RCTs (585 with silymarin and 613 with placebo groups) were included. Overall, silymarin significantly reduced the occurrence of anti-TB DILI at week 4 [RR: 0.33, 95% CI (0.15, 0.75)]. In addition, silymarin exerted protective effect on liver function in patients undergoing anti-TB drugs [SMD = − 0.15, 95% CI (−0.24, −0.07), P < 0.001 (ALT); SMD =−0.14, 95% CI (−0.23, −0.06), P = 0.001(AST); SMD =−0.12, 95% CI (−0.20, −0.03), P = 0.008 (ALP)]. Silymarin led to similar AEs in placebo groups [OR: 1.09, 95% CI (0.86, 1.39), P = 0.47]. Conclusion. Prophylactic therapy of silymarin is contributed to a noticeably reduced risk of development of anti-TB DILI four weeks after the initiation. In addition, silymarin significantly improved the liver function in patients who are receiving anti-TB drugs.

HISTOLOGICAL EVIDENCE FOR CELLULAR ADAPTATION TO NON-FREEZING COLD INJURY

1959 ◽  
Vol 37 (7) ◽  
pp. 811-819 ◽  
Author(s):  
O. Héroux
Keyword(s):  
Thermal Damage ◽  
Initial Level ◽  
Cellular Membrane ◽  
Cold Injury ◽  
Histological Changes ◽  
Inflammatory Reactions ◽  
Histological Evidence ◽  
Ionic Transfer ◽  
The Third ◽  
Parallel Increase

The development and the healing of non-freezing cold injury in ears of rats maintained at 6 °C for 118 days and followed at different times of exposure revealed histological changes of a different nature at 4–6 mm away from the edge of the ear from the changes at 1–3 mm. In the first 3 mm during the first 21 days of exposure there was a continuous drop in the number of prophases and telophases and a parallel increase in the number of blocked and degenerating metaphases. In the second week, inflammatory reactions appeared; in the third week, the edema and lymphocyte infiltration was quite severe, and at that time 10% of the epithelium was degenerating. At the end of the fourth week, in the non-necrotic part of the epidermis, the number of prophases and telophases had returned to the initial level and the number of blocked metaphases was back to normal. After 56 to 118 days, no signs of edema, necrosis, or blocked metaphases could be found. In summary, the cold injury developed in the first 3 or 4 weeks and healed in the following month. After 2 months, cold temperature had no damaging effect on the epidermal tissue.At 4–6 mm from the edge of the ear, no cold injury developed, but in the first week there was a slight degree of mitotic blocking which disappeared during the second week. Essentially the same picture was observed at the 1–3 mm location in the ears of rats kept at 15 °C.On the assumption that mitotic blocking is due to a disturbance of the ionic transfer through the cellular membrane, it is suggested that the primary cause of cold injury is a direct thermal damage to the membrane.

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