血管

The blood pressure of.1 of pathology physiology mechanism that SAS causes CVD breathes time-out to be able to bring about airframe in elevatory Morpheus anoxic, sympathetic is excessive and excited, element of serous catechu phenolic amine, kidney and hemal endodermis element are elevatory, bring about hemal easy of hemal convulsion; to shrink the function is disorder, can make blood-vessel flowing flesh happening reframes and fleshy, systemic blood-vessel obstruction adds element of the kidney when; is chronic and anoxic, system of hemal and nervous element is activationed, bring about blood pressure to lift. Obstruction of way of energy of life of patient of OSAS of disease of blood of 1.2 low oxygen increases, cause air current to interrupt, breath pauses, at the same time airframe gets used to low oxygen environment gradually, breathing centre drops to low oxygen and sensitivity of disease of blood of tall carbonic acid, breath suspends a frequency increasing, farther aggravating airframe is anoxic. 1.3 heads are self-adjusting the function drops normal person changes quickly in systematic circulation blood pressure when, the head can be passed adjust independently functional generation protects effect, make change of cerebral blood flow not big.

SAS诱发CVD的病理生理机制。1血压升高睡眠中呼吸暂停可导致机体缺氧，交感神经过度兴奋，血浆儿茶酚胺、肾素以及血管内皮素升高，导致血管痉挛；血管舒缩功能紊乱，可使血管平滑肌发生重构和肥厚，全身血管阻力增加；慢性缺氧时肾素—血管紧张素系统被激活，导致血压升高。1.2低氧血症OSAS患者气道阻力增加，造成气流中断、呼吸暂停，同时机体逐渐适应低氧环境，呼吸中枢对低氧和高碳酸血症敏感性下降，呼吸暂停次数增加，进一步加重机体缺氧。1.3脑自动调节功能下降正常人在体循环血压快速变化时，脑可通过自主调节功能产生保护效应，使脑血流量变化不大。

The first part consists of three experiments:(1) The rings were incubated in KH, 20, 50 mmol/L 〓 for 1 house, relaxation in response to the EDHF stimuli A23187 in 30nmol/L U46619-induced preconrtaction in the presence of 7 μ mol/L indomethacin, a cyclooxygenase inhibitor, 300μmol/L LNNA, a nitric oxide biosyhnthesis inhibitor, and 1mmol/L tetraethylammonium , a 〓 blocker, or 3 μmol/L glibenclamide , a 〓 blocker, was compared with the control;(2) After the arteries were incubated in KH, UW solution or HTK solution at 4℃ for 4 hours, endothelium-derived relaxation (percentage of 30nmol/L U46619 precontraction) was induced by A23187 in the present of 7 μmol/L indomethacir and 300μmol/L LNNA;(3) After incubation with KH, UW solution and STH (either at 37℃ in oxygenated organ chamber or at 4℃ in a refrigerator for 4 hours), endothelium-derived relaxation (percentage of 30nmol/L U46619 precontraction) was induced by A23187 in the present of 7 μ mol/L indomethacin and 300 μmol/L LNNA.

第一部分研究结果：（1）单纯浸泡于KH的冠状动脉A23187能引发66.67％的血管舒张反应，经TEA及20mmol／L、50mmol／L钾离子作用后，血管舒张反应程度显著降低，但经GBM作用后改变不明显；（2）与保存于KH的冠状动脉相比，A23187引发的血管舒张反应程度，保存于UW液的明显下降，保存于HTK液的无明显变化；（3）在37℃条件下，血管环浸泡于STH出现缓慢轻微的舒张反应，浸泡于UW液初期出现短暂收缩反应，但此后主要以舒张为主：在37℃条件下，血管经UW液保存后，U46619引发的收缩反应程度降低；不论在37℃或4℃条件下，A23187引发的血管舒张反应，经UW液保存后明显下降，但用STH保存后变化不明显。

The degradating and redistributing of ECM were migration of VSMC and vascular remodeling through inhibiting the production of PDGF-BB and the activation of MMPs so to prevent the vascular stenosis.⑤Orthotopic hybridism in situ: The expression of MMP-3 increased after operation, the tendency and intensity were parallel to the expression of NF-κB. Tongxinluo could decrease the expression of MMP-3 and NF-κB. The study showed that the producting and activating of MMP-3 were modulated by NF-κB. The inhibition to the producting and activating of MMp-3 of Tongxinluo was mediated by inhibiting the activating of NF-κB. Conclusion ①The rabbit vascular stenosis model could be established successfully by plain balloon damage, the operation process was easy, economical and practical.

