海豹油软胶囊防治高脂血症实验研究

目的研究海豹油软胶囊对实验性高脂血症的预防和治疗作用。方法预防实验：灌服高脂乳剂建立大鼠高脂血症模型的同时,连续30d灌胃给予低、中、高剂量的海豹油,试验结束时检测大鼠血清中总胆固醇（TC）、三酰甘油（TG）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）。治疗实验：灌服高脂乳剂15d建立大鼠高脂血症模型后,继续给予高脂乳剂的同时按预防实验方法进行。结果预防实验：海豹油低、中、高剂量组均能明显降低高脂血症大鼠血清TG、TC,明显升高血清HDL-C,降低血清LDL-C（P〈0.05）。治疗实验：海豹油低、中、高剂量组对高脂血症大鼠血清TC和TG水平均有明显的降低作用（P〈0.001）,各剂量对HDL-C水平无明显影响（P〉0.05）,高剂量组对LDL-C水平有降低作用（P〈0.05）。结论海豹油软胶囊具有防治高脂血症的作用。     

乌药叶对高脂血症模型大鼠血脂指标及肝组织形态学的影响

目的探讨乌药叶对高脂血症大鼠调节血脂及组织形态学的影响。方法将成年雄性高脂大鼠随机分成4组,设乌药叶0.33、0.66和2.00 g/kg·bw 3个剂量组和1个模型对照组,另设1个正常对照组,实验期45 d。结果在实验末期,中、高剂量组大鼠甘油三脂(TG)、总胆固醇(TC)和低密度酯蛋白胆固醇(LDL-C)均明显低于模型对照组,差异有统计学意义(P0.05或P0.01);中、高剂量组大鼠TG和高剂量组大鼠TC、LDL-C与正常对照组比较,均无统计学意义(P0.05);高剂量组大鼠高密度酯蛋白胆固醇(HDL-C)/LDL-C和HDL-C/TC均明显高于模型对照组,差异有统计学意义(P0.05)。高剂量组大鼠脂体比和中、高剂量组大鼠肝重、肝体比均明显低于模型对照组,差异有统计学意义(P0.05或P0.01);随乌药叶剂量增加,大鼠肝损伤和肝细胞肿胀、变性等病变程度明显减轻,且越靠近肝中央静脉效果越好,高剂量组大鼠肝组织病理变化总得分明显低于模型对照组,差异有统计学意义(P0.01)。模型对照组大鼠在实验末期TG明显低于实验前(P0.05);正常对照组大鼠在实验30 d、45 d TC、HDL-C、HDL-C/TC均明显低于实验前(P0.05或P0.01)。结论乌药叶具有明显促进高脂饮食大鼠TG、TC和LDL-C降低的作用;能明显拮抗高脂饮食大鼠HDL-C/LDL-C和HDL-C/TC降低的作用;明显拮抗高脂饮食大鼠脂体比、肝重、肝体比升高的作用,能明显减轻高脂饮食对大鼠肝的损伤,减轻肝细胞肿胀、变性等病变程度。高脂饮食所致高脂血症大鼠随实验进程TG有一定程度的下降趋势;成年雄性SD大鼠随周龄增长主要是因为其HDL-C下降而导致TC、HDL-C/TC下降。     

复方山泽降脂方降脂作用实验研究

目的探讨效验复方山泽降脂方（SZ）对实验性高脂血症大鼠血脂的调节作用。方法用脂肪乳剂灌胃造成大鼠实验性高脂血症动物模型,以复方山泽降脂方3.5、7、14 g.kg-1低、中、高剂量组给予大鼠灌胃28 d后,经腹主动脉取血,测血清总胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白（LDL-C）、高密度脂蛋白（HDL-C）。结果与高脂模型组比较,高剂量SZ能显著降低血清TC、TG、LDL-C水平和动脉硬化指数（AI）（P〈0.01或P〈0.05）,但对HDL-C的影响不大。结论复方山泽降脂方对高脂血症大鼠的脂质代谢有一定的调节作用,提示其对高脂血症的防治具有应用价值。     

