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The deteriorism of septic challenge is decided by the severity to unbalance.

不同时间脓毒症细胞因子失衡程度不同,脓毒症的发展趋势亦不同。

A pustule, again, is a dome-shaped skin elevation containing pus: a mixture of white blood cells, dead skin cells, and bacteria.

一脓疱,又是一个圆顶形皮肤海拔含脓:混合白血细胞,死皮细胞和细菌。

From occurrence and development mechanism, this article considers that the prevention and treatment for pyemia after severe empyrosis includes full body fluid anabiosis, early gastro-intestinal tract feeds, preventing intestinal tract endotoxin shifting, cutting the scab as soon as possible, eliminating necrosis, applying the antibiotic reasonably, immunity recuperation, maintaining the cellular immunity function, enhancing organism nutrition support, multi-organ function protection and improving organism prognosis.

本文通过对脓毒症的发生发展机制的阐述,认预防和治疗严重烧伤脓毒症全面的临床措施包括:快速、充分的体液复苏治疗和预防烧伤休克;早期胃肠道营养,以防止肠道内毒素移位;尽早切痂,清除坏死组织,封闭创面,合理应用抗生素,预防感染;免疫调理提高机体免疫能力,维护细胞免疫功能;加强机体营养支持治疗和多器官功能的保护,改善机体预后。

The inflammation reaction hyperplactic stage and lymphatic nodular stage are of nonspecific morphological changes and should be diagnosed with the help of positive tuberculin test and obvious increase of adenosine deaninase ; tuberculous nodular stage has a great number of epithelioid cells,and Langhans cells, caseous necrosis stage is characterized by a great deal of necrotic tissue and debris,a small number of fragmented epithelioid cells, and mainly by antiacid bacteria fibrinous hyperplastic stage is featured by a few fibrous tissue, cells and mucous oweing to hardness to get puncture, which neans tuberculous restoration,and scar formation.

炎性增殖反应期非特异性形态学变化,需要结合结核抗体阳性和腺苷酸脱氨酶明显增高有助于诊断,结核结节期主要可有较多类上皮样细胞及郎罕氏细胞;而干酪样脓样坏死主要见大量坏死组织及碎屑、少数残碎不全类上皮样细胞,此期主要能查到抗酸菌为特征;纤维增殖期,抽出物难取,仅见少数纤维组织、纤维细胞和黏液间质为其特征,提示结核恢复、瘢痕形成所致。

The inflammation reaction hyperplactic stage and lymphatic nodular stage are of nonspecific morphological changes and should be diagnosed with the help of positive tuberculin test and obvious increase of adenosine deaninase ; tuberculous nodular stage has a great number of epithelioid cells,and Langhans cells,caseous necrosis stage is characterized by a great deal of necrotic tissue and debris,a small number of fragmented epithelioid cells,and mainly by antiacid bacteria fibrinous hyperplastic stage is featured by a few fibrous tissue,cells and mucous oweing to hardness to get puncture,which neans tuberculous restoration,and scar formation.

炎性增殖反应期非特异性形态学变化,需要结合结核抗体阳性和腺苷酸脱氨酶明显增高有助于诊断,结核结节期主要可有较类上皮样细胞及郎罕氏细胞;而干酪样脓样坏死主要见量坏死组织及碎屑、少残碎不全类上皮样细胞,此期主要能查到抗酸菌特点;纤维增殖期,抽出物难取,仅见少数纤维组织、纤维细胞和黏液间质为其特征,提示结核恢复、瘢痕形成所致。

The inflammation reaction hyperplactic stage and lymphatic nodular stage are of nonspecific morphological changes and should be diagnosed with the help of positive tuberculin test and obvious increase of adenosine deaninase ; tuberculous nodular stage has a great number of epithelioid cells,and Langhans cells, caseous necrosis stage is characterized by a great deal of necrotic tissue and debris,a small number of fragmented epithelioid cells, and mainly by antiacid bacteria fibrinous hyperplastic stage is featured by a few fibrous tissue, cells and mucous oweing to hardness to get puncture, which neans tuberculous restoration,and scar formation.

