缺氧的

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。

MethodsThe model of cerebral ischemia and anoxia in mice was established by decollation and ligating common bicarotid artery the effect of BVF on the survival time of the mice,and the time of catching their breath after mice decollated,and mouse brain capillary vessel permeability were observed.

方法采用小鼠断头、结扎双侧颈总动脉等脑缺血缺氧模型，观察苦菜总黄酮对脑缺血缺氧小鼠存活时间、断头小鼠喘息时间及脑毛细血管通透的影响；TBA法、NBT法测定小鼠脑缺血缺氧后脑组织MDA含量和SOD活性。

Methods The model of cerebral ischemia and anoxia in mice was established by decollation and ligating common bicarotid artery the effect of BVF on the survival time of the mice,and the time of catching their breath after mice decollated,and mouse brain capillary vessel permeability were observed. The content of maiondialdehyde,activity of superoxide dismutasein the brain tissues of cerebral ischemia and anoxia mice were measured by TBA,NBT technology respectively.

采用小鼠断头、结扎双侧颈总动脉等脑缺血缺氧模型，观察苦菜总黄酮对脑缺血缺氧小鼠存活时间、断头小鼠喘息时间及脑毛细血管通透的影响；TBA法、NBT法测定小鼠脑缺血缺氧后脑组织MDA含量和SOD活性。

Methods The changes of NOS neuron of mouse brain in proconditioning to hypoxia were detected by histochemistry method.

采用组化法测定小鼠脑内一氧化氮合酶神经元在缺氧(1次缺氧，4次缺氧)预适应中的变化。

Methods］By observing the cytoplasmic Ca2+ concentration change of single cardiocyte in I/R status and the effect of Na+/H+ permutoid retarder to Ca2+ concentration in different phases (diabetes pure oxygen-lack deficit group called DM group,the oxygen deficit/reaeration on entire journey for medicine group called DM-EIPA group, the first group giringmedicine before reaeration on called DM-EIPA 1 group, and the second group giringmedicine before reaeration on called DM-EIPA 2 group) to detect the protection mechanism of Na+/H+ permutoid retarder to diabetic mouse cardiac muscle cell oxygen deficit/reaeration injury.

方法］ 通过观察糖尿病鼠单个心肌细胞在缺氧/复氧时细胞胞浆Ca2+浓度的动态变化以及Na+/H+交换体阻滞剂在不同时相（糖尿病单纯缺氧组即DM组，缺氧/复氧全程给药组即DM-EIPA组，复氧前给药1组即DM-EIPA 1组，复氧前给药2组即DM-EIPA 2组）对Ca2+浓度的影响来研究Na+/H+交换体阻滞剂对糖尿病鼠心肌细胞缺氧/复氧损伤的保护机制。

Change of sodium pump activity is involved in hypoxic injury in rat cortical neurons. High affinity sodium pump is re lated to the protection of hypoxic injury and low affinity sodium pump is related to the hypoxic injury.

Na，K-ATP酶活性改变参与了皮质神经元的缺氧性损伤，其中高汞和力Na，K-ATP酶与皮质神经元缺氧性损伤保护作用有关，而低亲和力Na，K-ATP酶则与其缺氧性损伤有关。

In a second experiment (n = 7), 100 nM DEX was administered posthypoxia. In a third experiment (n = 7 each group), an 2 antagonist, yohimbine was given with and without 100 nM DEX prehypoxia administration.

第一个试验，在缺氧状态前给予0、10、100nM 的右旋美托咪定（每组 n=7），第二个试验（ n=7），缺氧后给予100nM 右旋美托咪定，第三个试验（ n=7）， 100nM 右旋美托咪定联合或不联合育亨宾（一种α2受体拮抗剂）在缺氧后给予。

The result indicates that Bassia rapa L. 65%, 95% alcohol extract and water extract can prolong the survival time of mice in hypoxia under ordinary pressures significantly. It can also prolong the survival time of mice with acute cerebral ischemia and sodium nitrite significantly, and increase the number of erythrocytes and the content of hemoglobin. It demonstrates that Bassia rapa L. extract has anti-hypoxia activity.

结果表明，芫根水提取物、65%乙醇提取物及95%乙醇提取物均能明显延长模型小鼠在常压缺氧、急性脑缺血性缺氧及亚硝酸钠中毒时的存活时间，并可增加外周血象中红细胞数与血红蛋白含量，显示芫根提取物具有抗缺氧活性。

Methods The model of cerebral ischemia and anoxia in mice was established by decollation and ligating common bicarotid artery the effect of BVF on the survival time of the mice,and the time of catching their breath after mice decollated,and mouse brain capillary vessel permeability were observed.

采用小鼠断头、结扎双侧颈总动脉等脑缺血缺氧模型，观察苦菜总黄酮对脑缺血缺氧小鼠存活时间、断头小鼠喘息时间及脑毛细血管通透的影响；TBA法、NBT法测定小鼠脑缺血缺氧后脑组织MDA含量和SOD活性。

ResultsBVF could remarkably lengthen the survival time of cerebral ischemia and anoxia mice, and the time of catching their breath after mice decollated,could evidently decrease mouse brain capillary vessel permeability and the content of MDA, increase activity of SOD in the brain tissues of cerebral ischemia and anoxia mice.

方法采用小鼠断头、结扎双侧颈总动脉等脑缺血缺氧模型，观察苦菜总黄酮对脑缺血缺氧小鼠存活时间、断头小鼠喘息时间及脑毛细血管通透的影响；TBA法、NBT法测定小鼠脑缺血缺氧后脑组织MDA含量和SOD活性。

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。