麝香保心丸对高尿酸血症大鼠内皮功能的影响

目的观察麝香保心丸对高尿酸血症大鼠模型血管内皮功能的影响。方法用2%氧嗪酸钾饲料饲养成功诱导高尿酸血症大鼠模型,然后随机分高尿酸血症模型组和高尿酸血症+麝香保心丸干预组,分别用苦味酸法和硝酸还原酶法检测血清尿酸浓度与血浆一氧化氮(NO)含量,用免疫组化法检测主动脉组织内皮型一氧化氮合成酶(eNOS)表达。结果 2%氧嗪酸钾饲料饲养6周可成功诱导高尿酸血症大鼠模型,高尿酸血症大鼠血浆NO含量明显减少,主动脉eNOS表达亦下调。用麝香保心丸干预可明显改善大鼠内皮功能。结论麝香保心丸可改善高尿酸血症大鼠的血管内皮功能。     

排酸冲剂对高尿酸血症大鼠血尿酸水平的影响

目的研究排酸冲剂对高尿酸血症大鼠血尿酸水平的影响。方法将60只大鼠随机分为空白对照组、模型组、秋水仙碱对照组、排酸冲剂组,采用次黄嘌呤致大鼠高尿酸血症法,观察排酸冲剂降血尿酸作用。结果排酸冲剂能明显降低高尿酸血症大鼠血尿酸水平。结论排酸冲剂具有抗痛风急性发作的作用。     

清热利湿解毒通络法对高尿酸血症大鼠血清生长指标的影响

目的探讨清热利湿解毒通络法组方对高尿酸血症大鼠血清生化指标的影响。方法将高尿酸血症大鼠分为正常对照组,模型组,阳性药(别嘌醇片组),清热利湿解毒通络法高剂量组,中剂量组,低剂量组。观察用药对高尿酸血症大鼠血清尿酸(UA)、尿素氮(BUN)、肌酐(Scr)、超氧化物歧化酶(SOD)、丙二醛(MDA)、黄嘌呤氧化酶(XOD)水平的影响。结果三个剂量均能明显降低高尿酸血症大鼠血清中UA、BUN、Scr含量,降低血清中MDA含量,提高血清中SOD活性,但对XOD活性无明显影响;明显减少高尿酸血症大鼠肾脏中尿酸结晶沉积,使肾脏病变程度明显减轻。结论清热利湿解毒通络法组方对酵母和腺嘌呤所致的大鼠高尿酸血症有明显的治疗作用。     

雌性大鼠和雄性大鼠高尿酸血症动物模型的动态比较

目的 采用酵母膏联合氧嗪酸钾构建雌性大鼠和雄性大鼠高尿酸模型,观察持续高尿酸血症对雌性和雄性大鼠血清生化指标及心脏、肾脏、尾动脉和主动脉的病理改变的影响。方法 以酵母膏21 g/(kg·d)给予喂养,氧嗪酸钾以200 mg/(kg·d)持续腹腔注射28 d建立高尿酸血症雌性和雄性大鼠模型。结果 酵母膏21 g/(kg·d)喂养联合氧嗪酸钾200 mg/(kg·d)持续腹腔注射28 d,雌性大鼠血清尿酸水平可维持在更高水平,高血清尿酸水平使大鼠心脏、肾脏和动脉也发生了一系列病理改变,且雌性大鼠病理改变较雄性大鼠明显。结论 雌性大鼠的造模效果优于雄性大鼠,应为建立高尿酸血症动物模型的首要选择。     

高尿酸血症与高血压

正高尿酸血症作为一种代谢疾病,其患病率逐年增加。血清尿酸水平升高与冠心病、高血压等心血管病密切相关。因此,详实了解高尿酸血症与高血压之间的相互关系,对于我国人群慢性疾病的防治意义重大。1尿酸与原发性高血压的关系流行病研究显示,高血压患者中高尿酸血症的患病率在20%~40%之间,而痛风患者中高血压的患病率在25%~50%之间。在动物实验中,大鼠形成轻度的高尿酸血症后出现了高血压,而对高尿酸血症的干预又可防止高血压的形成。在     

