异丙肾上腺素对大鼠心肌纤维化和相关细胞因子的影响

目的: 探讨异丙肾上腺素(isoprote renol, Iso)对 大鼠,心肌纤维化和相关细胞因子的影响。方法: 20只SD大鼠随机分成正常对照组(空白组)、异丙肾上腺素组(Iso组),每组10只。Iso组经皮下注射Iso 后,对两组行组织学观察心功能、胶原容积分数(CVF)、胶原蛋白含量和血浆中血管紧张素II(An­gll)、一氧化氮(NO)浓度的测定。结果: 与空白组相 比,Iso组心肌细胞间有大量胶原增生, 心功能有所降低,CVF、胶原蛋白含量和Angil含量增加,NO含量降低,最大上升速率(+ dp/dt_max)和心室收缩压(LVSP)未见明显改变。结论: Iso能促进大鼠,心肌纤维化和相关细胞因子浓度的变化。     

κ-阿片受体与β1-肾上腺素受体交互作用抑制异丙肾上腺素诱导的心肌肥大

目的: 观察选择性 kappa 阿片受体(kappa opi-oid receptor,κ-OR)与 β 肾上腺素受体(β adrenergicreceptor, β-AR)在心肌细胞肥大方面的交互作用。方法: 以 体 外 培 养 的 乳 鼠 心 肌 细 胞 为 模 型, 10 μmol°L^-1 的异丙肾上腺素(β肾上腺素受体激动剂,β-AR)诱导心肌肥大, 观察 1μmol°L^-1的 U50,488H(κ-OR激动剂,U50)对其作用。进一步探索在100 nmol°L^-1ICI118, 551(β₂ -AR 阻断剂)存在情况下,κ-OR的激活对心肌肥大的作用。用 Lowry's 法测心肌细胞的蛋白质含量;用消化分离法,并利用计算机图象分析系统测心肌 细胞的体积;用[³H]leucine 掺入法测定心肌细胞蛋白的合成。结果: 异丙肾上腺素使心肌细胞总蛋白含量、体积、蛋白合成明显增加;1 μmol°L^-1 的 U50, 488H 使 ISO 诱导的心肌细胞总蛋白含量、体积、蛋白合成减少, 这种作用可被选择性 κ-OR阻断剂-nor-BNI(norbinaltorphimine)抑制。在 ICI118, 551 存在的情况下, U50 也能起到减弱 ISO 诱导心肌细胞肥大的作用。结论: U50,488H 通过激活 κ-OR 与β₁ -AR 交互作用抑制 ISO 所诱导的心肌细胞肥大。     

洛泰对异丙肾上腺素诱导大鼠急性心肌缺血的保护作用1

目的 观察三七总皂甙的新剂型——洛泰(血塞通粉针剂,主要成分为三七总皂甙)对大鼠急性心肌缺血的保护作用。方法 采用微量异丙肾上腺素(ISO)恒速静注造成大鼠急性心肌缺血的模型,动态观测Ⅱ导联心电图S-T段的变化,以ST段降低及ΣST为指标反映缺血程度。结果 静脉注射洛泰50,100mg·kg^-1,对ISO诱导大鼠急性心肌缺血有一定程度的保护作用,呈剂量依赖性,其中以100mg·kg^-1组对心电图的改善作用较明显。灌胃给予洛泰对ISO诱导大鼠实验性急性心肌缺血也有一定程度的减轻作用,但没有统计学差异。结论 采用改进的大鼠急性心肌缺血模型具有稳定性和重复性好、快捷有效、易掌握、耗费药品少等优点,适宜于初筛药物。同时实验结果提示静脉和灌胃两种途径给予洛泰对大鼠急性心肌缺血均具有一定程度的保护作用。     

