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排序方式: 共有182条查询结果,搜索用时 15 毫秒
1.
粉防己碱对野百合碱致大鼠肺动脉构形重建的逆转作用 总被引:2,自引:0,他引:2
以野百合碱复制Wistar大鼠肺动脉高压模型,用特殊染色方法观察粉防已碱对野百合碱致大鼠肺动脉构形重建的逆转作用,结果表明粉防已碱可选择性的降低野百合碱诱导的大鼠肺动脉高压的作用,并明显地逆转肺血管及肺组织损伤,降低肺动脉高压和右心室肥大,对体循环压力无影响 相似文献
2.
松龄血脉康抑制肺动脉高压的实验研究 总被引:1,自引:0,他引:1
为观察松龄血脉康胶囊对肺动脉高压大鼠肺动脉压的影响,取100只健康Wistar大鼠,其中60只背部注射野百合碱monocrotaline,MCT80mg/kg复制出肺动脉高压模型。再将其分为两组,各30只,其中一组以标准饲料喂养,另一组加用松龄血脉康胶囊1.5g·kg-1·d-1。其余40只健康大鼠做为正常对照组,在实验当天、7天、14天、21天、28天、35天从各组中随机抽取5只行右心导管测肺动脉压。结果:注射MCT后肺高压组28天时达高峰,但加用松龄血脉康组上升幅度明显小于未用药组。结论:松龄血脉康有显著抑制大鼠肺动脉高压发展的作用 相似文献
3.
Summary The monocrofaline-induced structural changes of small pulmonary arteries in rat and their relationship with pulmonary hypertension
and right ventricular hypertrophy were observed by determining the right ventricular systolic pressure, and by light and electron
microscope and morphometry. One to 38 days after last injection of monocrotaline (MCT), a medial thickening and lumen marrrowing
of the circular muscular arteries (CMA), accompanying terminal (TB) and respiratory bronchioles (RB), were found. And there
after the lumen of CMA, accompanying TB, became dilated, and its medial thickness (MT) decreased, whereas the histopathologic
changes of the partially muscular arteries (PMA), accompanying RB, became severe, their MT increased continuously, and finally
reached the peak value on Day 50. At the first day after last MCT treatment, inflammation and muscularization were found in
PMA and nonmuscular arteries (NMA), and became more severe with the cause of disease. Therefore, the intra-acinar pulmonary
arteries, both CMA and PMA, increased in number while the NMA decreased in number significantly because of the structural
remodeling. Four days after MCT treatment, the right ventricular systolic pressure began to rise, and reached its peak value
on Day 50. Eight days after MCT injection, right ventricular hypertrophy developed, and became most significant from Day 23
to Day 30. The results suggest that structural remodeling, i.e. muscularization, of intra-acinar pulmonary arteries plays
an important role in the development of pulmonary hypertension and right ventricular hypertrophy. 相似文献
4.
目的 研究慢性"炎症性"肺动脉高压大鼠在肺动脉高压形成过程中肺动脉蛋白激酶C(PKC)亚型的表达.方法 建立野百合碱诱导的慢性"炎症性"肺动脉高压大鼠模型,应用Western blot技术检测肺动脉高压形成过程中大鼠肺动脉四种PKC亚型(PKCα、PKCβⅡ、PKCδ和PKCε)的表达变化.结果 PKCα、PKCβⅡ和PKCδ亚型在正常和肺动脉高压大鼠肺动脉中均有表达,而PKCε亚型未检测到.在肺动脉高压形成过程中,大鼠肺动脉胞浆和胞膜组分表达的PKCα均逐渐上升,到第14天达到高峰后略有下降,且胞膜表达量的升高远比胞浆明显.胞浆PKCβⅡ和PKCδ表达量均在第8天达最高,而胞膜中二者均表现出持续升高的趋势.结论 PKCα、PKCβⅡ和PKCδ亚型可能参与了慢性"炎症性"肺动脉高压的形成,其表达变化可能与其转位有关. 相似文献
5.