成年SD大鼠糖尿病心肌病模型的建立

目的：探索成年SD大鼠糖尿病心肌病（DCM）模型建立的方法。方法20只健康SD成年大鼠作随机分为DCM组（n=10）、对照组（n=10）。对照组喂养普通饲料,DCM组高脂饲料喂养12周。DCM模型的建立：对照组以枸橼酸缓冲液腹腔注射,DCM组使用等量1%链脲菌素腹腔注射。通过病理组织学证实为DCM心肌病理学改变。结果与对照组比较,DCM组的血清FBG、TC、LDL-C、TG均明显增高（P〈0.05）,而对照组的血清HDL-C较DCM组高（P〈0.05）。与对照组比较,DCM组的大鼠心肌细胞排列紊乱,间质基质集聚与纤维化增多。第6周末,两组的空腹血糖差异无统计学意义（P〉0.05）,DCM组的IRI、胰岛素均高于对照组（P〈0.05）。结论高脂、高糖膳食并小剂量STZ腹腔注射建立DCM模型,其方法成功率高,简单易行。     

绿豆癀对大鼠高脂血症的影响

目的 观察绿豆癀对大鼠高脂血症的影响。方法 将Wistar大鼠随机分为对照组,模型组,绿豆癀高、中、低剂量组和绿豆粉组。采用喂饲高脂饲料方法建立大鼠高脂血症模型,末次喂饲后禁食12 h,测定血清三酰甘油（TG）、低密度脂蛋白–胆固醇（LDL-C）、高密度脂蛋白–胆固醇（HDL-C）的量。结果 绿豆癀高剂量能明显降低血清LDL-C（P＜0.01）,而且其效果明显比绿豆粉组好（P＜0.05）;绿豆癀各剂量和绿豆粉均能明显降低血清TG、升高血清HDL-C（P＜0.01、P＜0.05）,绿豆癀高、中剂量的效果更佳,与绿豆粉相比有明显差异（P＜0.01）。结论 绿豆癀对大鼠高血脂症具有明显的调节作用。     

LED 红光照射对高脂血症大鼠血脂的影响

目的研究LED红光[波长（630±15） nm]照射对高脂血症大鼠血脂及肝脏病理学改变的影响。方法36只雄性SD大鼠,随机分为正常对照组（12只）和高脂模型组（24只）。正常对照组喂饲普通饲料,高脂模型组喂饲高脂饲料,连续喂养6周。造模成功后,将高脂模型组大鼠随机分为高脂对照组（不给予照射）和LED治疗组（每天照射30 min,连续28 d）。分别于照射的第15天和第29天测定TC、TG、LDL-C、HDL-C的含量。于照射第29天处死大鼠,称取肝脏湿重并进行大体及镜下观察。结果 LED照射的第15天后,LED治疗组与高脂对照组相比,血清TC、TG、LDL-C的含量降低,HDL-C的含量升高,但只有LDL-C有统计学意义（ P ＜0屯．05）。 LED照射的第29天, LED治疗组与高脂对照组相比,血清TC、TG、LDL-C的含量明显降低,HDL-C的含量升高,差异有统计学意义（ P ＜0．01）。肝重、肝指数也明显降低（ P ＜0．05）。经LED照射后,LED治疗组大鼠肝脏脂肪变性的程度较高脂对照组有明显改善。结论LED红光照射可以降低高脂血症大鼠血清TC、TG、HDL-C、LDL-C的含量,并对高脂血症大鼠肝脏脂肪变性有一定的治疗作用。     

