运动性和高血压性肥大心脏心肌肌膜乳酸转运特征比较

目的：探讨运动性和高血压性心肌肥大重塑时细胞表型代谢变化特征。方法：采用Ｌ－１４Ｃ乳酸盐测定运动Ｗｉｓｔａｒ大鼠,自发性高血压大鼠（ｓｐｏｎｔａｎｅｏｕｓｌｙ ｈｙｐｅｒｅｎｓｉｖｅ ｒａｔｓ,ＳＨＲ）、运动ＳＨＲ和对照Ｗｉｓｔａｒ Ｋｙｏｔｏ（ＷＫＹ）大鼠的心肌肌膜囊泡（ｓａｒｃｏｌｅｍｍａｌ ｖｅｓｉｃｌｅ,ＳＬＶ）单羧酸盐乳酸转运载体变化。结果：Ｗｉｓｔａｒ大鼠经每日２ｈ的１０周游泳运动后,     

外周损伤引起成年大鼠体感皮层的功能重组

为了了解外周神经损伤对体感皮层分域组构的影响,在成年大鼠上观察了切断坐骨神经(SC)前、即刻和切断后数周内后爪皮层代表区的改变。在盐酸氯胺酮麻醉下,用微电极记录后爪皮肤轻触刺激在对侧体感皮层工区诱发的多单位反应,得出后爪的皮层代表区图。在16例中,8例大鼠观察了切断SC的即时效应。结果表明,不但SC代表区丧失皮肤反应性,原隐神经(SA)代表区的皮肤反应性也明显下降或消失,同时神经元自发活动也明显减弱。另8例大鼠在切断后数周内做了1～3次重复测定。在最初几天,原SA代表区范围内多数记录点的皮肤反应性仍未恢复,但在原SC代表区内,一些记录点转而对SA皮肤轻触刺激起反应。在随后数周内SA代表区进行性地扩张,占领了大部分原SC代表区。这一结果说明成年大鼠外周神经损伤可导致体感皮层发生显著的重组改变。     

自发性高血压大鼠中枢5－HT_（1A）受体的特性

本文用放射性配基［３Ｈ］８－ＯＨ－ＤＰＡＴ的结合实验显示,自发性高血大鼠（ＳＨＲ）海马、下丘脑及低位脑干的５－ＨＴ１Ａ受体结合位点数较正常Ｗｉｓｔａｒ大鼠为多,其中以海马最为显著;脑干的５－ＨＴ１Ａ受体虽较正常Ｗｉｓｔａｒ大鼠多,但不太明显。ＳＨＲ下丘脑中５－ＨＴ１Ａ受体除结合位点较正常Ｗｉｓｔａｒ鼠多外,亲和力也有增大。以上结果表明,ＳＨＲ与正常Ｗｉｓｔａｒ大鼠之间各脑区中５－ＨＴ１Ａ受体的差别可能与高血压病的发生有关。     

自发性高血压大鼠中枢5—HT1A受体的特性

本文用放射性配基［＾３Ｈ］８－ＯＨ－ＤＰＡＴ的结合实验显示,自发性高血大鼠海马,下丘脑及低位脑干的５－ＨＴ１Ａ受体结合位点数较正常Ｗｉｓｔａｒ大鼠为多,其中以海马最为显著,脑干的５－ＨＴ１Ａ受体虽较正常Ｗｉｓｔａｒ大鼠多,但不太明显。ＳＨＲ下捕脑中５－ＨＴ１Ａ受体除结合位点较正常Ｗｉｓｔａｒ鼠多外,亲和力也有增大。以上结果表明,ＳＨＲ与正常Ｗｉｓｔａｒ大鼠之间各脑区中５－ＨＴ１Ａ受体的差别可能与高     