A group of Wistar albino rats was injected subcutaneously with monocrotaline to induce vasoconstrictive hypertensive pulmonary vascular disease characterized by medial hypertrophy of small pulmonary arteries, the appearance of muscular pulmonary arterial vessels of arteriolar dimensions (less than 20 microns) in diameter), and exudative changes in the lung parenchyma. The vascular abnormalities were quantified by measuring the percentage medial thickness of small pulmonary arteries, the number of muscular pulmonary arterial vessels below 20 microns in diameter per cm2 of lung section and by determining the smallest arterial vessels in each case showing muscularity. A second group of rats was born in a decompression chamber and kept in hypobaric hypoxia for a month of the neonatal period, developing hypoxic hypertensive pulmonary vascular disease as a consequence. The animals in this group were allowed to recover in room air for a period of 3 months and were then injected with the same dose of monocrotaline as that given to the first group. The rats previously exposed to hypoxia exhibited an exaggerated response to the alkaloid, showing in particular many more small muscular pulmonary arterial vessels which were of a smaller diameter than those found in the eupoxic rats treated with the alkaloid. The experiment demonstrates the perinatal hypoxia exaggerates the effects of agents inducing vasoconstrictive pulmonary hypertension with a shift of the segment of the pulmonary arterial tree involved to the periphery as in hypoxia. Reports of a similar phenomenon are noted as occurring in babies born at high altitude, spending their infancy there and subsequently developing primary pulmonary hypertension later in life. 相似文献
6.
Steven B Yee Umesh M Hanumegowda Jon A Hotchkiss Patricia E Ganey Robert A Roth 《Toxicological sciences》2003,72(1):43-56
Synergistic liver injury develops in Sprague-Dawley rats from administration of a small, noninjurious dose (7.4 x 10(6) EU/kg) of bacterial lipopolysaccharide (LPS) given 4 h after a nontoxic dose (100 mg/kg) of the pyrrolizidine alkaloid, monocrotaline (MCT). Previous studies demonstrated that liver injury is mediated through inflammatory factors, such as Kupffer cells and tumor necrosis factor alpha (TNF-alpha), rather than through simple interaction between MCT and LPS. In the present study, the hypothesis that neutrophils (polymorphonuclear leukocytes or PMNs) are causally involved in this injury model is tested, and the interdependence between PMNs and other inflammatory components is explored. Hepatic PMN accumulation and the appearance of cytokine-induced neutrophil chemoattractant-1 in plasma preceded the onset of liver injury, suggesting that PMNs contribute to toxicity. Hepatic PMN accumulation was partially dependent on TNF-alpha. Prior depletion of PMNs in MCT/LPS-cotreated animals resulted in attenuation of both hepatic parenchymal cell (HPC) and sinusoidal endothelial cell (SEC) injury at 18 h. PMN depletion did not, however, protect against early SEC injury that occurred before the onset of HPC injury at 6 h. This observation suggests that SEC injury is not entirely dependent on PMNs in this model. In vitro, MCT caused PMNs to degranulate in a concentration-dependent manner. These results provide evidence that PMNs are critical to the HPC injury caused by MCT/LPS cotreatment and contribute to the progression of SEC injury. 相似文献
7.
Tian-tai ZHANG Bing CUI De-zai DAI Research Division of Pharmacology China Pharmaceutical University Nanjing China 《Acta pharmacologica Sinica》2004,(2)
INTRODUCTION The calcium-independent transient outward potas-sium current (Ito) is activated by depolarization and playsa key role in controlling the amplitudes and cardiac ac-tion potential duration (APD). Ito contributesto the phase1 repolarization of action potential in myocytes, theprolongation of APD is the result of decrease in Ito den-sity[1]. Ito which is encoded by genes of Kv1.4, Kv4.2,and Kv4.3[2], based on differences in kinetics, as wellas recovery from inactivation… 相似文献
8.
