Thermoregulatory reactions to cooling in rats with hereditary arterial hypertension

Experiments on rats with hereditary stress-induced arterial hypertension showed that hypertension shortened the latency and increased the amplitude of constrictive reaction of skin blood vessels to rapid cooling characterized by more rapid and considerable increase in blood norepinephrine content compared to slow cooling. Decreased thermal threshold of metabolic reaction suggests that arterial hypertension is accompanied by changes in both the vascular walls and tissues involved in metabolic reaction to cooling.     

Endocrine-metabolic relations in rats with inherited stress-induced arterial hypertension

Laboratory of Endocrinology, Institute of Clinical and Experimental Medicine, Siberian Branch, Academy of Medical Sciences of the USSR. Laboratory of Genetic Bases of Neuroendocrine Regulation, Institute of Cytology and Genetics, Siberian Branch, Academy of Sciences of the USSR, Novosibirsk. (Presented by Academician of the Academy of Medical Sciences of the USSR V. P. Kaznacheev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 109, No. 6, pp. 575–576, June, 1990.     

An homozygous mutation in KCNK3 is associated with an aggressive form of hereditary pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a rare devastating disease characterized by a high genetic heterogeneity with several related genes recently described, including BMPR2,TBX4 and KCNK3. The association between KCNK3 and PAH has been recently identified, but the prognosis and phenotype associated with these mutations have been poorly described. We studied a series of 136 idiopathic and hereditary PAH Spanish patients for BMPR2, TBX4 and KCNK3 mutations. We report the results of KCNK3 in which we were able to describe two new mutations (p.Gly106Arg and p.Leu214Arg) in three patients. The first one was found in a patient belonging to a consanguineous Romani family, who carried a homozygous mutation in KCNK3 and developed a severe and early form of the disease. To the best of our knowledge, this is the first time that a homozygous mutation in KCNK3 is reported in a PAH patient. The second one was found in a patient who presented at the young adult age a severe form of the disease. The present report supports the contribution of KCNK3 mutations to the genetic etiology of PAH and strongly suggests that mutations in KCNK3 follow incomplete dominance with worsening of the clinical features in homozygous patients.     

Peculiarities of active avoidance conditioning in rats with various forms of inherited arterial hypertension

Peculiarities of active avoidance conditioning were studied in NISAG rats (hereditary stress-induced arterial hypertension) and spontaneously hypertensive SHR rats. Conditioning was successful in 90% normotensive Wistar rats and in only 9.1% NISAG rats. Hypertensive SHR rats were intermediate between Wistar and NISAG rats by their learning capacity (66.7%). Our results suggest that differences in learning capacity of hypertensive rats are determined by genetic characteristics of animal behavior and emotional state, rather than blood pressure elevation. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 142, No. 10, pp. 386–388, October, 2006     

脂肪间充质干细胞早期干预对野百合碱诱发的肺动脉高压大鼠肺小动脉功能的影响

 目的：观察脂肪间充质干细胞(ADMSCs)早期干预对野百合碱(MCT)诱发的大鼠肺动脉高压(PAH)进程中肺小动脉功能的影响。方法：采用SD大鼠腹股沟皮下脂肪,经胶原酶消化法分离培养ADMSCs。雄性SD大鼠90只,随机分为正常对照组、PAH组和ADMSCs早期干预组(ADMSCs-EI组)。一次性腹腔注射MCT 40 mg/kg建立PAH动物模型。ADMSCs-EI组于MCT注射后1周,经左颈外静脉一次性给予ADMSCs(1×106)。分别于ADMSCs移植后1、2、3周,右心导管法测定大鼠的肺动脉平均压(MPAP),并采用离体血管张力法检测大鼠肺小动脉的内皮依赖性舒张(EDdR)、非内皮依赖性舒张(EDiR)以及收缩功能(VCF)。收缩或舒张的敏感性用pD2值表示。结果：与对照组比较,腹腔注射MCT后2周,PAH组大鼠肺小动脉EDdR明显减弱;同时,与PAH组比较,ADMSCs早期移植后1周,ADMSCs-EI组大鼠肺小动脉EDdR明显增强（均P<005）。与对照组比较,腹腔注射MCT后3、4周,PAH组大鼠MPAP显著升高,肺小动脉EDdR和EDiR显著减弱;同时,与PAH组比较,ADMSCs早期移植后2、3周,ADMSCs-EI组大鼠MPAP显著降低,肺小动脉EDdR和EDiR显著增强（均P<005）;但是,VCF在3组间均无显著差异（P>005）。结论： ADMSCs早期干预可以明显改善受损的肺小动脉EDdR及EDiR,并有效地降低MCT诱发的PAH大鼠的肺动脉压力。     

