不同形式蛋氨酸对凡纳滨对虾肝胰腺蛋氨酸腺苷转移酶活性的影响

试验在低鱼粉饲料中添加不同形式蛋氨酸[晶体蛋氨酸(MET)、邻苯二甲酸醋酸纤维素包被蛋氨酸(CAP)、棕榈酸甘油酯包被蛋氨酸(TPA)、树脂包被蛋氨酸(RES)和羟基蛋氨酸(MHA)],评价对凡纳滨对虾肝胰腺蛋氨酸腺苷转移酶活性的影响。配制5种等氮、等能饲料饲喂凡纳滨对虾,以晶体蛋氨酸为对照组进行50 d的养殖试验。分别在第28 d和50 d时,取对虾肝胰腺测定蛋氨酸腺苷转移酶活性。结果表明,微胶囊化对晶体蛋氨酸在肠道有一定的缓释作用,可以改善晶体蛋氨酸和蛋白质结合态蛋氨酸的吸收效率。     

对乙酰氨基酚对大鼠原代肝细胞的影响

对乙酰氨基酚(AP)是临床常用的解热镇痛药,治疗剂量时对肝脏无影响,过量则导致肝损伤[1-3].目前,许多学者以活体动物为研究对象,通过血清及肝组织匀浆中肝功能的变化,来揭示肝损伤的机制.但实验动物存在个体差异,使肝损伤机制的研究受到局限.体外培养的大鼠原代肝细胞保留着活体内的大部分功能,而且不存在个体差异,在肝损伤机制和筛选保肝药物的研究中越来越得到广泛应用.     

对乙酰氨基酚致猫中毒的诊疗报告

<正>对乙酰氨基酚具有解热、镇痛作用,口服吸收迅速,0.5～2 h血药浓度达峰值,血浆蛋白结合率25%～50%。90%～95%在肝脏代谢,主要以与葡萄糖醛酸化合物结合的形式从肾脏排泄,其余部分与硫酸盐、谷胱甘肽结合后,失去毒性。猫由于体内缺乏     

对乙酰氨基酚性肝损伤机制的研究进展

对乙酰氨基酚（Acetaminophen,简称AP）在英国被叫做扑热息痛,是一个解热镇痛药。对乙酰氨基酚的镇痛作用机制尚未十分明了,可能是通过抑制中枢神经系统中前列腺素（PG）的合成以及阻断痛觉神经末梢的冲动而产生镇痛作用。对乙酰氨基酚本身无毒性,但高剂量的对乙酰氨基酚可使CYP2E1活性增强,从而产生大量的毒性物质（NAPQI、亲电子基、氧自由基）进而引起肝细胞的严重损伤。iNOS抑制剂和N-乙酰半胱氨酸等影响CYP450活性的药物或物质可显著降低对乙酰氨基酚对肝的毒性。     

刺糖对对乙酰氨基酚诱导的肝损伤的保护作用

对乙酰氨基酚（N-acetyl-para-aminophenol,APAP）过量使用能够引起肝脏损伤,本研究旨在探讨刺糖对APAP所致小鼠急性肝损伤的保护作用及潜在的作用机理。采用水提法提取刺糖的有效成分,通过苯酚硫酸法和铝盐显色法进行刺糖提取物成分鉴定;49只雌性小鼠随机分为7组,正常对照组、模型组、刺糖不同浓度的提取物（600、300和150 mg/kg体重）+APAP组、水飞蓟宾阳性对照组及刺糖对照组（600 mg/kg体重）,灌胃3 d,末次给药1 h后,腹腔注射APAP 300 mg/kg体重,24 h后处死小鼠并采集血样和肝脏组织样品。检测血清谷丙转氨酶（ALT）和谷草转氨酶（AST）的活性;用HE染色制作病理标本,观察肝脏病理学变化。结果显示,刺糖提取物能够极显著降低小鼠血清中AST、ALT的含量（P<0.01）,APAP所引起的病理变化明显改善。本研究结果表明,刺糖对APAP所致的小鼠急性肝损伤有一定的保护作用。     