驻邕武警某部官兵高尿酸血症患病情况调查

目的了解武警某部官兵高尿酸血症的患病情况及相关因素。方法对2013年8~11月在我门诊部进行健康体检的武警某部1 365名官兵进行血尿酸相关检查,分析高尿酸血症的相关因素。结果 1 365名武警官兵中检出高尿酸血症180例,检出率为13.19%,男性检出率明显高于女性(P0.01);高尿酸血症见于各年龄组,但以40岁以上人群高发;高尿酸血症组中吸烟、嗜酒、肥胖者的比例均高于血尿酸正常组(P0.01)。结论武警某部官兵高尿酸血症患病率处于较高水平,在部队中应加强预防高尿酸血症的健康教育,纠正吸烟、嗜酒等不良生活习惯,适量运动,控制体重,以降低高尿酸血症的发生率。     

高尿酸血症对大鼠血压和血清脂联素的影响

目的观察高尿酸血症对大鼠血压和血清脂联素的影响,探讨高尿酸血症导致的血清脂联素的变化与血管内皮功能的关系。方法 36只雄性SD大鼠随机分为3组。使用高酵母膏饲料联合氧嗪酸钾悬液腹腔注射6周诱导大鼠高尿酸血症(n=12)。别嘌醇组(n=12)在给予酵母提取物和氧嗪酸钾同时给予别嘌醇灌胃。普通饲料饲养的大鼠作为对照(n=12)。测量大鼠收缩压。6周后处死大鼠,全自动生化分析仪检测血清尿酸,ELISA法检测血清脂联素、一氧化氮和内皮素1,免疫组织化学法检测大鼠主动脉内膜层内皮型一氧化氮合酶的表达量。结果与正常对照组相比,模型组大鼠血尿酸、内皮素1、收缩压显著升高,血清脂联素、一氧化氮及主动内膜层内皮型一氧化氮合酶表达量显著降低。与模型组相比,别嘌醇组血尿酸、内皮素1、收缩压降低,血清脂联素和一氧化氮水平升高,主动脉内膜内皮型一氧化氮合酶表达增加。脂联素与血尿酸、内皮素1、收缩压呈负相关。结论高尿酸血症诱导的大鼠高血压与血清脂联素、一氧化氮的降低及内皮素的升高有关。     

血尿酸水平与代谢综合征的相关性

目的探讨血尿酸水平与代谢综合征及其心血管并发症的相关性。方法分析资料完整的1000例代谢综合征患者,按NCEP-ATPⅢ诊断标准,分别探讨与高尿酸血症的关系及高尿酸血症与代谢综合征心血管并发症之间的关系。结果代谢综合征患高尿酸血症者占53%。代谢综合征的5项诊断标准中,以高血压、甘油三酯、腹型肥胖与高尿酸血症的关系最密切。男性高尿酸血症发病率高于女性,年长者高于年青者,合并心血管并发症者高尿酸血症较无心血管并发症者发病率明显增加。结论高尿酸血症与代谢综合征及其心血管并发症密切相关,高尿酸血症可能为代谢综合征的重要组成部分和重要的心血管疾病危险因素。     

老年退休人员高尿酸血症的患病率及影响因素分析

目的调查老年退休人群高尿酸血症的患病情况,并对其相关危险因素进行分析。方法选择健康体检的5412例老年退休人员,分别进行高尿酸血症及相关危险因素的问卷调查、体格检查和血液检测,根据血尿酸水平分为高尿酸血症组1581例,血尿酸正常组3831例,采用非条件logistic回归分析高尿酸血症的影响因素。结果 5412例受检者中,高尿酸血症患病率为29.21%,男性和女性患病率分别为37.87%和24.98%(P=0.000),高尿酸血症组超重、血糖异常、肾功能下降、血尿素升高、天冬氨酸转氨酶升高、高TG血症、高TC血症、低HDL-C血症、高LDL-C血症的患病率较血尿酸正常组明显升高(P<0.05),多因素logistic回归分析显示,性别、超重、肾功能下降、高TG血症、高TC血症、血尿素升高为高尿酸血症的危险因素(P<0.01)。结论该地区老年退休人群的高尿酸血症患病率较高,提示对于老年高尿酸血症患者的治疗应采取综合防治的措施,以降低患病率。     