①单纯球囊损伤可成功建立典型家兔血管狭窄模型，操作方法简单，经济实用；②以VSMC增殖、迁移为主的内膜增厚以及以ECM降解、合成与再分布所致的血管重构是导致受损血管狭窄的根本原因；③通心络能明显抑制VSMC的增殖、迁移和ECM降解、合成，阻止血管内膜增生和血管重构，防止受损血管狭窄；该作用可能与其减少和阻止PDGF-BB的产生和活性，以及抑制MMPs的表达和恢复MMPs/TIMPs平衡有关；④通心络能显著抑制球囊损伤后血管内膜增生和血管重构，可能与其保护血管内皮，改善内皮功能，增加血清NO含量有关；⑤通心络抑制内膜增生和血管重构，减轻受损血管狭窄，还可能是通过抑制NF-κB的活化途径而起作用的。

Sex of arteriosclerosis of result lower limbs is out-of-the-way 2 dimension behave disease on supersonic image for pathological changes blood-vessel inside in film is shown irregular add thick, local show strong echo spot, and to hemal antrum inside protuberant, hemal antrum internal diameter shows irregular stricture, pathological changes paragraph solid sex is low it is thus clear that inside hemal antrum echo smooth group fills up; color much general straps blood stream to show resemble showing to; of blood stream signal is not had inside hemal antrum multilayer helix CTA shows pathological change paragraph hemal area does not have comparative agent, show what side raises artery to take travel and initiative place at the same time.

结果下肢动脉硬化性闭塞症二维超声图像上表现为病变血管内中膜呈不规则增厚，局部呈强回声斑，并向血管腔内突起，血管腔内径呈不规则狭窄，病变段血管腔内可见实性低回声光团充填；彩色多普勒血流显像显示血管腔内无血流信号；多层螺旋CTA显示病变段血管区域无对比剂，同时显示侧支动脉的走行及起始部位。

The transform of phenotype of VSMC: The mRNA expressions of SM22α-a notate gene of contractile VSM-were all detected on normal aortas,but decreased normally when the aortas were destroyed and cultured in vitro for 10 days,especially in the serum groups,whose SM22αmRNA could not be detected by RT-PCR.Here,BQ123 can increased their expressions.This demonstrated that serum culture and the secretion of ET-1 can produce the transform of phenotype from contractile to synthesize type.

血管平滑肌表型的转化：RT-PCR检测发现，血管平滑肌收缩表型标志基因SM22α在正常血管平滑肌中都有表达，但在内皮损伤后体外培养10天的血管表达明显减弱，其中血清培养组血管基本不表达，加内皮素受体阻断剂BQ123后，各组SM22α的表达均有所上调，这表明内皮素分泌和血清培养促进了血管平滑肌的表型由收缩型向分泌型的转化。

Wheel' pattern were shown around mixed fibrous filter membranes, number of vessel ramification was 112.5±11.31 and ratio of vessel area/CAM area was 6.19±1.29﹪, but there were not localized allantoic vessels developing in the control group, the number of vessel ramification and ratio of vessel area/CAM area in control group were 82.6±8.05 and 1.78±0.33 respectively, so there was significant difference between PMP and control groups. In above mentioned conditions, the number of vessel ramification and ratio of vessel area/CAM area in VEGF group were 128.4±10.02 and 7.44±1.36 respectively, so there was no difference between PMP and VEGF groups.