葛根素对对乙酰氨基酚诱导的急性肝损伤的保护作用研究

【目的】 研究葛根素（puerarin,PU）对对乙酰氨基酚（acetaminophen,APAP）所致小鼠急性肝损伤的保护作用,为临床上防治APAP引起的肝损伤提供新思路。【方法】 将40只4周龄体重（20±2） g的SPF级雄性昆明小鼠随机分为正常组（CON）、模型组（APAP）、葛根素低剂量组（L-PU）、葛根素高剂量组（H-PU）4组,每组10只。CON组正常饲养,L-PU和H-PU组分别以50和100 mg/kg葛根素灌胃,每天1次,连续给药7 d。最后一次给药后禁食16 h,APAP、L-PU和H-PU组均以200 mg/kg对乙酰氨基酚灌胃1次。继续禁食12 h,麻醉后经眼眶采血,颈椎脱臼处死小鼠,迅速采集肝脏,观察肝脏形态、计算肝脏指数;测定血清丙氨酸氨基转移酶（alanine aminotransferase,ALT）、天冬氨酸氨基转移酶（aspartate aminotransferase,AST）活性,评价肝损伤情况;测定肝脏过氧化氢酶（catalase,CAT）活力及总抗氧化能力（total antioxidant capacity,T-AOC）,评定肝脏氧化应激情况;测定谷胱甘肽转移酶（glutathione S-transferase,GST）及细胞色素P450家族2亚家族E成员1（cytochrome P450 2E1,CYP2E1）含量,分析APAP在肝脏的代谢情况;测定凋亡相关蛋白半胱氨酸蛋白酶-3（caspase-3）和caspase-9含量,评定肝脏细胞凋亡情况;制作肝脏病理组织切片,HE染色后观察肝脏组织学变化。【结果】 与CON组相比,APAP组肝脏质地坚硬,有明显出血,肝脏组织结构受到严重破坏,肝索排列紊乱,肝小叶结构不清晰,肝细胞大量坏死,肝脏指数及血清中ALT、AST水平显著上升（P<0.05）,CAT活力、T-AOC及GST水平显著下降（P<0.05）,caspase-3、caspase-9及CYP2E1含量显著上升（P<0.05）。与APAP组相比,L-PU和H-PU组小鼠肝脏形态结构及组织结构基本保持正常,且H-PU组效果更显著;L-PU和H-PU组小鼠肝脏指数和血清中AST、ALT水平显著降低（P<0.05）,肝脏中CAT活力、T-AOC显著提高（P<0.05）,caspase-9水平显著降低（P<0.05）;此外,L-PU和H-PU组在提高小鼠GST水平的同时也显著降低了CYP2E1水平（P<0.05）。【结论】 葛根素对APAP所致的小鼠肝损伤具有明显的保护作用,可能与葛根素发挥抗氧化、抗凋亡、加速APAP解毒作用有关。     

菊苣多糖对小鼠药物性肝损伤保护作用的筛选

试验研究对菊苣种子、根、茎及叶4个部位多糖通过含量测定及抗氧化能力试验进行保肝作用的筛选,选取最优部位多糖探究其对药物性肝损伤(DILI)的保护作用。以50 mg/kg或100 mg/kg的剂量预防性给予昆白小鼠菊苣多糖3 d,腹腔注射对乙酰氨基酚(APAP) 300 mg/kg诱导药物性肝损伤,测定血清、肝脏的生化指标、氧化指标和考察肝脏病理变化。结果显示,菊苣多糖呈剂量依赖性降低APAP引起血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性的升高,抵抗APAP造成的肝脏氧化损伤,提高肝脏超氧化物歧化酶(SOD)、谷胱甘肽(GSH)的活性,降低过氧化氢酶(H_2O_2酶)活性、丙二醛(MDA)含量,缓解APAP引起的肝脏细胞的病理变化的发生,保护肝脏抵御APAP造成的损伤。     

兽用扑热息痛注射液的稳定性实验研究

扑热息痛，又名对乙酰氨基酚、醋氨酚．简称APAP，它是一种白色、无臭单斜形结晶，味微苦，密度1293g／cm^3，熔点169～170.5℃。溶于甲醇，乙醇、丙酮和乙酸乙酯，易溶于热水几乎不溶于冷水和石油醚中。作为一种解热镇痛药物，其解热作用缓慢而持久．与阿斯匹林相比，具有刺激性小，极少有过敏反应等优点。在解热镇痛药物里面，扑热息痛具有良好的应用前景，由于长期使用的阿斯匹林有刺激胃肠道，     

猫黄疸的诊断治疗新思路

一转诊病例患猫呈严重溶血性黄疸、高胆红素血症,症状多变,化验报告与症状变化矛盾,诊断及治疗出现困境。通过调理食欲,对症治疗、驱虫,症状出现转机,食欲增加,黄疸消退速度加快,溶血症状得到改善,配合精心护理,患猫得以痊愈。文章对治疗过程加以记录分析,以期为黄疸病例诊疗提供新思路。     

瘤胃保护性蛋氨酸对奶牛的营养作用

瘤胃保护性蛋氨酸(RPMet)经过瘤胃后在小肠转化为蛋氨酸(Met),可增加进入小肠的Met数量,改善小肠氨基酸平衡,提高血清中必需氨基酸浓度、奶牛氮的利用率及其生产性能等.本文综述了RPMet对奶牛的营养作用.     

