缬沙坦和螺内酯对高血压大鼠心肌胰岛素样生长因子-1的作用

目的观察自发性高血压大鼠(SHR)和WKY大鼠心肌胰岛素样生长因子1(IGF1)的浓度和表达及缬沙坦与螺内酯对SHRIGF1的影响,探讨IGF1与心肌肥厚的病理机制。方法将18只6周龄SHR随机分成3组,每组6只。其中2组分别灌胃缬沙坦30mg·kg-1·d-1和螺内酯20mg·kg-1·d-1,SHR阳性对照组给正常饮水,并与雄性同周龄WKY大鼠比较。实验期为13周,放射免疫法检测心肌IGF1的浓度,免疫组化法检测4组大鼠心肌IGF1的表达。结果SHR对照组IGF1表达和浓度均明显高于WKY组(P<0.01),缬沙坦组和螺内酯组的IGF1较SHR对照组下降(P<0.01),而且缬沙坦组比螺内酯组下降的更明显(P<0.05),两组血压、LVMBW均显著低于SHR组(P<0.01)。结论IGF1在肥厚心肌中表达明显增加,而缬沙坦和螺内酯在降压的同时可以抑制IGF1的表达,提示IGF1在心肌肥厚发展中起一定作用。     

长期服用苯那普利的高血压患者左室肥厚逆转与血管紧张素转换酶基因和Chymase基因多态性的相关性研究

目的 探讨长期服用苯那普利的原发性高血压患者左室肥厚逆转与血管紧张素转换酶(ACE)基因插入/缺失(I/D)多态性和Chymase(CMA)基因A/B多态性的关系。方法 收集157例原发性高血压伴左室肥厚患者24个月的随访资料;应用聚合酶链反应和限制性片段长度多态性方法检测ACE基因I/D多态性以及CMA基因A/B多态性;超声心动测量左室舒张末期内径(LVDd)、舒张期室间隔厚度(IVST)及左室后壁厚度(LVPWT)。结果 (1)治疗后血压明显下降而心率改变不明显;(2)能明显逆转LVH;(3)ACE基因型间除左室质量(LVM)下降值及左室质量指数(LVMI)下降值在DD基因型明显大于Ⅱ型和ID型以外,其余各临床指标下降值在ACE基因型间的差异均无统计学意义;(4)CMA基因型间各临床指标下降值的差异均无统计学意义;(5)ACE基因中各基因型与CMA基因中各基因型间不存在交互作用;(6)多元线性逐步回归分析表明,仅ACE基因型与LVMI下降值有关。结论 长期服用苯那普利可以明显降低血压、逆转LVH;其中ACE基因为DD型的患者较其他基因型患者更易于LVH逆转,而CMA基因多态性与LVH逆转不相关;两种基因间不存在交互作用。     

老年高血压患者血压昼夜节律对左室肥厚的影响

【摘要】 目的 研究老年高血压患者的血压昼夜节律变化对左室肥厚的影响。方法 选取我院126例高血压患者,根据心脏彩超提示左室肥厚情况分为肥厚组（n=52例）和非肥厚组（n=74例）。比较两组动态血压指标及血压变异性,进行多因素分析探讨血压变异性对左室肥厚的影响。 结果 高血压肥厚组24h平均收缩压（24hSBP）、白天平均收缩压（dSBP）、夜间平均收缩压（nSBP）、24h收缩压标准差（24hSSD）、24h舒张压标准差（24hDSD）、白天收缩压标准差（dSSD）、夜间收缩压标准差（nSSD）均高于非肥厚组,差异有统计学意义（P＜005）。Logistic回归分析显示,24h SBP 与dSSD、nSSD为左室肥厚的独立危险因素（P＜005）。结论 老年高血压患者的24h SBP 与dSSD、nSSD是影响左室肥厚的独立危险因素,平稳控制血压对防止左室肥厚的发生有一定影响。     