Content of HSP70 in rats with hereditary stress-induced arterial hypertension

Sensitivity of normotensive Wistar rats and NISAG rats (with hereditary arterial hypertension) to heat stress is compared at the organism and cell levels. High temperature sensitivity of NISAG rats correlates with a low content of the main heat shock protein HSP70. This relationship can serve as a biochemical marker of predisposition to arterial hypertension. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 8, pp. 171–173, August, 1997     

POEMS综合征合并肺动脉高压临床分析

目的 分析POEMS综合征合并肺动脉高压患者的临床特点.方法 回顾性分析北京协和医院确诊POEMS综合征患者的临床资料,并将超声心动图证实合并肺动脉高压的患者与肺动脉压正常的患者以及未行超声心动检查的患者的临床表现进行比较,描述合并肺动脉高压的POEMS综合征患者的临床特点.结果 POEMS综合征117例,合并肺动脉高压49例,肺动脉压正常33例,未行超声心动检查35例;肺动脉高压患病率41.9%.肺动脉高压组临床表现主要为胸闷、憋气,发生率42.9%(21/49),显著高于另外两组(P≤0.05),但一半以上患者无明显胸闷、憋气;肺动脉高压组并发胸水、腹水、心包积液发生率较另外两组高(P≤0.01),其他临床表现无显著差异.结论 POEMS综合征超声心动图检测肺动脉高压患病率高达40%以上,但半数以上患者无胸闷、憋气,提示在POEMS综合征诊治过程中应重视肺动脉高压的筛查和早期发现.     

脂肪间充质干细胞对野百合碱诱发的肺动脉高压大鼠肺动脉钙离子通道的影响

 目的：探讨脂肪间充质干细胞(adipose tissue-derived mesenchymal stem cells,ADMSCs)移植对野百合碱（monocrotaline,MCT）诱发的肺动脉高压（pulmonary arterial hypertension,PAH）大鼠肺动脉钙离子通道的影响。方法：胶原酶消化法分离培养ADMSCs。雄性SD大鼠24只,分为正常对照组（Ctr组）、PAH组和ADMSCs组,每组8只。右心导管法测定大鼠的平均肺动脉压(MPAP);称重法测右心室肥厚指数（RVHI）;分别用RT-PCR及Western blotting法测定大鼠肺动脉干电压门控性钙离子通道α1c亚基（CaVα1c）肌浆/内质网Ca2+ ATP酶2a（SERCA-2a）、三磷酸肌醇受体1（IP3R-1）、瞬时受体电位通道1（TRPC1）和TRPC6 mRNA和蛋白的表达水平。结果：（1）MCT注射4周后,与Ctr组相比, PAH组大鼠MPAP和RVHI均显著升高（P<0.05）;ADMSCs移植2周后,与PAH组相比,ADMSCs组MPAP和RVHI均明显降低（P<0.05）。（2）与Ctr组相比,PAH组大鼠肺动脉CaVα1c、TRPC1和TRPC6 mRNA及蛋白表达水平均明显增强（P<0.05）,SERCA-2a 和IP3R-1 mRNA及蛋白表达水平均明显降低（P<0.05）;与PAH组相比,ADMSCs组CaVα1c、TRPC1和TRPC6的表达均明显降低（P<0.05）,SERCA-2a 和IP3R-1的表达均明显增强（P<0.05）。结论：ADMSCs能有效地降低MCT诱发的PAH大鼠的肺动脉压力,减轻右心室肥厚。ADMSCs降低肺动脉压力可能与钙离子通道变化有关。     

The intestinal tract and the pathophysiology of arterial hypertension: an experimental study on Dahl rats

Salt depleted rabbits and humans excrete an oral sodium load more quickly via the kidneys than an intravenous one. This has been ascribed to the presence of a sodium sensor in the gastrointestinal tract which in some way can influence renal function. The purpose of this study was to investigate this response in the Dahl rats. Renal and faecal sodium excretion was followed in the two strains of rats (normotensive, saltresistant (SR/Jr) and hypertensive, saltsensitive (SS/Jr) rats). After 4 days on a low salt diet they were given NaCl(l.5 mmol kg^-1 body wt) either by gavage or intravenously. SR/Jr rats showed an increased renal sodium excretion both after oral and intravenous sodium repletion. The excretion was 2–3 times greater after the oral than after the intravenous administration. The SS/Jr rats augmented their renal sodium excretion only after the oral load, although the sodium excretion was significantly less than in SR/Jr rats. In fact, during the first 8 h after giving sodium orally the renal excretion of sodium was on an average eight times larger in the SR/Jr than in the SS/Jr rats. Renal excretion of sodium was similar in the two strains after intravenous administration. We conclude that the hypertensive SS/Jr rats have great difficulties in excreting an oral sodium load, a phenomenon that may be of importance in the pathophysiology of arterial hypertension in this strain of rats.     