SHRsp内脏阻力血管平滑肌钙通道动力学特征

用膜片箝全细胞钡电流方式比较成年雄性卒中易感型自发性高血压大鼠（ＳＨＲｓｐ）及正常大鼠（Ｗｉｓｔａｒ）肠系膜动脉Ａ４－Ａ５分支阻力血管平滑肌电压依赖性钙通道的动力学特性。结果发现：１）两种大鼠该段均存在有Ｌ型与Ｔ型钙通道。２）峰值电流（ｐｅａｋＩＢａ２＋）幅度和密度ＳＨＲｓｐ均大于Ｗｉｓｔａｒ大鼠。３）通道激活时间常数（τａ）ＳＨＲｓｐ小于Ｗｉｓｔａｒ大鼠,失活时间常数（τｉ）于箝制电压（ＨＰ）＝－４０ｍＶ时,两种大鼠无区别,ＨＰ＝－８０ｍＶ时,ＳＨＲｓｐ显著大于Ｗｉｓｔａｒ。４）和Ｗｉｓｔａｒ大鼠相比较,ＳＨＲｓｐ的稳态激活曲线（Ｄ∞）与稳态失活曲线（Ｆ∞）,均呈现左移。ＳＨＲｓｐ肠系膜动脉阻力血管平滑肌电压依赖性钙通道的如此特征更有利于胞外钙离子进入胞内。而关于内脏阻力血管的实验结果迄今鲜有报道。     

坐骨神经阻滞引起成年大鼠初级体感皮层代表区的快速改变

为了探讨成年大鼠坐骨神经（ＳＣＩ）去传入后初级体感皮层是否发生快速重组,在氯胺酮麻醉下,利用微电极测定后爪代表区,然后用普鲁卡因阻滞对侧ＳＣＩ。结果表明,阻滞后１ｈ、４ｈ和８ｈ,隐神经代表区（ＳＡＲ）比对照分别增大３２．５％（ｎ＝７）、９３．０％（ｎ＝１７）和１００％（ｎ＝４）。此外,在原ＳＡＲ和新生ＳＡＲ记录的平均多单位诱发反应的峰潜伏期,后者比前者延长４．３ｍｓ。作者推测在快速出现的皮层重组机制中,皮层－皮层多突触通路的去抑制可能起重要作用     

大鼠力竭运动中丘脑底核和皮层神经元电活动的变化

目的：探讨力竭过程中丘脑底核（SIN）对皮层兴奋性的调控作用。方法：采用皮层脑电（ECoG）及局部场电（LFPs）同步记录技术,对一次性力竭运动过程中大鼠SIN、皮层神经元电活动变化规律进行同步、动态观察。结果：运动开始阶段大鼠能够自主跟随跑台进行运动,运动持续约45min时（45±11．5min）,自我驱动下的运动能力明显降低;此时STN兴奋性显著增加（P〈0．01）,皮层兴奋性显著下降（P〈0．01）。如果给予大鼠一定的外部刺激后仍可继续运动一段时间直至力竭;力竭即刻皮层兴奋性降到最低值（P〈0．01）,而SIN兴奋性变化不显著（P〉0．05）。结论：大鼠在力竭运动过程中,皮层运动区神经元电活动随着运动疲劳的发生呈现广泛的抑制现象,而SIN神经元电活动在疲劳初期则明显增强,SIN通过负诱导作用参与了运动性中枢疲劳的调控,且STN神经元兴奋性增强可能是皮层实现保护性抑制机制的重要途径之一。     

坐有神经阻滞引起成年大鼠初级体感皮层代表区的快速改变

为了探讨成年大鼠坐骨神经去传入后初级体感皮层是否发生快速重组,在氯胺酮麻醉下,利用微电极测定后爪代表区,然后用普鲁卡因阻滞对侧ＳＣＩ。结果表明,阻滞后１ｈ,４ｈ和８ｈ,隐神经代表区比对照分别增大３２．５％,９３．０５和１００％。此上,在原ＳＡＲ和新生ＳＡＲ记录的平均多单位诱发反应的峰潜伏期,后者比前者延长４．３ｍｓ。作者推测在快速出现的皮层重组机制中,皮层－皮层多突触通路的去抑制可能起重要作用。     