正常与缺血性心肌梗死及心肌肥厚大鼠超声心动图参数变化趋势比较

目的 通过对正常和心血管疾病状态下的大鼠进行连续超声心动图检测,获得客观准确的大鼠心脏超声参数的变化趋势。方法 建立缺血性心肌梗死和压力负荷增高诱导心肌肥厚的大鼠模型,分别在术前、术后1、2和4周进行超声心动图检测,在相同时间点对正常大鼠进行超声心动图检测,并记录超声参数数据。结果 正常大鼠各心脏参数随时间的变化均有所升高,属正常生长状态。心肌梗死大鼠心脏变化以心室重构和功能障碍为主,心室内径和心室容积随时间变化显著增加,射血分数和短轴缩短率显著降低,差异均有统计学意义（P＜0.05）。心肌肥厚大鼠心脏变化以形态改变为主,左室前、后壁厚度随着时间的延长显著增加,收缩末期容积显著下降,射血分数和短轴缩短率代偿性升高,差异均有统计学意义（P＜0.05）。结论 应用超声心动图可获得正常和疾病状态下较为客观准确的大鼠心脏超声数据,为后续应用大鼠实验模型研究各种心血管疾病提供了数据参考。     

纤维鼻咽镜联合切割吸引器对腺样体肥大患儿血清TNF-α、IL-4、LTB4水平的影响

目的探讨纤维鼻咽镜联合切割吸引器对腺样体肥大患儿血清肿瘤坏死因子-α(TNF-α)、白细胞介素-4(IL-4)、白三烯B4(LTB4)水平的影响。方法选取2017年2月至2019年7月在本院进行治疗的腺样体肥大患儿80例,按照随机数字表法分为观察组与对照组,各40例。对照组行传统经口腺样体刮除术,观察组行纤维鼻咽镜联合切割吸引器切除术,比较两组患儿血清TNF-α、IL-4、LTB4水平。结果术后,两组血清TNF-α、IL-4、LTB4水平均降低,且观察组低于对照组,差异有统计学意义(P<0.05);观察组术中出血量少于对照组,鼻腔恢复通气与咽痛持续时间短于对照组,差异有统计学意义(P<0.05);观察组并发症发生率略低于对照组,差异无统计学意义。结论纤维鼻咽镜联合切割吸引器的应用可减少术中出血量,促进恢复,降低腺样体肥大患儿血清TNF-α、IL-4、LTB4水平,且安全性较高。     

APOε2 and education in cognitively normal older subjects with high levels of AD pathology at autopsy: findings from the Nun Study

Asymptomatic Alzheimer''s disease (ASYMAD) subjects are individuals characterized by preserved cognition before death despite substantial AD pathology at autopsy. ASYMAD subjects show comparable levels of AD pathology, i.e. β-amyloid neuritic plaques (Aβ-NP) and tau-neurofibrillary tangles (NFT), to those observed in mild cognitive impairment (MCI) and some definite AD cases. Previous clinicopathologic studies on ASYMAD subjects have shown specific phenomena of hypertrophy in the cell bodies, nuclei, and nucleoli of hippocampal pyramidal neurons and other cerebral areas. Since it is well established that the allele APOε4 is a major genetic risk factor for AD, we examined whether specific alleles of APOE could be associated with the different clinical outcomes between ASYMAD and MCI subjects despite equivalent AD pathology. A total of 523 brains from the Nun Study were screened for this investigation. The results showed higher APOε2 frequency (p < 0.001) in ASYMAD (19.2%) vs. MCI (0%) and vs. AD (4.7%). Furthermore, higher education in ASYMAD vs. MCI and AD (p < 0.05) was found. These novel autopsy-verified findings support the hypothesis of the beneficial effect of APOε2 and education, both which seem to act as contributing factors in delaying or forestalling the clinical manifestations of AD despite consistent levels of AD pathology.     