阿托伐他汀强化降脂对脑卒中患者颈动脉内膜中层厚度的影响

目的：观察阿托伐他汀强化降脂对脑卒中患者颈动脉内膜中层厚度（CIMT）的影响。方法：随机将120例脑卒中患者分为阿托伐他汀常规剂量组（10mg／d）组62例,强化降脂组（40mg／d）58例;分别于用药前及用药5个月后测定总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、三酰甘油（TG）;以超声观察CIMT的变化。结果：两组治疗前血脂、CIMT比较差异无统计学意义。两组治疗后TC、LDL-C和TG水平明显低于用药前（P〈0.05或P〈0.01）,但强化降脂组TC、LDL-C下降程度大于常规剂量组（P〈0.01）。两组治疗后CIMT均减少,但强化降脂组内比较差异有统计学意义（P〈0.01）。强化降脂组治疗后CIMT与常规剂量组比较差异有统计学意义（P〈0.01）。结论：强化降脂组能更有效降低TC、LDL-C、CIMT副作用无明显增加,安全性好。     

阿托伐他汀钙对兔动脉粥样硬化的影响

目的观察阿托伐他汀钙对兔动脉粥样硬化血管内皮的保护作用。方法将30只4月龄雄性健康日本大耳白兔,随机分为3组,每组10只。空白对照组：给予普通饲料喂养;模型组：给予高脂饲料喂养（高脂饲料配方：1%胆固醇（TC）＋10%猪油＋7.5%蛋黄粉＋81.5%普通饲料）;治疗组：在给予高脂饲料喂养的同时加用阿托伐他汀钙5mg.kg-1.d-1。实验共进行12周。实验结束时,处死动物取血测定TC、三酰甘油（TG）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDL-C）、血清一氧化氮（NO）和内皮素-1（ET-1）水平,取主动脉进行病理学观察。结果与空白对照组比较,模型组、治疗组兔的血清TC、TG、LDL-C、ET-1水平显著升高（P〈0.01）,而HDL-C、NO水平显著降低（P〈0.01）;模型组兔血管内膜明显增厚,形成动脉粥样硬化斑块,内含大量泡沫细胞,具有典型的动脉粥样硬化表现;与模型组相比,治疗组兔血清TC、TG、LDL-C、ET-1水平显著降低（P〈0.01）,而HDL-C、NO水平显著升高（P〈0.01）;兔血管内膜轻度增厚,有较少量泡沫细胞,动脉粥样硬化病变程度较模型组明显减轻。结论阿托伐他汀钙除具有强大的降脂作用外,还通过升高NO水平降低ET-1水平,改善血管内皮功能发挥抗动脉粥样硬化作用。     

人工麝香对大鼠高脂血症影响的实验研究

目的：观察人工麝香对大鼠高脂血症的影响。方法：SD大鼠,随机分为6组,每组10只。空白组正常饲养,其余5组高脂乳剂灌胃同时给药,连续4周。末次给药后1 h,取血离心制备血清,检测TC、TG、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）含量,用双抗体夹心ELISA法测定血清C反应蛋白（CRP）、内皮素-1（ET-1）、肿瘤坏死因子α（TNF-α）的变化。结果：与模型组比较,人工麝香低、中、高剂量（3、6、12 mg/kg）能明显降低TC、TG的升高（P〈0.05）,对LDL-C的升高有一定的降低作用;人工麝香高剂量能明显降低大鼠血清CRP、ET-1、TNF-α（P〈0.05）。结论：人工麝香对大鼠高脂血症具有明显的调节作用。     

油茶皂苷对高脂血症大鼠血脂的影响

目的探讨油茶皂苷SQS用于高脂血症大鼠的降脂作用。方法采用高脂血症大鼠为研究对象,随机分成6组,分为SQS高、中、低剂量实验组、阳性组、阴性高脂模型组和正常组。末次给药1h后断头取血测定TC、TG、LDL-C及HDL-C含量的变化。结果 SQS 3个剂量组与高脂组比较,TC、TG水平均降低（P〈0.05）,而且随剂量增加而降低TC、TG的作用增强,存在明显的量效关系,降低LDL-C水平（P〈0.05）,增高HDL-C水平（P〈0.05）,明显降低高脂血症大鼠血清的TC/HDL比值。结论油茶皂甙能调节高脂血症动物模型血清脂质,可能具有防止动脉粥样硬化的作用,而且毒副作用较小,具有较好的应用前景。     