均苯四甲酸酐修饰β-环糊精微球电色谱柱的制备及应用

合成了均苯四甲酸酐修饰β-环糊精微球,通过红外光谱、X-射线光电子能谱、扫描电镜对其进行结构和形貌表征,获得了大小均匀、表面光滑、粒径为5~10μm的微球。以该微球为手性固定相,采用溶胶-凝胶法制备了颗粒固定化整体柱,并考察了柱制备过程中的影响因素,获得最佳的柱制备条件:聚乙二醇∶冰乙酸∶正硅酸甲酯为0.25 g∶2.5 m L∶1.5 m L,溶胶∶微球为2 m L∶1 g,水浴时间10 h,水浴温度40℃。利用该颗粒固定化整体柱对盐酸异丙肾上腺素和盐酸氯丙那林对映体进行手性拆分,达到了基线分离。     

Erratum to Stricker.

Reports an error in the article "The The Renin-Angiotensin System and Thirst: A Reevaluation. II. Drinking Elicited in Rats by Caval Ligation or Isoproterenol" by Edward M. Stricker (Journal of Comparative and Physiological Psychology, 1977, Vol. 91, No. 6, pp. 1220-1231), one line was printed incorrectly. On page 1228, the third line in the left-hand column reads "protin after 2 U/100 g hog renin"; the entire first sentence should read as follows: Three other nephrectomized rats were anesthetized 50 min after .33 mg/kg isoproterenol, 5 min after 2 U/100 g hog renin had been given. (The following abstract originally appeared in record 2005-09077-001) Ligation of the inferior vena cava and administration of isoproterenol have been shown to stimulate renin secretion and to augment water intake in rats. However, the present experiments suggested that the plasma renin activities produced by these treatments do not account for more than 20% of the observed drinking behavior. Direct measurements of arterial blood pressure further indicated that nephrectomized rats go into hypotensive shock after caval ligation or isoproterenol treatment. Drinking was elicited in these hypotensive animals by systemic injection of hypertonic NaCl solution, renin, or Pitressin, or by intracranial injection of angiotensin, but in each case a rapid increase in blood pressure also was observed. Thus, it appears that nephrectomy reduces water intake in these animals by undermining their general capacity to behave rather than by removing a specific dipsogenic stimulus. These and other results suggested that drinking elicited in rats by caval ligation or isoproterenol is not mediated by the renin-angiotensin system. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The Renin-Angiotensin System and Thirst: A Reevaluation. II. Drinking Elicited in Rats by Caval Ligation or Isoproterenol.

Ligation of the inferior vena cava and administration of isoproterenol have been shown to stimulate renin secretion and to augment water intake in rats. However, the present experiments suggested that the plasma renin activities produced by these treatments do not account for more than 20% of the observed drinking behavior. Direct measurements of arterial blood pressure further indicated that nephrectomized rats go into hypotensive shock after caval ligation or isoproterenol treatment. Drinking was elicited in these hypotensive animals by systemic injection of hypertonic NaCl solution, renin, or Pitressin, or by intracranial injection of angiotensin, but in each case a rapid increase in blood pressure also was observed. Thus, it appears that nephrectomy reduces water intake in these animals by undermining their general capacity to behave rather than by removing a specific dipsogenic stimulus. These and other results suggested that drinking elicited in rats by caval ligation or isoproterenol is not mediated by the renin-angiotensin system. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Amaranthus viridis Linn., a common spinach, modulates C-reactive protein, protein profile, ceruloplasmin and glycoprotein in experimental induced myocardial infarcted rats

BACKGROUND: Glycoprotein is one of the components of the cardiac extracellular matrix and plays an important role in cardiac remodelling during various cardiac diseases, including myocardial infarction (MI). This study was aimed at evaluating the preventive role of Amaranthus viridis Linn. on C‐reactive protein (CRP), total protein, albumin, globulin, ceruloplasmin and glycoproteins in the serum and heart of experimental induced myocardial infarcted (MI) rats. RESULTS: MI was induced in male Wistar rats by subcutaneous injection of 20 mg kg^?1 isoproterenol (ISO) kg^?1 body weight (BW) twice at an interval of 24 h. ISO‐induced MI rats showed a significant increase in the levels of serum CRP and ceruloplasmin and a significant decrease in the levels of serum total protein, albumin and globulin. Glycoprotein levels in the serum and heart were increased in ISO‐induced MI rats. Oral administration of 300 mg A. viridis kg^?1 BW day^?1 for a period of 45 days altered the metabolic derangement in ISO‐induced MI rats. CONCLUSION: This study exemplifies the protective effect of A. viridis on ISO‐induced cardiotoxicity in male Wistar rats. The data further reinforce the cardioprotective effect of A. viridis by altering CRP and glycoprotein levels. Copyright © 2012 Society of Chemical Industry     