高尿酸勃起功能障碍大鼠模型的建立

目的建立并评价高尿酸勃起功能障碍(ED)大鼠模型,为不同目的要求的研究提供建模参考。方法采用酵母粉(15 g/kg)饲料喂养,乙胺丁醇悬液(250 mg/kg)灌胃,氧嗪酸钾(200 mg/kg)皮下注射联合给药造模。先分别构建下述若干模型组,即模型Ⅰ、Ⅱ、Ⅲ、Ⅳ组,来进行对比研究。且不同的模型组依次相对应花费4 w、8 w、12 w及16 w的时间来进行造模。然后借助相关工具,对不同组的血尿酸水平进行精确检测,再借助阿扑吗啡(APO)实验,确定其中的高尿酸ED大鼠,最后对筛选出的样本进行阴茎海绵体内压(ICP)检测,以此来评估大鼠的勃起功能。结果模型Ⅰ、Ⅱ、Ⅲ、Ⅳ组血尿酸水平都呈现出上升态势,相比于空白对照组,差异存在统计学意义;而模型Ⅱ、Ⅲ、Ⅳ组APO(-)大鼠的勃起功能都呈显著的减弱态势,相比于空白对照组,差异存在统计学意义;模型Ⅲ、Ⅳ组APO(+)大鼠的勃起呈显著的减弱态势,相比于空白对照组,差异存在统计学意义;对比模型Ⅲ、Ⅳ组大鼠的勃起功能并未出现显著的差异,差异不存在统计学意义(P0.05)。结论造模8 w时APO(-)高尿酸血症大鼠勃起功能明显降低,造模12 w时APO(-)和APO(+)的高尿酸血症大鼠勃起功能均明显降低。造模12 w内高尿酸血症大鼠勃起功能下降与造模时间成正相关,且APO(-)高尿酸血症大鼠勃起功能更差。     

Effects of stress on growth of transplanted hepatic tumours and immune responses

Growth of transplanted hepatic tumours (T-9) was enhanced in immune rats under stress, compared with immune rats in an unstressed condition. Compared with unstressed immune rats, killer activity of mononuclear cells infiltrating the tumours against T-9 cells was significantly reduced in stressed immune rats. In contrast, killer activity of splenocytes obtained from stressed immune rats against T-9 cells was elevated compared with that from unstressed immune rats. In addition, natural killer cell activity of mononuclear cells infiltrating the tumours obtained from stressed immune rats was significantly reduced compared with that from unstressed immune rats. Cell populations infiltrating tumour tissues were identified by flow cytometric analysis. The percentage of CD8+ cells in mononuclear cells isolated from tumour tissues of stressed immune rats was reduced compared with that of unstressed immune rats. Furthermore, interleukin-2 responsiveness of splenocytes was suppressed in stressed immune rats, whereas T cell function as reflected by phytohaemagglutinin- or Concanavalin A-reactivity was unaffected by stress. Collectively, it is likely that stress suppressed the generation of cytotoxic cells from the spleen cells of immune rats.     