一种新的高盐致高血压动物模型及其血管重构改变

目的 :研究单纯高盐饲养对正常Wistar大鼠血压及血管结构的影响 ,并建立一种新的高盐致高血压大鼠模型。方法 :雄性Wistar大鼠 ,于哺乳期 (3周龄 )后 ,随机分成 2组 :正常盐 (含 0 .5 %NaCl饲料 )饲养组和高盐 (含 4 %NaCl饲料 )饲养组 ,持续饲养 18周 ,定期测量鼠尾收缩压和体重。实验结束时 ,经右颈动脉插管测平均动脉压。在血管灌注固定后 ,胸主动脉、肾动脉及肠系膜小动脉作形态学测量。结果 :高盐与正常盐饲养组间 ,大鼠体重在分组前后均无区别。高盐饲料饲养后第 8周起 ,高盐组鼠尾血压明显高于正常盐饲养组 ,并持续至实验结束 ,且随时间增加 ,血压增高更明显。颈动脉平均压测量结果进一步证实高盐饲养组血压明显高于正常盐饲养组。检测大、中、小血管的血管中层厚度、中层厚度与管腔比率、血管壁横截面积 ,高盐饲养组均明显较正常盐饲养组增大 ,但两组间血管腔径无区别。高盐饲养组左心室重量指数明显高于正常盐饲养组。结论 :长期高盐饲养可致正常Wistar大鼠血压升高。故单纯高盐饮食在正常生理状态下的Wistar大鼠可形成一种新的高血压模型 ,且高血压形成同时伴随有循环系统心脏和血管的重构现象。该高血压模型可能较盐敏感性高血压模型更接近人类的高盐摄入与高血压病的实际情况。     

培哚普利对长期高盐饮食Wistar大鼠血压和左室重构的影响

目的 观察长期高盐饮食对Wistar大鼠血压及左心室重构的影响,探讨左心室重构的机制及培哚普利对左心室重构的干预作用.方法 8周龄、SPF级健康雄性Wistar大鼠42只随机分为三组.对照组(n=14,给予0.5% NaCl的颗粒饲料)、高盐模型组(n=14,给予8% NaCl的颗粒饲料)、干预组(n=14,给予8% NaCl的颗粒饲料+培哚普利2~8 mg·kg-1·d-1.每两周测尾动脉压1次,共喂养24周.24周末处死大鼠,HE、Masson染色观察心肌组织形态及胶原纤维化情况.酶联免疫吸附试验(ELISA)测定血清高敏C反应蛋白(hsCRP)浓度,提取左心室心肌组织RNA及蛋白质,实时荧光定量PCR法及Western blot测定左心室心肌组织NF-κB mRNA及蛋白表达水平.结果 与对照组比较,高盐模型组血压、左心室质量指数(LVMI)、心肌纤维化面积(MIFI)、hsCRP、左心室NF-κB mRNA及蛋白表达水平明显升高(P<0.01);与高盐模型组相比,干预组血压、LVMI、MIFI、hsCRP、左心室NF-κB mRNA及蛋白表达水平均降低(P<0.01).结论 长期高盐饮食可导致Wistar大鼠血压升高和左心室重构,炎症反应可能参与高盐诱导的左心室重构;培哚普利可能部分通过抑制炎症反应而减轻高盐诱导的左心室重构.     

Enhanced angiotensin-converting enzyme activity and systemic reactivity to angiotensin II in normotensive rats exposed to a high-sodium diet