胡须信息在大鼠双侧初级体感皮层间的传递路径

大鼠的初级体感皮层(primary somatosensory cortex,SⅠ)虽然只接受来自对侧胡须的上行输入,但仍可以被同侧胡须刺激所激活.解剖学研究发现,在两侧SⅠ皮层之间有两条传递胡须信息胼胝体通路:一条是类颗粒区(perigranular zone,PGZ)通路;另一条是异颗粒区(dysgranular zone,DZ)通路.然而,哪一条通路在传递胡须刺激信息的过程中起主要作用还不清楚.本研究使用电压敏感染料(voltage-sensitive dye,VSD)成像技术来观察胡须刺激时整个SⅠ的神经元群体活动的空间分布和时间特性.实验发现,对侧胡须刺激首先激活barrel(颗粒区,granular zone,GZ),然后以兴奋波的形式传播到胡须感觉区(sub-barrel field cortex,BFC)外侧的DZ.而与首先激活BFC的对侧胡须刺激不同,同侧胡须刺激首先激活SⅠ的DZ.所激发的皮层兴奋以波的形式传播并扩散至BFC.失活另一侧皮层可以抑制这种同侧反应.电刺激另一侧半球皮层与刺激同侧胡须类似,也首先激活成像侧DZ.我们的实验结果显示,胡须刺激激活对侧SⅠ,在经过胼胝体传导后,另一侧半球的DZ(同侧于被刺激的胡须)被激活.连接双侧皮层DZ区的胼胝体连接在SⅠ对同侧胡须刺激的反应中起了主导作用.     

成年大鼠体感皮层局限损伤引起的代表区重组

本文目的是探讨在成年大鼠初级体感皮层（ＳＩ）内进行局限损毁能否引起损毁区周围的代表区重组。在氯胺酮麻醉下用微电极技术测定隐神经代表区（ＳＡＲ）和坐骨神经代表区（ＳＣＲ）,然后用铂电极对ＳＡＲ进行选择性电解损毁。三至四周后进行重复测定。结果表明,在１４例所观察的大鼠中,９例在原损毁区以外发现新生的ＳＡＲ,其面积为０．２０±０．０８ｍｍ２。这表明成年大鼠ＳＩ神经元在中枢损伤后具有一定的重组能力。     

MIJ和HFJ近交系大鼠心电图表现

目的 测定近交系MIJ、HFJ大鼠心电图,并与Wistar大鼠比较分析,观察MIJ和HFJ大鼠心电图表现.方法 大鼠麻醉后,仰卧位固定于大鼠固定板上,用短针电极刺入皮下2～3 mm位置,麻醉5 min后,用福田青岛FX-102B心电图机做心电图,并对心电图进行分析.结果 三种大鼠均为窦性心律,心律齐整,雄性HFJ、MIJ心率均高于同性别Wistar.HFJ和MIJ品系、性别间心率差异均无显著性.HFJ和MIJ心电轴与Wistar相同,主要在0°～90°间.三种大鼠的P波方向及QRS波群基本相同,但各波振幅和各波时限,在不同品系和性别之间存在较明显的差异.结论 近交系MIJ和HFJ大鼠各有其独特的心电图表现.     

非酒精性脂肪性肝炎大鼠肝脏血管内皮生长因子表达的意义

目的探讨血管内皮生长因子（VEGF）在非酒精性脂肪性肝炎（NASH）大鼠肝脏的表达及意义。方法 20只大鼠随机分为对照组（10只）和模型组（10只）,分别给予标准饮食和高脂饮食16周,进行肝脏病理学检查和血生化指标分析;采用超高频小动物超声诊断仪检测肝脏及其血流动力学改变,利用分子生物学方法检测肝组织VEGF表达水平。结果模型组大鼠ALT、AST和TC增高（P〈0.05）。肝组织病理表现为大小泡混合性脂肪变性,伴肝细胞气球样变性、炎性细胞浸润、碎片状坏死和少量纤维组织增生。超声结果为肝脏增大,肝缘圆钝,实质回声细密增强,后方组织明显衰减,与脂肪肝病理结果一致;门静脉内径增大,肝静脉内径减小（p〈0.05）,静脉流速降低。肝组织VEGF蛋白和mRNA表达明显增加（P〈0.05）,VEGF蛋白主要表达在肝细胞和窦内皮细胞。结论 NASH肝脏VEGF蛋白和mRNA表达明显增加,VEGF可能参与NASH肝脏血流动力学的异常。     

