缺氧血症的

ObjectiveSevere traumatic patients always had a severe blood loss, for maintaining blood supply of heart and head, the gut would appear ischemic and anoxemia through the mechanisms of intestinal ischemic, reperfusion and release of mediators of inflammation and so on, which could cause functional impairment of intestinal barrier and translocation of intestinal bacterium and endotoxin, accordingly, induce the occur of SIRS (systemic inflammatory response syndrome), sepsis and MODS (multiple organ dysfunction syndrome).

目的严重创伤常伴严重失血，机体为维持心、脑的血供，肠道首先出现缺血缺氧，通过肠道缺血、再灌注、炎症介质的释放等机制，引起肠道屏障功能障碍，肠内细菌及内毒素移位，从而导致SIRS、脓毒症和MODS的发生。

AbstractObjective:to analyze the relationship between normal term newborn and the degree of asphyxiation.

目的：分析足月新生儿高胆红素血症与窒息缺氧程度的关系。

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 damage of hepatic kupffer cells function and intestine mucosae protective screen function caused cooperatively by ischemia, hypoxia, microcirculatory disarrangement, inflammatory mediators (O〓, OH〓 etc) and cytokines (TNF-α, IL-1, IFN-γetc), the functional damage easily results in bacterial translocation and endotoxemia, as the damage mitigates the clearance of bacteria and toxin.

缺血、缺氧、微循环障碍、炎症介质及细胞因子（TNF-α、IL-1、IFN-γ等）共同作用，使肝脏Kuppfer细胞和肠粘膜屏障功能受损，对内毒素清除能力减弱致内毒素血症，是肝功能衰竭的重要病生环节，亦是继发多脏器衰竭的始动因素，但ALF致病确切机制目前尚不十分清楚。

The clinical manifestations except HIE's features are combined irregular, indefinite krauomania on the face and limbs; eyeball gaze, fremitus, respiratory temporary arrest,and blood calcium descending.

现将36例HIE其中合并抵钙血症23例分析如下。临床资料一、诊断标准缺氧缺血性脑病的诊断及分度参考韩玉昆等的新生儿缺氧缺血性脑病临床诊断依据和分度方法［'］。

One, the end that domestic oxygen cure treats to COPD patient and meaning are anoxic can cause cellular loss quickly, correct anoxic main to having the COPD patient that has disease of blood of sexual low oxygen effect, research shows LTOT ameliorable COPD accompanies the survival rate that breathes exhaustion patient chronically.

一、家庭氧疗对COPD患者治疗的目的及意义缺氧可迅速引起细胞损伤，纠正缺氧对具有进行性低氧血症的COPD患者具有重要功能，探究表明LTOT可改善COPD伴慢性呼吸衰竭患者的生存率。

The transition from the systemic inflammatory response syndrome to seere sepsis and septic shock inoles a myriad of pathogenic changes, including circulatory abnormalities that result in global tissue hypoxia.1,2 These pathogenic changes hae been the therapeutic target of preious outcome studies.12 Although this transition occurs oer time, both out of the hospital and in the hospital, in outcome studies interentions hae usually been initiated after admission to the intensie care unit.12 In studies of goal-directed hemodynamic optimization, in particular, there was no benefit in terms of outcome with respect to normal and supranormal hemodynamic end points, as well as those guided by mixed enous oxygen saturation.9,13 In contrast, een though we enrolled patients with lower central enous oxygen saturation and lower central enous pressure than those studied by Gattinoni et al.9 and with a higher lactate concentration than those studied by Hayes et al.,13 we found significant benefits with respect to outcome when goal-directed therapy was applied at an earlier stage of disease.

从全身炎症反应综合征转为严重脓毒症和脓毒性休克牵涉大量发病的变化，包括导致全身性缺氧的循环紊乱。这些发病的变化成为先前结果研究的治疗学目标。尽管这些转变随着时间的流失而逐渐出现，既可以在院外，也可在院内，在结果研究中，干预措施往往在进入ICU之后才启动。特别的，在那些目标导向血流动力学最优化研究中，依照结果，那些以正常或超正常血流动力学为终点的措施未能显示出益处，以混合静脉血氧饱和度为导向的研究同样如此。

Sleep apnea hypopnea is one of the most important factors for exacerbating hypoxemia,carbon dioxide retention and acidosis.

睡眠呼吸紊乱是造成OS患者高碳酸血症及缺氧难以纠正的重要原因。

This is because:① hypertension caused by macrovascular disease, microvascular disease, the body part can hypoxia, blood lactate levels, leading to uric acid by inhibiting renal tubular secretion, coupled with increased synthesis of uric acid in patients, renal clearance of uric acid will reduce the functionality;② some long-term use in patients with hypertension Thiazide diuretics, the result of hypovolemia, which was repeated absorption of uric acid, thus leading to hyperuricemia.

这是因为：①高血压引起的大血管病变、微血管病变，可使机体部分组织缺氧、血乳酸水平升高，导致肾小管分泌尿酸受到抑制，加之病人体内尿酸合成增加，肾脏清除尿酸的功能就会降低；②部分高血压患者在长期使用噻嗪类利尿剂后，造成血容量减少，致使尿酸被重复吸收，从而引起高尿酸血症。

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。