Effects of pharmacological amounts of S‐allylcysteine on lipids in normal and isoproterenol‐induced myocardial infarction in rats

The present study evaluates the effect of S‐allylcysteine on marker enzymes, serum and myocardial lipids in normal and isoproterenol‐induced myocardial infarction in male Wistar rats. A significant increase in the activities of marker enzymes such as creatine kinase, lactate dehydrogenase, aspartate transaminase and alanine transaminase in serum of isoproterenol (150 mg kg^?1)‐treated rats was observed. The levels of serum lipids (cholesterol, triglycerides, free fatty acids and phospholipids) were significantly increased, while the levels of myocardial cholesterol, triglycerides and free fatty acids were significantly increased in isoproterenol‐administered rats. The concentration of myocardial phospholipids was significantly decreased in isoproterenol‐administered rats. Oral pretreatment with S‐allylcysteine at doses of 50, 100 and 150 mg kg^?1 using an intragastric tube daily for a period of 45 days positively modulated the biochemical alterations caused by isoproterenol. The effect of S‐allylcysteine at a dose of 150 mg kg^?1 showed a better cardioprotective effect than the other two doses (50 and 100 mg kg^?1). α‐Tocopherol (60 mg kg^?1) administration orally using an intragastric tube to rats daily for 45 days also exhibited a significant cardioprotective effect. The effect of S‐allylcysteine was compared with α‐tocopherol. Oral administration of S‐allylcysteine (50, 100 and 150 mg kg^?1) to normal rats did not show any significant change in this study. Thus, from the present study it can be concluded that a pharmacological dose of S‐allylcysteine exerts a protective effect against isoproterenol‐induced myocardial infarction in rats. Copyright © 2006 Society of Chemical Industry     

Maternal defense is modulated by beta adrenergic receptors in lateral septum in mice.

Maternal defense (offspring protection) is a critical and highly conserved component of maternal care in mammalian systems that involves dramatic shifts in a female's behavioral response to social cues. Numerous changes occur in neuronal signaling and connectivity in the postpartum female, including decreases in norepinephrine (NE) signaling in subregions of the CNS. In this study using a strain of mice selected for maternal defense, we examined whether possible changes in NE signaling in the lateral septum (LS) could facilitate expression of maternal aggression. In separate studies that utilized a repeated measures design, mice were tested for maternal defense following intra-LS injections of either the β-adrenergic receptor agonist isoproterenol (10 μg or 30 μg) or vehicle (Experiment 1), the β-adrenergic receptor antagonist propranolol (2 μg) or vehicle (Experiment 2), or the β1-receptor antagonist, atenolol (Experiment 3). Mice were also evaluated for light–dark performance and pup retrieval. Thirty micrograms of the agonist isoproterenol significantly decreased number of attacks and time aggressive relative to vehicle without affecting pup retrieval or light–dark box performance. In contrast, the antagonist propranolol significantly increased maternal aggression (lowered latency to attack and increased total attack time) without altering light–dark box test. The β1-specific antagonist, atenolol, significantly decreased latency to attack (1 μg vs. vehicle) without altering other measures. Although the findings were identified in a unique strain of mice, the results of these studies support the hypothesis that changes in NE signaling in LS during the postpartum period contribute to the expression of offspring protection. (PsycINFO Database Record (c) 2011 APA, all rights reserved)