大鼠脑中5—羟色胺受体的检定及其在衰老时的变化

采用放射性配基结合分析法,对大鼠大脑皮质的5-HT受体作了检定,并观察了老年大鼠(36月龄)大脑皮质中该受体的变化。证实大鼠大脑皮质存在着丰富的、高亲和力和单一结合位点的5-HT受体。老年大鼠大脑皮质中5-HT受体的数目较成年大鼠(3月龄)明显减少,但亲和力无改变。应用荧光分光技术测定了成年和老年大鼠脑干和大脑皮质5-HT含量,证实老年大鼠上述两个脑区的5-HT含量均有降低。本研究的结果提示,老年大鼠中枢5-HT系统的功能减低,这一变化可能与老年期的一些表现如睡眠障碍、体温低、记忆力减退和易患精神疾病等有关。     

A comparison of sciatic nerve neuropathy in diabetic and aged rats

We compared the development of sciatic nerve neuropathy in young diabetic rats with that in non-diabetic aged rats. Diabetes was induced in six-month old rats by injection with alloxan and was moderately controlled by single daily injections of insulin. Blood insulin levels in diabetic rats were significantly reduced compared to the aged animals, and glucose was significantly higher in diabetic rats. Sciatic nerve conduction velocities were measured monthly. Both motor and sensory conduction velocities decreased in the diabetic rats to a level that was similar to those in 36-month old rats. The decreases in conduction velocities in the diabetic rats were most dramatic during months 6 through 12 of diabetes. After 6 and 12 months of diabetes, sciatic nerves were examined by electron microscopy and compared to nerves from 24- and 36-month old rats respectively. Ultrastructural changes in the sciatic nerves of diabetic rats at 6 months included disruptions of myelin and dense axoplasm. In comparison, the 24-month old rats only had distorted contours of the nerve fibres. After 12 months of diabetes, the axoplasm had large spaces and the myelin was thickened and deformed. The axoplasm of 36-month old rats was normal in appearance; however the myelin sheath was thickened and split into layers. The Schwann cells were vacuolated and irregular in shape. These observations indicate that diabetes results in the early onset of age-like changes in the sciatic nerve. It suggests that the control of hyperglycemia in humans may preserve sciatic nerve structure and function.     

Transplacental transport of alpha 2-macroglobulin (alpha 2M) and induction of alpha 2M in maternal and neonatal rats with acute inflammation.

The aims of this study were to investigate transplacental transport of alpha 2-macroglobulin (alpha 2M) in rats in rats and to examine the degree of alpha 2M induction in maternal and neonatal rats with acute inflammation. Serum was collected from healthy pregnant CD (IGS) rats, neonates of the pregnant rats and their cord blood. Additional serum samples were obtained from pregnant rats inoculated with an inflammatory agent, turpentine oil, their neonates and cord blood, and neonates inoculated with turpentine oil. The serum levels of alpha 2M were measured by means of an enzyme-linked immunosorbent assay. The average serum levels of alpha 2M in healthy neonates and cord blood were about 380 micrograms/ml. Serum a2M level in neonates inoculated with turpentine oil averaged about 580 micrograms/ml. Serum alpha 2M levels in maternal rats inoculated with turpentine oil, neonates from those rats and their cord blood were elevated, the values being 2,000 micrograms/ml or higher. It was demonstrated that induction of alpha 2M in neonatal rats was lower than in maternal rats when inoculated with turpentine oil. These results suggest that alpha 2M is transplacentally transported from maternal rats to fetal ones.     

