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首页> 外文期刊>Undersea and Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society >Structural alterations in adult rat carotid bodies exposed to hyperbaric oxygenation.
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Structural alterations in adult rat carotid bodies exposed to hyperbaric oxygenation.

机译：在成年大鼠颈动脉体结构更改暴露于高压氧化。

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摘要

Inhibition of carotid body (CB) function is the main mechanism involved in the attenuation of respiratory drive observed during hyperoxia. However, only a few studies at 5.0 atmospheres absolutes (ATA) have analyzed carotid body structure or function in hyperbaric oxygenation (HBO2) situations. We hypothesized that rats will present CB structural alterations when exposed to different lower hyperbaric oxygen doses enough to alter their chemosensory response to hypoxia. METHODS: Twenty-one adult male Wistar rats, divided into three groups, were maintained in room air or exposed to O2 at 2.4 or 3.0 ATA for six hours. Histological, ultrastructural and immunohistochemical analyses for neuronal nitric oxide synthase (nNOS) and F2-isoprostane were performed in the excised CBs. RESULTS: Histological analyses revealed signs of intracellular edema in animals exposed to both conditions, but this was more marked in the 3.0 ATA group, which showed ultrastructural alterations at the mitochondrial level. There was a significant increase in the volume density of intraglomic-congested capillaries in the 3.0 ATA group associated with an arteriolar vasoconstriction. In the 2.4 ATA group, there was a relative increase of glomic light cells and a decrease of glomic progenitor cells. Additionally, there was a stronger immunoreactivity for F2-isoprostane in the 3.0 ATA O2-exposed carotid bodies. The glomic cells stained positive for nNOS, but no difference was observed between the groups. Our results show that high O2 exposures may induce structural alterations in glomic cells with signs of lipid peroxidation. We further suggest that deviation of blood flow toward intraglomic capillaries occurs in hyperbaric hyperoxia.
机译：抑制颈动脉体(CB)函数主要参与的衰减机制呼吸驱动氧过多期间观察到的。然而,只有少数研究5.0大气压绝对(ATA)颈动脉体分析在高压氧化结构或功能(HBO2)的情况。当暴露在目前CB结构更改不同的低剂量高压氧足以改变他们的化学感觉的对缺氧的反应。方法:21岁成年雄性Wistar鼠分为三组,保存房间空气或暴露在2.4或3.0 ATA O26个小时。免疫组织化学分析神经元氮氧化合成酶(nNOS)和F2-isoprostane在切除哥伦比亚广播公司(CBs)执行的。组织学分析显示的迹象细胞内水肿动物接触条件,但这是在3.0更明显ATA集团表明超微结构在线粒体水平变化。体积密度的显著增加3.0 ATA intraglomic-congested毛细血管组与小动脉的有关血管收缩。glomic光细胞的相对增加减少glomic祖细胞。此外,有一个更强免疫反应性的F2-isoprostane 3.0ATA O2-exposed颈动脉的身体。nNOS呈阳性,但没有差异观察两组之间。高氧暴露可能引起结构改变glomic细胞脂质的迹象过氧化反应。向intraglomic毛细血管血流量发生在高压氧过多。

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