Decreased carnitine biosynthesis in rats with secondary biliary cirrhosis

Carnitine biosynthesis was investigated in rats with secondary biliary cirrhosis induced by bile duct ligation (BDL) for 4 weeks (n = 5) and in pair-fed, sham-operated control rats (n = 4). Control rats were pair-fed to BDL rats, and all rats were fed an artificial diet with negligible contents of carnitine, butyrobetaine, or trimethyllysine. Biosynthesis of carnitine and its precursors was determined by measuring their excretion in urine and accumulation in the body of the animals. Four weeks after BDL, total carnitine content was increased by 33% in livers from BDL rats when compared with control rats, but was unchanged in skeletal muscle and whole carcass. The plasma total carnitine concentration averaged 29.0 +/- 4.1 vs. 46.4 +/- 7.3 micromol/L in BDL rats and control rats, respectively. Urinary total carnitine excretion was reduced by 56% in BDL rats as compared with control rats. Carnitine biosynthesis was significantly decreased in BDL rats (0.45 +/- 0.19 vs. 0.93 +/- 0.08 micromol/100 g body weight/d in BDL and control rats, respectively). The tissue content of free and protein-linked trimethyllysine, a carnitine precursor, and trimethyllysine plasma concentrations were not different between BDL and control rats. However, urinary trimethyllysine excretion was increased 5-fold in BDL rats and approximated glomerular filtration. In contrast, urinary excretion of butyrobetaine, the direct carnitine precursor, was decreased by 40% in BDL rats as compared with control rats. Trimethyllysine biosynthesis was not different, but butyrobetaine biosynthesis was decreased by 51% in BDL as compared with control rats. In conclusion, carnitine biosynthesis is decreased in BDL rats as a result of a defect in the conversion of trimethyllysine to butyrobetaine.     

Effects of hypertension on cardiac performance in rats with myocardial infarction

To determine the effects of hypertension and myocardial infarction on cardiac performance, hemodynamic studies were performed on etheranesthetized, female spontaneously hypertensive rats and on two strains of normotensive rats, Wistar-Kyoto and American Wistar, 26 days after coronary arterial ligation. Baseline measurements of ventricular and arterial pressures and cardiac output (electromagnetic flowmeter) were obtained. Peak cardiac pumping and pressure-generating capacities were determined during a volume load and aortic occlusion, respectively. Infarct size was determined by planimetry. There was a progressive reduction in mean arterial pressure in relation to infarct size in both hypertensive and normotensive rats, but this reduction was twice as great in spontaneously hypertensive rats as in the normotensive rats, such that the arterial pressure of hypertensive rats with a moderate or large infarction decreased to within the “normotensive range.” However, spontaneously hypertensive rats still maintained significantly higher arterial pressures than did normotensive rats at comparable infarct sizes. There was also a progressive reduction in the peak pressure developed during an afterload stress, and this reduction was greater in hypertensive rats than in normotensive rats with a large infarct. Maximal flow-generating capacity was similarly altered in rats with infarction: Peak stroke volume index varied inversely with infarct size and the reduction in this index was significantly greater in spontaneously hypertensive rats than in normotensive rats with a large infarct. Moreover, peak stroke work index was reduced to a greater extent in spontaneously hypertensive rats than in both normotensive strains of rats at any infarct size. Thus, after myocardial infarction, greater reductions in both pressure and flow-generating capacities occurred in hypertensive rats than in normotensive rats.     

Evidence for alteration in the processing of dopamine in the anterior pituitary gland of aged rats: receptors and intracellular compartmentalization of dopamine

Receptors for dopamine and the subcellular localization of dopamine in the anterior pituitary gland were studied in young cycling female rats and in aged, constant estrous female rats. Dopamine receptors were quantified in membrane preparations of anterior pituitary tissue using [3H] spiperone as the ligand. On the basis of saturation isotherms, it was calculated that the equilibrium dissociation constant (Kd) and binding capacity for [3H]spiperone binding to pituitary membranes from young rats were 34.2 pM and 82 fmol/mg protein, respectively. The relative binding capacity of membranes from aged rats was 35% greater than that of membranes from young rats. There was no difference in the Kd values in aged and young rats. When the relative binding of [3H]spiperone by anterior pituitary membranes from individual animals was quantified by incubation with a saturating concentration of the ligand, it was found that [3H]spiperone binding in aged rats was significantly greater than that in young rats. When the subcellular localization of dopamine in anterior pituitary tissue was examined by means of density gradient centrifugation, it was found that the subcellular distribution of dopamine in tissue of aged rats was quantitatively different from that in young rats. In young rats, a small amount of dopamine was associated with light particles, whereas a large amount of dopamine was associated with heavy particles, which cosedimented with PRL-containing granules. In aged rats, the amount of dopamine associated with light particles was 5 times that found in young rats, whereas the amount of dopamine associated with heavy particles was the same as that in young rats. We speculate that altered intracellular compartmentalization of dopamine, leading to a marked accumulation of dopamine in the light particles, is related to increased secretion of PRL in aged rats.     

