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[大鼠内毒素诱导急性肺损伤时中性粒细胞变形能力的变化及山莨菪碱对中性粒细胞变形能力的影响]

[Changes of the deformability of neutrophil and the influence of anisodamine on neutrophil deformability during endotoxin-induced acute lung injury in rats].

作者信息

Xu X, Sun G, Qian G

机构信息

Department of Respiratory Disease, Xing Qiao Hospital, Chong Qing 400037.

出版信息

Zhonghua Jie He He Hu Xi Za Zhi. 1998 Oct;21(10):598-600.

Abstract

OBJECTIVE

To explore the mechanisms of change of deformability of polymorphonuclear leukocytes (PMN) and influence of anisodamine on deformability of PMN during endotoxin-induced acute lung injury (ALI) in rat. To explore the role of PMN in ALI.

METHOD

The model of ALI in rat was reproduced by intravenous injection of E Coli endotoxin. The deformability of PMN was measured by micropipette aspiration technique.

RESULT

The elastic modulus K1 of PMN at the 1st hour (33 +/- 12 Pa), 4th hours (37 +/- 12 Pa, 1 Pa = 0.0075 mmHg) and 6th hours (38 +/- 13 Pa) after injection of E Coli endotoxin are all significantly higher than that in the control group (26 +/- 9 Pa P < 0.01). The viscosity modulus (mu) of PMN at the 4th hours (5 +/- 3 Pa.s) and 6th hours (6 +/- 3 Pa.s) after injection of E Coli endotoxin are all significantly higher than the control group (3.1 +/- 2.6 Pa.s, P < 0.01). The elastic shear modulus (G) of PMN at the 4th hours (54 +/- 20 Pa) and the 6th hours (56 +/- 21 Pa) after injection of E Coli endotoxin are all significantly higher than the control group (47 +/- 17 Pa, P < 0.05). The K1(33 +/- 12 Pa) and mu(4 +/- 3 Pa.s) in anisodamine group are all significantly lower than endotoxin group in the same time phases (P < 0.05).

CONCLUSION

The deformability of PMN decrease remarkably during ALI, which will enhance PMN sequestration in lungs, lead to ALI. It may be one of important pathogenic mechanism of ALI. The anisodamine can inhibit the decrease of deformability of PMN effectively and may have some therapeutic effect on ALI.

摘要

目的

探讨大鼠内毒素诱导急性肺损伤(ALI)过程中多形核白细胞(PMN)变形能力变化的机制及山莨菪碱对PMN变形能力的影响。探讨PMN在ALI中的作用。

方法

通过静脉注射大肠杆菌内毒素复制大鼠ALI模型。采用微量吸管吸液技术测定PMN的变形能力。

结果

注射大肠杆菌内毒素后第1小时(33±12帕斯卡)、第4小时(37±12帕斯卡,1帕斯卡=0.0075毫米汞柱)和第6小时(38±13帕斯卡)PMN的弹性模量K1均显著高于对照组(26±9帕斯卡,P<0.01)。注射大肠杆菌内毒素后第4小时(5±3帕斯卡·秒)和第6小时(6±3帕斯卡·秒)PMN的黏度模量(μ)均显著高于对照组(3.1±2.6帕斯卡·秒,P<0.01)。注射大肠杆菌内毒素后第4小时(54±20帕斯卡)和第6小时(56±21帕斯卡)PMN的弹性剪切模量(G)均显著高于对照组(47±17帕斯卡,P<0.05)。山莨菪碱组同一时间点的K1(33±12帕斯卡)和μ(4±3帕斯卡·秒)均显著低于内毒素组(P<0.05)。

结论

ALI过程中PMN变形能力显著降低,这将增强PMN在肺内的滞留,导致ALI。这可能是ALI重要的发病机制之一。山莨菪碱可有效抑制PMN变形能力的降低,对ALI可能有一定治疗作用。

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