A high salt diet is associated with reduced activity of the renin–angiotensin–aldosterone system (RAAS). However, normotensive rats exposed to high sodium do not show changes in systemic arterial pressure. We hypothesized that, despite the reduced circulating amounts of angiotensin II induced by a high salt diet, the cardiovascular system's reactivity to angiotensin II is increased in vivo, contributing to maintain arterial pressure at normal levels. Male Wistar rats received chow containing 0.27% (control), 2%, 4%, or 8% NaCl for six weeks. The high-sodium diet did not lead to changes in arterial pressure, although plasma levels of angiotensin II and aldosterone were reduced in the 4% and 8% NaCl groups. The 4% and 8% NaCl groups showed enhanced pressor responses to angiotensin I and II, accompanied by unchanged and increased angiotensin-converting enzyme activity, respectively. The 4% NaCl group showed increased expression of angiotensin II type 1 receptors and reduced expression of angiotensin II type 2 receptors in the aorta. In addition, the hypotensive effect of losartan was reduced in both 4% and 8% NaCl groups. In conclusion these results explain, at least in part, why the systemic arterial pressure is maintained at normal levels in non-salt sensitive and healthy rats exposed to a high salt diet, when the functionality of RAAS appears to be blunted, as well as suggest that angiotensin II has a crucial role in the vascular dysfunction associated with high salt intake, even in the absence of hypertension.     

Early urinary biomarkers of renal tubular damage by a high‐salt intake independent of blood pressure in normotensive rats

Dietary sodium intake has been associated with progression to chronic kidney disease (CKD) as well as hypertension. A high‐salt intake causes renal damage independent of hypertension. Because traditional renal biomarkers are insensitive, it is difficult to detect renal injury induced by a high‐salt intake, especially in normotensive patients. Here, we investigated whether newly developed renal biomarkers could be detected earlier than traditional biomarkers under a high‐salt intake, in normotensive rats. Male Wistar Kyoto rats (WKY) received a regular (0.8% NaCl) or salt‐loaded (2, 4, and 8% NaCl) diet from 9 to 17 weeks of age. A urine sample was obtained once a week and urinary vanin‐1, neutrophil gelatinase‐associated lipocalin (NGAL), and kidney injury molecule‐1 (Kim‐1) were measured. At 17 weeks of age, 8% salt‐loaded WKY showed histopathological renal tubular damage and elevated Rac1 activity in renal tissues. Although there was no significant increase in serum creatinine, urinary albumin, N‐acetyl‐β‐D‐glucosaminidase (NAG), or Kim‐1 during the study period among the groups, urinary vanin‐1 and NGAL significantly increased in 8% salt‐loaded WKY from 10 to 17 weeks of age. These results suggest that urinary vanin‐1 and NGAL, which might be induced by salt per se, are potentially earlier biomarkers for renal tubular damage in normotensive rats under a high‐salt intake.     

Arterial structural changes in hypertensive rats induced by capsaicin and salt loading

1. The objective of the present study was to investigate the arterial structural changes in a salt-sensitive hypertensive rat model induced by treatment with capsaicin. 2. Newborn male Wistar rats were treated with 50 mg/kg capsaicin subcutaneously for 2 days. Control rats were treated with vehicle solution (5% ethanol and 5% Tween 80 in saline). After weaning at 3 weeks, rats were divided into four groups: (i) control with a normal salt diet (0.5% NaCl; CON + NS); (ii) control with a high-salt diet (4% NaCl; CON + HS); (iii) capsaicin plus normal salt diet (CAP + NS); and (iv) capsaicin plus a high-salt diet (CAP + HS). Treatment with different salt diets was initiated at 3 weeks of age and lasted for 18 weeks. Tail-cuff systolic blood pressure (BP) and bodyweight were examined. At the end of the treatment period, blood vessels were prepared by perfusion fixation. Heart weight and vascular dimensions were measured in the thoracic (artery) aorta, renal artery and mesenteric artery. 3. Two weeks after the initiation of the salt diet treatment, BP became significantly higher in the CAP + HS group than in any of the other groups and this difference was maintained until the end of the treatment period. 4. Beginning at 8 weeks after the initiation of the salt diet treatment (11 weeks of age), BP became higher in the CON + HS group than in the CON + NS and CAP + NS groups. Blood pressure was not significantly different between the CON + NS and CAP + NS groups. 5. Media thickness, media thickness to lumen ratio and cross-sectional area of the aorta, renal artery and mesenteric artery were significantly increased in the CAP + HS group compared with the other groups. Heart weight was also increased in the CAP + HS and CON + HS groups compared with the other groups. 6. Similar structural changes in the blood vessels and heart were also found in the CON + HS group compared with the CON + NS group. Lumen diameter was not altered by the treatments in any of the arteries studied. 7. We conclude that treatment with capsaicin increased the sensitivity of the BP of these rats to salt and this increase in BP is correlated with hypertrophy of the arteries (vascular remodelling) with no change in lumen size. A long-term high-sodium load induced hypertension in normal Wistar rats, which was accompanied by cardiovascular hypertrophy.     

