Tirofiban, a Glycoprotein IIb/IIIa Antagonist, Has a Protective Effect on Decompression Sickness in Rats: Is the Crosstalk Between Platelet and Leukocytes Essential?
Tirofiban, a Glycoprotein IIb/IIIa Antagonist, Has a Protective Effect on Decompression Sickness in Rats: Is the Crosstalk Between Platelet and Leukocytes Essential?
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DOI：
10.3389/fphys.2018.00906
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发表时间：
2018
影响因子：
4
通讯作者：
Vallée N
中科院分区：
文献类型：
--
作者：
Lambrechts K;de Maistre S;Abraini JH;Blatteau JE;Risso JJ;Vallée N
在其最严重的形式中，减压病（DCS）可能全身性扩展和/或引起严重的神经功能缺损，包括瘫痪甚至死亡。无菌性和缺血性炎症现象似乎与气泡与生物体的反应是连续的，血小板活化在DCS的发展中起决定性作用。根据通常提出的假设，气泡可以通过直接接触激活血小板，或者是磨损血管上皮的原因，这将暴露基底板糖原，然后促使血小板激活。本研究的目的是使用大鼠模型证实GPIIb/IIIa整合素特异性抗血小板药物可以预防DCS。关于药物对大鼠临床状态的发生率存在显著差异（p = 0.016），与对照大鼠相比，用替罗非班（TIR）治疗的大鼠具有更好的临床结果（p = 0.027），即使使用的三种抗GPIIb/IIIa剂具有有限的呼吸窘迫。TIR限制了高压暴露后血小板计数的下降。TIR有助于防止DCS。TIR对GPIIb/IIIa具有特异性，而依替巴肽和阿昔单抗可抑制与免疫系统通讯的αVβ3和αMβ2。虽然抑制GPIIb/IIIa可以突出血小板依赖性炎症通路，改善DCS的结果，我们想知道是否抑制αVβ3和αMβ2通信是不是一个错误的方法来限制DCS的死亡率。
In its severest forms, decompression sickness (DCS) may extend systemically and/or induce severe neurological deficits, including paralysis or even death. It seems that the sterile and ischemic inflammatory phenomena are consecutive to the reaction of the bubbles with the organism and that the blood platelet activation plays a determinant role in the development of DCS. According to the hypotheses commonly put forward, the bubbles could either activate the platelets by direct contact or be the cause of abrasion of the vascular epithelium, which would expose the basal plate glycogen and then prompt the platelets to activate. The purpose of this study is to confirm anti-platelet drugs specific to GPIIb/IIIa integrin could prevent DCS, using a rat model. There is a significant difference concerning the incidence of the drug on the clinical status of the rats (p = 0.016), with a better clinical outcome for rats treated with tirofiban (TIR) compared with the control rats (p = 0.027), even if the three anti-GPIIb/IIIa agents used have limited respiratory distress. TIR limited the decrease in platelet counts following the hyperbaric exposure. TIR help to prevent from DCS. TIR is specific to GPIIb/IIIa whereas eptifibatide and abciximab could inhibit αVβ3 and αMβ2 involved in communication with the immune system. While inhibiting GPIIb/IIIa could highlight a platelet-dependent inflammatory pathway that improves DCS outcomes, we wonder whether inhibiting the αVβ3 and αMβ2 communications is not a wrong approach for limiting mortality in DCS.
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影响因子：
4.6
作者：
de Maistre S;Vallée N;Gempp E;Lambrechts K;Louge P;Duchamp C;Blatteau JE
通讯作者：
Blatteau JE
影响因子：
20.1
作者：
Bledzka K;Smyth SS;Plow EF
通讯作者：
Plow EF
影响因子：
3.7
作者：
Blatteau, Jean-Eric;Brubakk, Alf O.;Vallee, Nicolas
通讯作者：
Vallee, Nicolas
影响因子：
1.6
作者：
Harifi G;Sibilia J
通讯作者：
Sibilia J
影响因子：
1.5
作者：
Gempp, Emmanuel;Lacroix, Guillaume;Louge, Pierre
通讯作者：
Louge, Pierre