促红素对肝硬化大鼠血清—氧化氮含量的影响

目的探讨血红蛋白（Ｈｂ）对肝硬化大鼠血清一氧化氮（ＮＯ）含量及血流动力学的影响。方法应用５７Ｃｏ标记微球观察促红素长期治疗对肝硬化大鼠血流动力学参数的影响；应用荧光法测定大鼠血清ＮＯ含量。结果肝硬化大鼠全部出现高动力循环状态，且血清ＮＯ含量显著高于对照组、血Ｈｂ含量显著低于对照组；促红素治疗组，高动力循环状态明显改善，与未治疗组比较，Ｈｂ含量显著升高，血清ＮＯ含量显著降低。结论促红素致Ｈｂ增加，进而加速ＮＯ灭活对肝硬化高动力循环状态可能具有潜在治疗作用     

Endocrine and metabolic effects of life-long food restriction in rats

The effects of chronic (40%) food restriction from 6 weeks of age were studied in 28-month-old male Fischer-344 rats; the results were compared with ad libitum-fed, old and young male rats at 28 and 3 months of age, respectively. Pituitary luteinizing hormone was similar in all old rats and was significantly lower than in young rats. In old ad libitum-fed, but not in food-restricted rats, serum levels of LH, testosterone and T4 were significantly lower than in young rats. Serum levels of T3 did not differ between young and old rats. Type-II 5'-deiodinase activity in brown adipose tissue was similar in both groups of old animals and was significantly depressed as compared with that in young rats. Serum levels of triglycerides were significantly depressed in food-restricted rats, but were significantly increased in ad libitum-fed rats as compared with young rats. Both groups of old rats had significantly elevated serum levels of cholesterol over that in young rats, but the level was significantly lower in food-restricted as compared to ad libitum-fed animals. The results are consistent with the notion that life-long food restriction tends to preserve the activity of many metabolic functions.     

Catabolic defect of triglyceride is associated with abnormal very-low-density lipoprotein in experimental nephrosis

Very-low-density lipoprotein (VLDL)-triglyceride (TG) kinetics were examined in puromycin aminonucleoside-induced nephrotic rats in order to establish the nature of the hypertriglyceridemia associated with this condition. Nephrotic rats had a plasma TG concentration 10-fold higher than the controls. In nephrotic rats TG secretion rate was elevated only 1.2-fold above the controls, suggesting that the catabolism of TG was also impaired. Lipolytic activities were determined in postheparin plasma (PHP) of the control and the nephrotic rats. There were no significant differences in either the activity of lipoprotein lipase (LPL) or hepatic lipase (HL). VLDL-TG was endogenously radiolabeled in donor rats with [2-3H]-glycerol. The half life (T1/2) was then determined by monitoring the clearance of plasma [3H]-VLDL-TG in normal recipient animals. The T1/2 of VLDL-TG from nephrotic rats was twice that of normal rats. The defect in VLDL-TG clearance could be partially rectified by preincubation with high-density lipoprotein (HDL) from normal rats, but not with HDL from nephrotic rats. VLDL from either nephrotic or normal rats were incubated with PHP of normal rats to assess the effectiveness of VLDL-TG as a substrate for PHP. The lipolytic rate for nephrotic VLDL was significantly lower than that for normal VLDL, suggesting that VLDL from nephrotic rats was somewhat resistant to the action of LPL and HL. When VLDL from nephrotic rats was preincubated with HDL from normal rats, the low lipolytic rate of VLDL-TG improved significantly. This was not observed when HDL from nephrotic rats was used for the preincubation. The results suggested that physical and/or chemical change of VLDL particles due to nephrosis results in a catabolic defect of VLDL-TG.     

