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大鼠皮肤挤压伤引起的血管通透性增加。

Increased vascular permeability evoked by crush injury in the skin of the rat.

作者信息

Cummings R, Lykke A W

出版信息

Br J Exp Pathol. 1970 Feb;51(1):19-27.

PMID:4392188
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2072207/
Abstract

The vascular exudative response to cutaneous crush injury was studied in the rat by estimating the leakage of circulating Evans' blue as well as by labelling abnormally permeable vessels with circulating colloidal carbon. The time-course of increased vascular permeability evoked by moderate crush injury is characterized by a monophasic response which has a rapid onset and lasts no more than 4 hr. Increments in the intensity and/or duration of the stimulus are matched by increased intensity and duration of the monophasic response, but with strong crushing the initial phase is followed by a second or delayed response occurring 3-6 hr after injury. Labelling with circulating colloidal carbon indicates that in both phases of the permeability response, the effects are confined to venules. Antagonists of histamine and serotonin partially suppress exudation in the initial ½ hr after injury, whereas antagonists of kinins and serotonin partially suppress the delayed phase of exudation.

摘要

通过评估循环伊文思蓝的渗漏以及用循环胶体碳标记异常通透的血管,对大鼠皮肤挤压伤后的血管渗出反应进行了研究。中度挤压伤引起的血管通透性增加的时间进程以单相反应为特征,该反应起病迅速,持续时间不超过4小时。刺激强度和/或持续时间的增加与单相反应强度和持续时间的增加相匹配,但在强力挤压时,初始阶段之后会出现第二个或延迟反应,发生在损伤后3 - 6小时。用循环胶体碳标记表明,在通透性反应的两个阶段,作用均局限于小静脉。组胺和5 -羟色胺拮抗剂在损伤后的最初半小时内部分抑制渗出,而激肽和5 -羟色胺拮抗剂部分抑制渗出的延迟阶段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58b1/2072207/cf51994c2b49/brjexppathol00427-0033-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58b1/2072207/cf51994c2b49/brjexppathol00427-0033-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/58b1/2072207/cf51994c2b49/brjexppathol00427-0033-a.jpg

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引用本文的文献

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Mechanisms responsible for increased vascular permeability in acute inflammation.急性炎症中血管通透性增加的相关机制。
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本文引用的文献

1
Studies on inflammation. II. The site of action of histamine and serotonin along the vascular tree: a topographic study.炎症研究。II. 组胺和5-羟色胺沿血管树的作用部位:一项局部解剖学研究。
J Biophys Biochem Cytol. 1961 Dec;11(3):607-26. doi: 10.1083/jcb.11.3.607.
2
Experimental suppression of the acute inflammatory changes of thermal injury.热损伤急性炎症变化的实验性抑制
J Pathol Bacteriol. 1959 Jul;78:121-32. doi: 10.1002/path.1700780113.
3
Vascular permeability changes in inflammation: the role of endogenous permeability factors in mild thermal injury.
炎症中的血管通透性变化:内源性通透性因子在轻度热损伤中的作用
Br J Exp Pathol. 1960 Oct;41(5):487-506.
4
Mediators of the inflammatory response and their modification by therapeutic agents.炎症反应的介质及其被治疗药物的修饰。
Proc R Soc Med. 1967 Aug;60(8):775-8. doi: 10.1177/003591576706000828.
5
Pyridinolcarbamate, a bradykinin antagonist in veins. A preliminary report on pharmacologic and clinical observations.吡啶醇氨基甲酸酯,一种静脉中的缓激肽拮抗剂。药理学和临床观察的初步报告。
Am Heart J. 1966 Mar;71(3):297-312. doi: 10.1016/0002-8703(66)90469-8.
6
The drug inhibition of increased vascular permeability.该药物对血管通透性增加的抑制作用。
J Pathol Bacteriol. 1968 Oct;96(2):371-9. doi: 10.1002/path.1700960215.
7
An electron-microscope study of the vascular response to mild thermal injury in the rat.大鼠轻度热损伤血管反应的电子显微镜研究
J Pathol Bacteriol. 1968 Jan;95(1):175-83. doi: 10.1002/path.1700950120.
8
A study of the anti-inflammtory action of pyridinolcarbamate (Anginin).吡啶醇胺(安吉林)抗炎作用的研究。
J Pathol. 1969 Mar;97(3):527-36. doi: 10.1002/path.1710970311.
9
Inflammation in healing. 1. Time-course and mediation of exudation in wound healing in the rat.愈合过程中的炎症。1. 大鼠伤口愈合过程中渗出的时间进程及介导因素。
Br J Exp Pathol. 1969 Jun;50(3):309-18.