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热损伤后红细胞延迟破坏的机制。一项体外实验性扫描电子显微镜研究。

Mechanisms of delayed red cell destruction after thermal injury. An experimental in vitro sem study.

作者信息

Baar S

出版信息

Br J Exp Pathol. 1974 Apr;55(2):187-93.

Abstract

Factors likely to affect the life span of erythrocytes in thermally injured patients have been investigated by an model. Normal blood was incubated with phospholipase A, prostaglandins, adrenaline, noradrenaline and adrenochrome. After incubation the samples were heated for 10 min at 48°, 49° and 50°. Glutaraldehyde fixed samples were examined by Stereoscan electronmicrography. Phospholipase A reduced the normal thermal deformation point from 49° to 48°. Prostaglandin E, noradrenaline and adrenochrome increased the required temperature to 50°. Adrenaline had no effect. Lowering the zeta potential by treatment with neuraminidase increased the thermal deformation point to 50°. This effect was abolished if the cells were also treated with trypsin. Possible applications of these findings to red cell survival in burned patients are discussed.

摘要

通过一个模型对可能影响热损伤患者红细胞寿命的因素进行了研究。将正常血液与磷脂酶A、前列腺素、肾上腺素、去甲肾上腺素和肾上腺色素一起孵育。孵育后,将样品在48°、49°和50°下加热10分钟。通过立体扫描电子显微镜检查戊二醛固定的样品。磷脂酶A将正常热变形点从49°降至48°。前列腺素E、去甲肾上腺素和肾上腺色素将所需温度提高到50°。肾上腺素没有效果。用神经氨酸酶处理降低ζ电位可将热变形点提高到50°。如果细胞也用胰蛋白酶处理,这种效果就会消失。讨论了这些发现对烧伤患者红细胞存活的可能应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70cf/2072518/8cea68c52d05/brjexppathol00404-0110-a.jpg

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