高血压心肌肥厚患者心脏交感神经分布与勿动蛋白A表达变化的关系

目的探讨高血压心肌肥厚患者心脏交感神经分布与神经元轴突生长抑制因子勿动蛋白A(neurite out-growth inhibitor-A,Nogo-A)的表达变化。方法从我院老年患者尸体标本库中,随机入选男性高血压患者10例,并根据患者去世前1周心脏超声结果分为心肌肥厚组4例和非心肌肥厚组6例。检测超声心动图,并计算左心室重量指数。免疫组织化学分析测定酪氨酸羟化酶(tyrosine hydroxylase,TH)与Nogo-A的表达。结果与非心肌肥厚组比较,心肌肥厚组患者室间隔厚度、左心室后壁厚度、左心室重量指数明显升高(P<0.05);心肌肥厚组患者心肌TH阳性表达明显降低[(6.35±3.85)%υs(22.17±8.19)%,P<0.05],Nogo A表达明显增加[(11.34±7.16)%υs(2.17±4.10)%,P<0.05]。心肌肥厚患者心肌Nogo-A表达与心肌TH表达呈负相关(r=-0.33,P<0.05)。结论老年高血压心肌肥厚患者心肌交感神经分布减低,然而心肌神经元轴突生长抑制因子Nogo-A表达增加,两者间存在密切相关性。     

Influence of Mesterolone on Satellite Cell Distribution and Fiber Morphology within Maturing Chicken Pectoralis Muscle

Mesterolone is a synthetic oral anabolic androgenic steroid used to treat hypogonadism. There are frequent reports of mesterolone abuse in human and equine sports to increase muscle mass and strength. However, limited information is available about how this drug exerts its effects on skeletal muscle. Satellite cells (SCs) are mononuclear myogenic stem cells that contribute to postnatal muscle growth and repair. As SC activation and subsequent differentiation to new myonuclei is a major event during muscle hypertrophy, this study investigated the influence of mesterolone on SC distribution within the pectoralis muscle of chickens. Specifically, this study tested the hypotheses that mesterolone induces avian skeletal muscle hypertrophy, and that mesterolone increases the number of SCs in avian skeletal muscle. Robust immunocytochemical techniques and morphometric analyses were used to calculate the numbers of SCs and myonuclei. Also, DNA concentration and Pax7 protein levels were measured to confirm immunocytochemical findings. Mesterolone significantly increased pectoralis mass and fiber size. All SC indices and number of myonuclei increased significantly by mesterolone administration. In addition, greater DNA concentration and Pax7 protein expression were found in mesterolone‐treated birds. This study indicates that mesterolone can induce avian skeletal muscle hypertrophy and that this is correlated with increased number of SCs. We suggest that SCs are key cellular intermediaries for mesterolone‐induced muscle hypertrophy. Anat Rec, 2012. © 2012 Wiley Periodicals, Inc.     

Angiotensin I Converting Enzyme Gene Cosegregates with Blood Pressure and Heart Weight in F2 Progeny Derived from Spontaneously Hypertensive and Normotensive Wistar-Kyoto Rats

The present investigation examines the association of angiotesin I converting enzyme (ACE) genotypes with blood pressure and heart weight in an F2 population of rats derived from a cross between spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. ACE genotype of rats in the F2 population was determined using a microsatellite polymorphism. Our investigation revealed that cardiac mass was not correlated with blood pressure at 12 weeks of age within the SHR, WKY, F1 or F2 groups of rats. In male rats, ACE genotype accounted for approximately 20% of the difference in mean blood pressure between SHR and WKY rats. There was no effect in females. It was also responsible for 21%-29% of the difference in heart weight both in female and male animals. The allele derived from the SHR parent appeared recessive to the allele from WKY parent for both heart weight and blood pressure. These results suggest that a gene in the region of the ACE locus is one of the genetic factors influencing blood pressure and heart weight in SHR.