Effect of exogenous melatonin on neuroendocrine-reproductive function of middle-aged female rats

The possible role of melatonin in the regulation of the reproductive system of female rats during ageing was investigated in middle-aged female rats showing irregular duration of the oestrous cycle (n = 30). Blood samples were obtained by jugular venepuncture during the oestrous cycle in control rats. After this experiment was completed, the female rats were treated with melatonin for 2 months and blood samples were obtained at different stages of the oestrous cycle. Plasma LH, FSH and prolactin concentrations were significantly increased in the afternoon of the day of pro-oestrus after melatonin treatment compared with control rats. Moreover, FSH concentrations too were significantly increased on the morning of pro-oestrus and oestrus in melatonin treated rats compared with control rats. Similarly, oestradiol concentrations were significantly higher on the morning of pro-oestrus in melatonin treated rats compared with controls. Another group of rats showing irregular duration of the oestrous cycle was used to study the possible effect of melatonin treatment on the timing of pro-oestrous surges of LH and FSH. The results showed that LH and FSH peak values occurred at 5 h after melatonin treatment. Pituitary responsiveness to LHRH in a 90 min test was also studied in middle-aged rats showing irregular duration of the oestrous cycle that had been injected for 1 month with either melatonin or saline. Prolactin response was unaffected by exogenous melatonin, but a stimulatory effect of melatonin on LH and FSH pituitary responsiveness to LHRH was observed. The results indicate an improved function of the neuroendocrine-reproductive axis in middle-aged rats after melatonin treatment.     

Cross-linking of DNA in liver and testes of rats fed 1,3-propanediol

1,3-Propanediol (PAD) was fed to rats for 15 weeks, and its effects on hepatic and testicular DNA were studied. The control rats were fed a casein-based diet that contained 10% tocopherol-stripped corn oil with 30 IU of d,l-α-tocopherol acetate/kg; the experimental rats were fed the same diet with 500 ppm of PAD. Homogenates prepared from the livers of each group of rats converted 1,3-propanediol to malondialdehyde (MDA) with equal efficacy, but homogenates of testes did not catalyze this conversion. After 10–15 weeks of feeding the diets, the hepatic DNA of the rats fed PAD had less template activity, more bound tryptophan and more DNA-protein and interstrand DNA cross-links than that of the control rats. As measured by template activity and bound tryptophan, testicular DNA of the experimental rats was not different from that of the control rats; however, there was slightly more cross-linking in the testicular DNA of experimental rats than in that of control rats. Testes of the experimental rats contained more lipid-soluble fluorophores than did those of the control rats. The results are consistent with the conclusion that PAD was converted to MDA in vivo and that MDA is the reactive species that caused the observed biological damage.     

Renal production of thromboxane and prostaglandins in a rat model of type 2 diabetes

In an investigation of the involvement of prostanoids in the pathogenesis of nephropathy in type 2 diabetes, we repeatedly measured the urinary excretion of prostanoids in both diabetic and healthy rats as the rats aged. Seven rats of the Otsuka Long-Evans Tokushima Fatty strain were used as rats with a model of type 2 diabetes and seven rats of the Long-Evans Tokushima Otsuka strain were used as rats without diabetes. Thromboxane (TX) B2 and 6-keto-prostaglandin (PG) F1alpha, the amounts of which reflect renal production of TXA2 and PGI2, respectively, and PGE2 in urine collected in metabolic cages were assayed when rats were 14, 30, 46, and 54 weeks old. Plasma glucose and urinary protein excretion also were measured periodically. The mean plasma glucose concentration of the diabetic rats was higher than that of the healthy rats throughout the study. At 30 weeks and later, urinary protein excretion by the diabetic rats was greater than that of the healthy rats, and it increased with age. Urinary excretion of TXB2 by the diabetic rats was higher than that of the healthy rats at 14 weeks (52.4+/-23.5 vs. 27.0+/-2.6 ng/day; mean +/- SD, P = .015) and the difference continued to the end of the experiment. Urinary excretion of 6-keto-PGF1alpha by the diabetic rats was high at 14 weeks (52.3+/-12.8 vs. 26.9+/-4.6 ng/day; mean +/- SD, P<.001) but decreased with age and was the same as that of the healthy rats at 54 weeks. The urinary excretion of PGE2 by the two groups of rats was not significantly different. These results suggest that altered renal production of TXA2 and PGI2 is involved in the pathogenesis of diabetic nephropathy in rats with type 2 diabetes.     