Effects of propylene glycol-containing diets on acetaminophen-induced methemoglobinemia in cats

Soft-moist cat foods contain 7 to 13% propylene glycol (PG) on a dry-weight basis. These diets induce Heinz body formation in feline RBC. In this study, we evaluated cats on a control diet and on a commercial diet containing 8.3% PG. All cats on the PG diet developed an increase in the number of circulating Heinz bodies. We then administered acetaminophen to cats on each diet to determine whether RBC from cats on PG diets were more susceptible to oxidant stress. Methemoglobin concentrations were significantly greater in cats in PG diets after acetaminophen administration. These data indicate that RBC from cats fed PG diets are more susceptible to oxidative stress.     

The role of para-aminophenol in acetaminophen-induced methemoglobinemia in dogs and cats

Acetaminophen (APAP) overdose in most species is associated with hepatotoxicity because of the metabolite N -acetyl- p -benzoquinoneimine (NAPQI). In dogs and cats, APAP overdose primarily causes methemoglobinemia and hemolysis. Although NAPQI has been proposed as the responsible intermediate in dogs and cats, it lacks chemical or pharmacokinetic characteristics that favor methemoglobin formation. We hypothesized that para -aminophenol (PAP) rather than NAPQI induces methemoglobinemia and that deficient arylamine N -acetyltransferase (NAT) activity in dogs and cats contributes to this species-dependent methemoglobinemia. Erythrocytes from dogs, cats, mice, and rats were exposed in vitro to APAP, NAPQI, and PAP. Only PAP induced methemoglobin and it induced more methemoglobin formation in dog and cat than rat and mouse erythrocytes. PAP also induced more methemoglobin in erythrocytes from Nat1/Nat2 knockout mice than wildtype (WT) mouse erythrocytes ( P  <   0.05), but less than in dog and cat erythrocytes ( P  <   0.01). APAP and PAP toxicity were compared in vivo in WT and Nat1/Nat2 knockout mice. APAP caused no hematotoxicity while PAP induced more methemoglobin in NAT1/NAT2 knockout mice than in WT mice ( P  <   0.05). These results support the hypothesis that PAP is the metabolite responsible for APAP-induced methemoglobinemia and that deficient NAT activity in dogs and cats contributes to this species-dependent toxicity.     

Evaluation of prophylactic and therapeutic effects of silymarin and N-acetylcysteine in acetaminophen-induced hepatotoxicity in cats

Avizeh, R., Najafzadeh, H., Razijalali, M., Shirali, S. Evaluation of prophylactic and therapeutic effects of silymarin and N -acetylcysteine in acetaminophen-induced hepatotoxicity in cats. J. vet. Pharmacol. Therap. 33 , 95–99.
Cats most commonly receive toxic amounts of acetaminophen (APAP) because owners medicate them without consulting a veterinarian. The aim of this study was to compare the hepatoprotective action of silymarin and N -acetylcysteine (NAC) against APAP poisoning. Twenty healthy cats were randomly allotted to five equal groups. Animals in group A were given APAP (single dose 150 mg/kg, p.o.); groups B and C consisted of cats that received NAC (100 mg/kg, p.o.) or silymarin (30 mg/kg, p.o.) concurrent with APAP administration respectively; groups D and E were treated like groups B and C, respectively, but 4 h after APAP administration. The serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), methemoglobin, and total and direct bilirubin were measured before APAP administration and 4, 24, and 72 h later. A single oral administration of APAP significantly elevated serum concentrations of ALT, AST, ALP, LDH, methemoglobin, and total and direct bilirubin. In both the groups receiving APAP plus NAC or silymarin, levels of serum enzyme activities, methemoglobin, and total and direct bilirubin remained within the normal values. It was concluded that silymarin as well as NAC can protect liver tissue against oxidative stress in cats with an APAP intoxication.     

舒眠宁对猫麻醉效果的研究

将舒眠宁应用于猫,观察其麻醉诱导时间、维持麻醉时间、苏醒时间、各项生理参数及麻醉效果。给猫肌注舒眠宁0.08 mL/kg后,诱导、维持麻醉、苏醒时间分别为(3.8±0.3)m in,(59±16)m in和(16±13)m in,对各项生理参数影响不明显。在拟进行绝育或去势术的猫静注舒眠宁0.04 mL/kg后,诱导、维持麻醉、苏醒时间分别为(30±5)s、(30±16)m in和(20±12)m in,所监测的生理参数均在正常范围内。将舒眠宁和舒泰分别以0.08 mL/kg和10 mg/kg给猫肌注后,舒泰组出现眼球震颤,舌、头部不自主运动,开口困难、大量流涎等副作用,舒眠宁组则无明显副作用;舒泰比舒眠宁对猫的心率影响大;舒眠宁的肌松效果好于舒泰。     

Serum gamma-glutamyl transpeptidase activity in healthy cats and cats with induced hepatic disease