Mechanism of the Pancreas-parotid Gland Interaction

In order to elucidate the mechanism of interaction between the pancreas and parotid gland, male Wistar rats of tlie same litters were used to produce parabiotic pairs. Six pairs which survived tlie procedure more than 30 days were available for experimentation. In one of each pair of rats, acute pancreatitis was induced. Amylase concentration in the sera, pancreas and parotid glands in these rats was estimated and histocytological studies of these organs were performed. The following results were obtained: 1. The serum amylase level was elevated in the rats with experimentally induced pancreatitis. It was slightly elevated in the rats without pancreatitis. 2. Organ amylase concentration in the pancreas and parotid gland was reduced in the rats with and without pancreatitis. The reduction of pancreas tissue amylase in the rats without pancreatitis was slight and insignificant. 3. In hght microscopy, the pancreas in the rats without pancreatitis was not significantly altered compared to that of the control rats. The parotid gland in the rats without pancreatitis showed apparent atrophie degenerative changes, which were less severe than in the rats with pancreatitis. Electron microscopy revealed that the pancreas in rats without pancreatitis showed similar findings with those of the control rats. In the parotid gland, the findings in the rats without pancreatitis were less severe, but similar to those in the rats with pancreatitis. A humoral transmission mechanism is participating in the development of an interactive response between the pancreas and parotid gland.     

克山病病区粮喂饲大鼠维生素E营养状态评价及补充硒和维生素E的影响

克山病病区粮,或在其中补充硒或维生素E(VE)喂饲大鼠21～22周,以非病区粮组大鼠为对照。结果表明:病区粮组大鼠心、肝、脾、肾、骨骼肌、肾上腺和胰腺形态改变不明显;病区粮组大鼠心重:体重比值高于非病区粮组和补充硒或VE组大鼠;病区粮组大鼠24小时尿中肌酸排泄量高于非病区粮组在补充VE组大鼠尿中没有检出肌酸;病区粮组大鼠和非病区粮组大鼠红细胞体外过氧化氢溶血率相同,但都处于高水平,补充硒可明显降低溶血率,补充VE则溶血率更进一步降低。综合上述结果得出结论,病区粮喂养大鼠体内VE储存不能满足其需要。     

比索洛尔对抗β1-肾上腺素能受体自身抗体阳性心衰大鼠心功能的影响

目的 探讨比索洛尔对抗β1-肾上腺素能受体（β1-AR）自身抗体阳性心衰大鼠心功能的影响。方法 采用缩窄腹主动脉的方法,建立慢性心力衰竭的大鼠模型。将心衰组大鼠（90只最终入组65只）随机分为心衰治疗组（40只）和心衰非治疗组（25只）。心衰治疗组接受比索洛尔4周的治疗。心衰非治疗组接受同剂量的蒸馏水同样时间的治疗。应用ELISA法检测大鼠血清β1-AR自身抗体的阳性率和滴度;应用BL-420E生物机能实验系统于治疗前及治疗后4周检测心功能。结果 ①治疗组组内抗β1-AR自身抗体阳性者较阴性者左室舒张末压低,左室变化的最大速率升高,但无统计学意义;非治疗组组内抗β1-AR自身抗体阳性者较阴性大鼠的心功能进一步恶化,左室舒张末压明显升高（P<0.01）,左室变化的最大速率下降（P<0.05）。②治疗组中抗β1-AR自身抗体阳性者与非治疗组中抗β1-AR自身抗体阳性者比较,前者较后者左室舒张末压明显下降（P<0.01）;左室变化的最大速率均显著升高（P<0.05）。结论 比索洛尔治疗后,心衰大鼠抗β1-AR自身抗体阳性者的心功能较非治疗组中抗β1-AR自身抗体阳性者的心功能明显改善。同为治疗组的抗β1-AR自身抗体阳性者的心功能较阴性者的左室舒张末压低,左室变化的最大速率升高。