结果显示：当 PMP的浓度为80 μg/ml时，孵育72小时后混合纤维素滤膜周围可见到放射状密集生长的血管网，血管分支数为112.5±11.31 ，血管面积为（6.19±1.29）﹪，而在对照组无特异性密集血管生成，血管分支数为82.6±8.05，血管面积为1.78±0.33，二组比较有显著性差异（P＜0.05）；而与VEGF组比较，后者的血管分支数为128.4±10.02，血管面积为7.44±1.36，二组比较差异无显著性。

Angiogenesie and vasculogenesis comprise the mechanisms that responsible for the development of new blood vessels. Vasculogenesis is the process of in situ formation of blood vessels from endothelial progenitor cells or angioblast. Angiogenesis involves extension of the already formed primitive vasculature by the sprouting of new capillaries through migration and proliferation of previously differentiated ECs.

新血管形成的机制有血管生成和血管新生，前者是血管内皮前体细胞或成血管母细胞在原位分化为内皮细胞并形成血管的过程，后者则是已经分化的成熟内皮细胞移行并增生使原有血管延伸。

The changes on vessal"s structure and function with EH is called vascularremodeling, including:①vas wall incrassation, especially on middle-level,lead the proportion between wall and cavity increased, the resistance of bloodstream and the reaction to the shrink substance is tone up;②resistance vasis decreased, especially on dia 12-25μm"s vas, and bring a series of functionabnormity with it.

与高血压伴随的血管结构和功能的变化，即是血管重构(Vascular Remodeling，VR)主要包括：①血管壁增厚，尤其是中层肥厚，导致壁与腔之间的比例明显加大，血流阻力和血管对缩血管物质的反应性增强；②阻力血管变得稀少，尤其是直径12-25μm的阻力血管数目明显减少，随之产生一系列血管功能异常。

Histomorphometric studies were done to measure the following indexes: the IOD values of pulmonary, skeletal muscular and pleural small vascular walls from staining of AT1 and AT2 receptors, the pulmonary vascular density, muscularization of the nonmuscular vessels, percent wall thickness and proliferation of pulmonary small vascular walls.

结果：先心病患儿肺小血管壁AT1、AT2受体染色的IOD值均高于对照组(P=0.000)；先心病患儿骨骼肌和胸膜小血管壁AT1、AT2受体染色的IOD值均高于肺小血管(P＜0.05)；先心病患儿肺小血管壁AT1受体染色的IOD值与肺血管密度、非肌性肺血管肌化程度、肺小血管壁厚百分比和肺小血管壁细胞的增殖度相关(r分别为-0.783、0.742、0.521、0.657)，AT2受体仅与肺血管密度和血管壁厚百分比相关(r分别为-0.487、0.516)。

Between women with or without endometriosis, the expression of VEGFmRNA of eutopic endometrium in the secretoiy phase was significantly higher than that in the proliferative phase(P.05). eutopic endometrium of women with endometriosis both in the proliferative phase and secretoiy phase expressed higher level VEGFmRNA than that in control group(P.05). Conclusion:①The expression of VEGF is adjusted by female'hormone.②VEGF is a very important factor that may contribute to the pathegenesis of endometriosis by promoting neovascularization,explanting of ectopic endometrium , increasing activity of angiopoiesis in eutopic endometrium③VEGF is a efficient organism maker to reflect invading growth, prognosis and metastasis potency of EMs.④VEGF may paly an important role in both pathogenesis and progress of endometriosis.

EM 患者VEGF 水平受女性性激素周期性调节；VEGF 是导致EM 发生特别是在位内膜血管活性增强、异位内膜种植、新生血管形成的重要机制，提示血管生成是EMs 发生中的一个重要因素；VEGF 可能不仅参与EM 的形成，并与进一步发展存在关系，提示血管生成在异位子宫内膜的种植、浸润中可能起着重要的病理生理作用，是EM 发病的必要环节；VEGF 是反映EM 侵袭生长、转移潜能、预后的有效生物指标，提示通过使用抗血管生成药物或抗血管生长因子抗体，来阻断血管生成，极有可能成为EM 在现有药物和手术治疗基础上的一种有效治疗策略和靶点。

This one mode pays close attention to network credence foundation of the businessman very much.

这一模式非常关注商人的网络信用基础。

Cell morphology of bacterial ghost of Pasteurella multocida was observed by scanning electron microscopy and inactivation ratio was estimated by CFU analysi.

扫描电镜观察多杀性巴氏杆菌细菌幽灵和菌落形成单位评价遗传灭活率。