Acute arrhythmogenesis after myocardial infarction in normotensive rats: influence of high salt intake

A high salt diet is a known risk factor for cardiovascular diseases that leads to cardiac hypertrophy and creates a substrate for arrhythmias and sudden death. However, acute arrhythmogenesis after infarction has not been studied. Male Wistar rats (21 days) received drinking water (MI) or 1% NaCl solution (MI-Salt-C) for 4 weeks. Water was given to another group for 4 weeks, and on the day before surgery, animals received a 1% NaCl solution (MI-Salt-A). Non-invasive systolic blood pressure (SBP) was obtained before surgery. Myocardial infarction (MI) was produced by permanent occlusion of the left coronary artery. Electrocardiogram was monitored during the first 30 min post-occlusion to evaluate arrhythmias. Although SBP was not altered by salt intake (SHAM: 114±2, MI: 112±2, MI-Salt-C: 115±2, MI-Salt-A: 116±4 mm Hg), ventricular hypertrophy was observed in the animals receiving chronic salt diet (SHAM: 0.22±0.008, MI: 0.23±0.007, MI-Salt-C: 0.28±0.01; MI-Salt-A: 0.23±0.01 g/cm; P<0.05). Ventricular premature beats increased in both salt-loaded groups compared to MI group (MI: 805±81, MI-Salt-C: 1145±98; MI-Salt-A: 1023±77; P<0.05). Atrioventricular blockade was only observed in animals subjected to high salt intake (MI-Salt-C: 38.9%; MI-Salt-A: 42.1%). High salt intake was associated with increased post-infarct arrhythmias; however, this effect was unrelated to ventricular hypertrophy.     

SODIUM INTAKE MODULATES RENAL VASCULAR REACTIVITY TO ENDOTHELIN-1 IN DAHL RATS

1. The systemic and renal haemodynamic responses to endothelin-1 (ET1) were evaluated and compared to Angiotensin II (AII) in anaesthetized Dahl salt-sensitive (DS) and salt-resistant (DR) rats on either low (0.1% NaCl in diet) or high (8% NaCl in diet) salt intake. 2. Baseline mean arterial pressure on low salt diet was similar in both strains, while on high salt diet it was 73 +/- 4 mmHg in DR rats and 119 +/- 8 mmHg in DS rats (P less than 0.05). Baseline renal blood flow (RBF) and renal vascular resistance (RVR) were similar in all groups. 3. AII in bolus injection induced a short, dose-dependent increase in blood pressure and renal vascular resistance and a fall in renal blood flow. The maximal pressure increase was significantly greater in DS rats on high salt diet than that in each of the other groups (P less than 0.05). The fall in renal blood flow and the increase in renal vascular resistance were attenuated in both strains on low salt diet. 4. ET1 induced an initial decrease followed by a prolonged increase in blood pressure; both phases were similar in all groups. However, renal vascular reactivity to ET1 was markedly modulated by salt intake. On low salt diet, following a bolus injection of ET1 (1 nmol/kg), RBF decreased by 34% in DR and by 20% in DS rats, while on high salt diet RBF decreased by 76% in DR and by 80% in DS rats (P less than 0.05 high vs low salt).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium regulation of alpha 2-adrenoreceptors in Dahl rats. Effect of feeding a low or high salt diet