The length‐dependent activation of contraction is equally impaired in impuberal male and female rats in monocrotaline‐induced right ventricular failure
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Oleg Lookin Alexander Balakin Daniil Kuznetsov Yuri Protsenko 《Clinical and experimental pharmacology & physiology》2015,42(11):1198-1206
The length‐dependent activation of contraction is attenuated in the failing myocardium of adult male rats. This pathological change is not seen in adult female rats, possibly because of a protective effect of sex hormones. The present study evaluated length‐dependent changes in isometric twitch, Ca2+ transient (CaT) and action potential (AP) in the right ventricular myocardium of impuberal healthy male and female rats (control) and in rats treated with a single injection of 50 mg/kg monocrotaline (MCT). Compared with sex‐matched control rats, MCT‐treated male and female rats exhibited increased right ventricular weight (134% and 142% of control, respectively), decreased left ventricular weight (72% and 79%), twitch attenuation (48.8 ± 2.7% and 57.5 ± 1.2%) and prolongation (125 ± 3% and 127 ± 2%), CaT attenuation (37.8 ± 0.4% and 39.1 ± 1.1%) and prolongation (114 ± 1% and 116 ± 1%) and AP prolongation at 90% repolarization (195 ± 2% and 203 ± 1%). The MCT‐treated male rats exhibited a 50% lower integral magnitude and an approximately 25% larger time‐to‐peak ‘bump’ compared with control male rats. These parameters in MCT‐treated female rats tended to show similar changes to those seen in the control female rats, with no significant difference between the two groups. In all groups, integral magnitude and time‐to‐peak ‘bump’ increased with length. In conclusion, the length‐dependent activation of contraction was equally blunted in the failing right ventricular myocardium of impuberal male and female rats. This was related to changes in CaT and AP, which were similar between male and female rats. Therefore, puberty is necessary for manifestation of the protective effects of sex hormones on this remodelling. 相似文献
9.
野百合碱注射建立大鼠肺动脉高压模型的方法 总被引:1,自引:0,他引:1
目的探讨野百合碱注射建立大鼠肺动脉高压模型的方法和关键点。方法 SPF级雄性SD大鼠30只,随机分为实验组和对照组各15只。实验组大鼠颈背部皮下注射野百合碱50 mg/kg;对照组皮下注射0.9%氯化钠注射液1 ml。3周后大鼠行右心导管检查、病理检查和免疫组化检查。结果实验组大鼠表现为进行性右心功能衰竭,死亡2只,平均肺动脉压力、右心室收缩压均明显高于对照组[(40.05±1.78)mm Hg vs(18.63±1.80)mm Hg(1 mm Hg=0.133 k Pa),(62.99±2.03)mm Hg vs(28.04±2.26)mm Hg,P均<0.05]。病理切片HE染色,实验组大鼠肺血管中膜明显增生,管腔狭窄,中膜管壁厚度百分比、中膜管腔面积百分比、右心室肥厚指数[RV/(LV+IVS)]均明显大于对照组[(0.292±0.064)vs(0.106±0.026)、(0.0495±0.092)vs(0.200±0.045)、(0.473±0.041)vs(0.295±0.035),P均<0.05]。实验组大鼠肺血管增殖细胞核抗原免疫组化IA值明显高于对照组[(39.5±8.7)vs(18.5±5.3),P<0.05]。结论经颈背部皮下注射野百合碱建立大鼠肺动脉高压动物模型是一种操作简单、有效可靠的方法,把握几个关键点可以提高建模成功率。 相似文献
10.
目的 通过气道内滴注腺病毒转染肝细胞生长因子(adenovirus hepatocyte growth factor,Ad-HGF)干预野百合碱(monocrotaline,MCT)诱导的肺动脉高压(pulmonary hypertension,PAH)模型大鼠,观察Ad-HGF干预对平均肺动脉压(mean pulmonary artery pressure,mPAP)等指标的影响.方法 选用健康雄性SD大鼠40只,随机[采用随机单位(区)组设计方法]分为4组:正常对照组(normal,NOR组)10只,MCT诱导PAH组(PAH组)10只、单次和重复肝细胞生长因子(hepatocyte growth factor,HGF)干预治疗组(HGF和THGF组)各10只.NOR组和PAH组:气道内滴注0.2 mL磷酸盐缓冲液;HGF组和THGF组:气道内滴注0.2 mL Ad-HGF 1次和一周后重复一次共2次.再饲养两周后,测定各组大鼠的肺动脉压,计算右心室肥厚指数;苏木素伊红染色观察肺动脉管壁等;酶联免疫吸附(ELISA)法测定肺组织匀浆中HGF浓度.结果 与PAH组大鼠比较,HGF组和THGF组大鼠的mPAP、右心室肥厚指数、肺动脉管壁指数和面积指数明显降低,肺苏木素伊红染色肺小动脉管壁厚度减少,管腔面积增大,血管周围炎症细胞浸润减轻,肺组织匀浆HGF浓度明显升高,差异有统计学意义(P<0.05),且低于NOR组水平.结论 经气道内滴注转染Ad-HGF,能明显降低但不能完全逆转MCT诱导PAH大鼠的mPAP,减少肺小动脉管壁厚度,减轻右心室肥厚程度,从而达到延缓PAH进程的作用. 相似文献