Activities of serum gamma-glutamyl transpeptidase (GGT), alkaline phosphatase (ALP), and alanine aminotransferase (ALT) were determined in healthy cats and in cats before and after treatment: common bile duct ligation, carbon tetrachloride administration, sham surgery, or anesthesia only. Significant (P less than 0.01) increases in serum GGT, ALP, and ALT occurred in cats with ligated bile ducts. Significant (P less than 0.01) increases in serum ALT occurred in carbon tetrachloride-treated cats. Increases of serum GGT, ALP, or ALT were not observed in cats subjected to sham surgery or anesthesia only compared with these cats' baseline values and values in healthy cats. Tissue GGT activity was measured in liver, renal cortex, jejunal mucosa, and bile ducts. There was a 1.5-fold increase in GGT activity in livers of cats with ligated bile ducts, compared with that in livers of healthy cats.     

Myocardial damage in cats that died after anaesthesia

Summary

The necropsy findings of 85 cats that died up to six weeks after administration of injectable anaesthetics are described The most obvious findings in these cats were degeneration and necrosis of heart muscle fibres followed and related to time after the administration of the anaesthetics, by infiltration of predominantly mononuclear cells and by an increase in collagenous connective tissue. The lesions were most obvious on the inner side of the myocardium, indicating that hypoxic injury occurred during anaesthesia. The possible mechanism of the damage to the heart and its role in the pathogenesis of cardiomyopathy in the cat is discussed.     

Fine-needle aspirate cytology suggesting hepatic lipidosis in four cats with infiltrative hepatic disease

Four cats are reported in which cytology smears obtained by ultrasound-guided fine needle aspiration of the liver were interpreted as indicative of hepatic lipidosis. However, histopathology of hepatic tissue samples obtained with Tru-Cut-like needles or wedge biopsy revealed that the cats had inflammatory or neoplastic hepatic disease causing their clinical signs. Fine needle aspiration and cytology may not detect infiltrative lesions, particularly those that are nodular, multifocal, or localised around the portal regions. Fine needle aspirate cytology is a useful diagnostic procedure with many advantages, but care must be taken to avoid diagnosing hepatic lipidosis as the cause of illness when an infiltrative lesion is responsible.     

Metabolic and hormonal alterations in cats with hepatic lipidosis

Hepatic lipidosis in cats is a commonly diagnosed hepatobiliary disease of unknown cause. The purpose of this prospective study was to characterize the blood hormone and lipid status of cats with hepatic lipidosis, and to compare this status to that of cats with other types of liver disease and to control cats. Twenty-three cats with hepatic disease were assigned to 1 of 2 groups on the basis of cytopathologic or histopathologic examination of the liver: group 1, hepatic lipidosis (n = 18); or group 2, cholangiohepatitis (n = 5). Ten healthy young adult cats were used as controls. Food was withheld from control animals for 24 hours before blood collection. Concentrations of plasma glucagon and serum insulin, cortisol, thyroxine, triglycerides, cholesterol, phospholipids, and nonesterified fatty acids (NEFAs) were determined in all cats, in addition to routine hematologic and serum biochemical testing. Cats with hepatic lipidosis had higher serum NEFA concentrations than cats with cholangiohepatitis or control cats (P < .05). Cats with cholangiohepatitis had higher serum cholesterol and phospholipid concentrations than those of cats with lipidosis or control cats (P < .05); their plasma glucagon concentrations were higher than those of control cats (P < .05), but were not different from those of cats with hepatic lipidosis. Serum insulin concentrations were significantly higher in control cats than in diseased cats (P < .05), but neither serum insulin nor the insulin to glucagon ratio was significantly different among the cats with hepatic disease. The high concentration of NEFAs in cats with hepatic lipidosis suggests that at least 1 factor in the pathogenesis of this syndrome may involve the regulation of hormone-sensitive lipase.     

Epidermal and hepatic glucocorticoid receptors in cats and dogs

Low capacity, high affinity [³H] dexamethasone binding receptors were identified in cytosolic preparations of liver (mean number 45±10·1 fmol mg⁻¹ protein, apparent dissociation constant 0·4±0·1 nM) and skin (mean number 46·4±23·8 fmol mg⁻¹ protein, apparent dissociation constant 1 ± 0·2 nM) of clinically normal dogs. For clinically normal cats, approximately half these numbers of receptors with a lower affinity, were detected in liver (mean number 23·1±10·4 fmol mg⁻¹ protein, apparent dissociation constant 3·2±0·9 nM) and skin (mean number 23·90±10·9 fmol mg⁻¹ protein, apparent dissociation constant 2·2±1·5 nM). This difference between dogs and cats in [³H] dexamethasone binding receptors may contribute to the relative glucocorticoid resistance observed in cats.