Sodium regulation of alpha 2-adrenoreceptors was investigated in inbred salt-sensitive (S) and inbred salt-resistant (R) rats fed a high or low salt diet. The systolic blood pressure was higher in S rats than in R rats, and this difference was obviously greater on a high salt diet. In rats fed a low or high salt diet, S rats had higher alpha 2-adrenoreceptor density in the kidneys compared with R rats as measured by [3H]yohimbine binding and Scatchard analysis. The affinity of the receptors in the kidney for the antagonist, yohimbine, was nearly the same in these two strains either on a low or high salt diet. In the brain, the affinities or the numbers of receptors were not significantly different whether these two strains were fed a low or high salt diet. Inclusion of NaCl up to 80 mM in the assay medium did not alter the in vitro binding of [3H]yohimbine in the kidney or brain. On the other hand, inclusion of NaCl in the assay medium reduced the ability of epinephrine in competing with [3H]yohimbine for the receptor sites in the kidney and in the brain, and this effect of NaCl was the same in a given tissue between S and R rats, whether they were fed a low or high salt diet. These results suggest that: (1) in the kidneys, the receptor density and not the receptor affinity was different between S and R strains whether they were fed a low or high salt diet; (2) in the brain, the receptor density and affinity were the same between S and R rats regardless of the diet (low or high salt), indicating that the sodium salt diet modulates the peripheral but not the central alpha 2-adrenoreceptors; and this modulatory effect was observed only in S rats; (3) Na+ was able to reduce the affinity of the agonist (epinephrine) for the receptors in both S and R rats, and this effect of Na+ on central and peripheral alpha 2-adrenoreceptors was similar in prehypertensive rats and rats with salt-induced hypertension; and (4) the resistance of R rats to salt-induced hypertension was not due to the absence of Na+ binding component involved in the regulation of alpha 2-adrenoreceptor-adenylate cyclase complex.     

强化胰岛素治疗对糖尿病大鼠胰岛β细胞凋亡蛋白bcl-2和bax的影响

目的观察强化胰岛素治疗对糖尿病大鼠胰岛β细胞凋亡相关蛋白bcl-2和bax的影响。方法将36只Wistar大鼠随机分为对照组和高脂组,对照组给予基础饲料喂养,高脂组给予脂肪乳灌胃＋基础饲料喂养10d,然后给高脂组大鼠腹腔注射链脲佐菌素,3d后再将高脂组大鼠随机分为2个亚组,即糖尿病对照组和糖尿病治疗组,疗程4周。在脂肪乳灌胃第10天、注射STZ第3天和治疗4周末测大鼠各项指标;实验结束时用免疫组化法测大鼠胰岛β细胞凋亡相关蛋白bcl-2和bax的表达。结果大鼠在强化胰岛素治疗4周末,与糖尿病对照组相比,糖尿病治疗组的bcl-2蛋白表达升高,bax蛋白表达降低,两组差异均有统计学意义（均P〈0．05）。结论强化胰岛素治疗可增强2型糖尿病大鼠胰岛β细胞bcl-2蛋白表达,降低bax蛋白表达,减轻2型糖尿病大鼠胰岛β细胞凋亡。     

高脂高盐饮食对未成年鼠生长及代谢的影响

目的 观察高脂高盐饮食对未成年鼠生长发育、胰岛素敏感性及相关代谢指标的影响. 方法 40只体质量50g左右SD鼠（生长至3周末,刚断乳）随机分为三组：普通饮食组（NC组）12只、高脂组（FC组）14只、高脂高盐组（FSC组）14只,分别给予普通食物、高脂食物、高脂＋高盐食物喂养4周（鼠生长至7周末）,观察三组大鼠体质量、血压及内脏脂肪重量、血脂等,行口服葡萄糖耐量试验及胰岛素释放试验评价血糖及胰岛细胞功能. 结果 FSC组鼠体质量、内脏脂肪、血糖及胰岛素水平均较NC组明显增加,血脂紊乱加重并表现出显著的胰岛素抵抗,差异有统计学意义（均P＜0.05）. 结论 高脂高盐饮食可诱导未成年鼠腹型肥胖、高血压、血脂异常及糖耐量异常.