炎性增殖反应期非特异性形态学变化,需要结合结核抗体阳性和腺苷酸脱氨酶明显增高有助于诊断,结核结节期主要可有较多类上皮样细胞及郎罕氏细胞;而干酪样脓样坏死主要见大量坏死组织及碎屑、少数残碎不全类上皮样细胞,此期主要能查到抗酸菌为特点;纤维增殖期,抽出物难取,仅见少数纤维组织、纤维细胞和黏液间质为其特征,提示结核恢复、瘢痕形成所致。

The inflammation reaction hyperplactic stage and lymphatic nodular stage are of nonspecific morphological changes and should be diagnosed with the help of positive tuberculin test and obvious increase of adenosine deaninase ; tuberculous nodular stage has a great number of epithelioid cells,and Langhans cells, caseous necrosis stage is characterized by a great deal of necrotic tissue and debris,a small number of fragmented epithelioid cells

炎性增殖反应期非特异性形态学变化,需要结合结核抗体阳性和腺苷酸脱氨酶明显增高有助于诊断,结核结节期主要可有较多类上皮样细胞及郎罕氏细胞;而干酪样脓样坏死主要见大量坏死组织及碎屑、少数残碎不全类上皮样细胞,此期主要能查到抗酸菌为特点;纤维增殖期,抽出物难取,仅见少数纤维组织、纤维细胞和黏液间质为其特征,提示结核恢复、瘢痕形成所致。

Statistic indicates that half of the sepsis is caused by Gram-negative bacteria,and that lipopolysaccharide,which release from the cytoderm of Gram-negative bacteria,is considered to be the major molecule which is responsible for the endotoxin sepsis.

统计表明,临床半数的脓毒症是由于革兰氏阴性菌(Gram-negative bacteria)感染引起的,革兰氏阴性菌的细胞壁上的脂多糖(lipopolysaccharide,LPS),或称为内毒素,被认为是革兰氏阴性菌引起脓毒症的主要作用分子。

Results In animal study, lumbricus could inhibit the growth of staphylococci, bacillus coli and bacillus aeruginosus. The time of wound healing in experimental group was 4 days shorter than that in control group. At 4d and 7 day the numbers of the capillary, blood vessel endodermis and desmohemoblast desmocyte and splitting epithelium of trial group were much more than those of control group. At 4d the trial group′s numbers of splitting mesenchymal cell were much more than that of control group. From 3d on the wound healing and granulation filling of experimental group were much quicker than those of control group.

结果 动物实验中,地龙能抑制金黄色葡萄球菌、大肠杆菌及绿脓杆菌的生长;实验组创面愈合时间较对照组提前了4天;第4、7天实验组动物创面的毛细血管数、血管腔内皮细胞数及间质成纤维细胞数均较对照组明显增多,上皮细胞分裂象也高于对照组,第4天的间皮细胞分裂象也高于对照组;自第3天始创面愈合及肉芽充填速度实验组明显快于对照组。

One hand mechanical obstruct led to the increase of veinous resistance and the obstacle of microcirculation, the other hand the adhesive PMN was activated in excess, the white blood cells released a lot of enzymes, in which PMN-elastase can decompose the components of cell and many albumens, inclusive of immunoglobulin、alexin and fibrication. These components induced the injury of the pancreatic capillary vessels and cell and lysosome enzy made the tissue protein hydrolyze and produced unsaturated fatty acids, which destroyed the structure and function of cellar membrane. The inflammatory cellar factors activate other immunocytes to produce the injury and necrosis of tissue, which aggravated the pathological injury and led to shock、pyaemia and MODS. So ICAM-1 and LFA-1 played an important role in SAP. Frossard found that the expression of ICAM-1 in the rat model, especially in serum、pancreas and lung. All these showed ICAM-1 is an important factor in AP and concomitant lung injury.

胰腺小叶组织局部血管EC首先被激活,ICAM-1表达升高,与被激活的PMN表面表达的LFA-1相结合,&PMN-EC&相互作用加剧,一方面机械性阻塞毛细血管导致静脉阻力增加、微循环障碍;另一方面粘附的PMN过度吞噬或激活,当白细胞吞噬的颗粒不能被封闭隔离,连同细胞内的酶被释放出来,其中的PMN-elastase能够降解细胞基质中各种成分,水解多种蛋白,加重胰腺的毛细血管内皮细胞和腺泡的损伤;释放的溶酶体酶使组织蛋白水解,产生的不饱和脂肪酸引发脂质过氧化方应,破坏细胞膜的结构和功能;释放的炎性细胞因子,激发其他的免疫细胞的功能,导致进一步的组织损伤和坏死,加重SAP的病理损伤,最终导致休克、脓毒血症及多器官功能障碍等严重后果。

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