The role of platelets in the development and progression of pulmonary arterial hypertension

Pulmonary arterial hypertension is a multifactorial disease characterized by vasoconstriction, vascular remodeling, inflammation and thrombosis. Although an increasing number of research confirmed that pulmonary artery endothelial cells, pulmonary artery smooth muscle cells as well as platelets have a role in the pulmonary arterial hypertension pathogenesis, it is still unclear what integrates these factors. In this paper, we review the evidence that platelets through releasing a large variety of chemokines could actively impact the pulmonary arterial hypertension pathogenesis and development. A recent publication revealed that not only an excess of platelet derived cytokines, but also a deficiency may be associated with pulmonary arterial hypertension development and progression. Hence, a simple platelet blockade may not be a correct action to treat pulmonary arterial hypertension. Our review aims to analyse the interactions between the platelets and different types of cells involved in pulmonary arterial hypertension pathogenesis. This knowledge could help to find novel therapeutic options and improve prognosis in this devastating disease.     

Morphological and functional characteristics of cadmium-induced arterial hypertension

Laboratory of Geographic Pathology, Research Institute of Human Morphology, Academy of Medical Sciences of the USSR, Moscow. Department of Physiology of Man and Animals, M. V. Lomonosov Moscow State University. (Presented by Academician of the Academy of Medical Sciences of the USSR N. P. Avtsyn.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 4, pp. 420–423, April, 1991.     

氟西汀对BMPR2表达的影响以及对野百合碱诱导大鼠肺动脉高压的预防作用

目的探讨氟西汀对骨形态生成蛋白受体2(bone morphogenetic protein receptor 2,BMPR2)表达的影响以及对野百合碱(monocrotaline,MCT)诱导大鼠肺动脉高压(pulmonary arterial hypertension,PAH)的预防作用。方法将24只Wistar大鼠随机分成三组:对照组、MCT组和氟西汀处理组。采用多导生理记录仪测量血流动力学相关指标,HE染色方法观察肺动脉的形态学改变,以及利用RT-PCR方法检测肺动脉BMPR2的表达。结果与对照组相比,MCT组肺动脉压力、肺动脉中膜厚度百分比以及右心肥厚指数均明显升高,BMPR2在肺动脉上的表达明显减少(<0.01)。给予氟西汀处理后,氟西汀明显抑制了MCT诱发的肺动脉压力的升高、肺动脉重构和右心肥厚,并逆转了BMPR2的表达(<0.05)。结论肺动脉的构型重建可能与BMPR2的表达减少有关。氟西汀可能通过逆转BMPR2的表达有效地预防MCT诱导的PAH。     

Experimental study of myocardial collagen during nifedipine therapy of arterial hypertension

Light and electron microscopy of the left-ventricular myocardium obtained from spontaneously hypertensive SHR rats showed a pronounced increase in collagen content. These changes were more pronounced in animals treated with nifedipine in the mean therapeutic dose for 8 weeks. Collagen accumulated between muscle fibers and often formed perivascular cuffs. Hence, nifedipine promotes the formation of scleroproteins in the myocardium.     

Myocardial hypertrophy of the left ventricle during familial arterial hypertension

In patients with familial arterial hypertension and their relatives preclinical signs of myocardial hypertrophy were observed before the formation of stably increased blood pressure. We evaluated echocardiographic sings of left ventricular myocardial hypertrophy in normotensive relatives of patients with arterial hypertension. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 140, No. 12, pp. 625–626, December, 2005     

肺动脉高压患者生活质量及其影响因素

目的：了解肺动脉高压患者的生活质量状况并探讨其影响因素。方法：采用整群抽样的方法选择2014年6月至2015年6月期间在中南大学湘雅医院住院治疗的68例肺动脉高压患者作为研究对象。采用一般资料问卷、中文版简明健康调查量表(Short Form 36 Health Survey Questionnaire,SF-36)对其进行调查,运用单因素分析及多元线性回归法分析其影响因素。结果：肺动脉高压患者SF-36量表各维度评分均低于常模,差异均有统计学意义(P<0.05)。影响生活质量生理健康的因素为性别、6分钟步行试验距离(6-minute walking distance,6MWD)、是否合并右心衰竭、是否坚持氧疗;影响生活质量心理健康的因素为性别、文化程度、有无医疗保险。结论：肺动脉高压患者生活质量不高。医护人员应对女性、文化程度低、无医疗保险、6MWD短、合并右心衰竭、未坚持氧疗的患者给予更多的关注。