感觉神经损伤性盐敏感性高血压大鼠心、肾ACE和ACE2的表达

目的研究肾素-血管紧张素系统（RAS）基因血管紧张素转换酶（ACE）和血管紧张素转换酶2（ACE2）在感觉神经损伤性盐敏感性高血压大鼠心肌和肾脏中的表达情况,探讨ACE、ACE2在盐敏感性高血压发生发展中的作用。方法用乳鼠皮下注射辣椒辣素法建立模型。哺乳期后,大鼠被随机分成4组：对照＋正常盐饮食组（CON-NS）、对照＋高盐饮食组（CON-HS）、辣椒辣素＋正常盐饮食组（CAP-NS）、辣椒辣素＋高盐饮食组（CAP-HS）。四组大鼠分别接受4周不同的处理。至7周龄（分组饲养后第4周）处死大鼠,免疫组化检测大鼠心肌和肾脏ACE和ACE2蛋白的表达,反转录-聚合酶链式反应（RT-PCR）检测大鼠心肌和肾脏ACE和ACE2mRNA的表达。结果①至7周龄（分组饲养后第4周）各组动物体重差异无显著性（P〉0.05）。②各组动物在分组时（0周）鼠尾收缩压差异无显著性（P=0.583）,至7周龄（分组饲养后第4周）,CAP-HS组鼠尾收缩压明显高于其它三组（P〈0.01）。③心肌和肾脏ACE蛋白表达均升高。心肌组织,CAP-HS组与CON-NS比较,P〈0.01,与CON-HS和CAP-NS比较,P〈0.05;肾脏组织,CAP-HS组与其它三组比较,P〈0.01。④心肌和肾脏ACE2蛋白表达均降低。心肌和肾脏组织,CAP-HS组与CON-NS和CAP-NS比较,P〈0.01,与CON-HS比较,P〈0.05。⑤心肌和肾脏ACE mRNA表达均升高。心肌组织,CAP-HS组与CON-NS比较,P〈0.01,与CON-HS和CAP-NS比较,P〈0.05;肾脏组织,CAP-HS组与其它三组比较,P〈0.01。⑥心肌和肾脏ACE2 mRNA表达均降低。心肌和肾脏组织,CAP-HS组与CON-NS和CAP-NS比较,P〈0.01,与CON-HS比较,P〈0.05。结论感觉神经损伤性盐敏感性高血压大鼠心、肾ACE表达升高的同时有ACE2表达的降低,ACE和ACE2表达水平的差异可能与盐敏感性高血压的形成有关。     

低分子量肝素对妊高征大鼠肾脏病变的保护作用及机制初步探讨

目的:研究低分子量肝素(LMWH)对妊高征大鼠肾脏损伤的作用及其细胞内信号转导机制.方法:采用注射L-NAME方法制备妊高征动物模型,将妊娠大鼠随机分为正常妊娠组、妊高征组、LMWH治疗组,测定各组平均动脉压、尿蛋白、血肌酐及血尿素氮,观察LMWH对肾脏各指标的影响及肾脏出现的病理学变化;同时采用免疫组化、RT-PCR及Western Blot方法检测ERK1/2在各组的表达变化.结果:LMWH治疗组肾脏组织ERK1/2的蛋白及mRNA表达水平明显低于妊高征组(P＜0.01),而妊高征组肾脏组织ERK的蛋白及mRNA表达水平明显高于正常妊娠组(P＜0.01),ERK1与ERK2在各组大鼠肾脏中的表达无差异;治疗组平均动脉压及尿蛋白明显低于非治疗组(P＜0.05),但仍未达正常妊娠水平;HE染色和PAS染色为治疗组肾小球系膜增生、基底膜增厚较非治疗组明显减轻.ERK蛋白主要分布于肾小球中.结论:LMWH对妊高征大鼠肾脏损伤具有一定的防护作用,其机制可能是通过下调ERK1/2的表达来实现.