Obstructive apnea causes microvascular perfusion maldistribution in the lungs of rats.

Obstructive apnea causes microvascular perfusion maldistribution in the lungs of rats.
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阻塞性呼吸暂停导致大鼠肺部微血管灌注分布不良。

DOI:
10.1152/ajpregu.00243.2018
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发表时间:
2019
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
Teodorescu,Mihaela
Teodorescu,Mihaela
中科院分区:
--
文献类型:
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作者:
Conhaim,RobertL;Watson,KalE;Teodorescu,Mihaela

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阻塞性睡眠呼吸暂停(OSA)与显著的心血管后果相关,包括肺动脉高压,但对其对肺微血管灌注的影响知之甚少。为了研究阻塞性睡眠呼吸暂停对肺微血管灌注的影响,我们夹闭麻醉的自主呼吸大鼠的气管插管以模拟阻塞性呼吸暂停。夹子保持在原位10次呼吸,然后松开,让动物再次自主呼吸。我们每20秒重复一次该方案,直到大鼠经历总共5次呼吸暂停发作,每次10次呼吸。然后,我们将108个荧光乳胶颗粒(直径4 μm)注入股静脉,这些颗粒被困在肺微循环中。我们取出肺,使其风干,并使用分散指数(DI)分析(我们以前开发的一种方法)量化肺切片中的颗粒分布。DI的对数(logDI)是灌注分布不均的量度。较大的log(DI)值对应于较大的分布不均。呼吸暂停肺的平均logDI值为1.28(SD 0.24)。未发生呼吸暂停的大鼠的平均logDI值为0.85(SD 0.08)(P≤ 0.05)。在呼吸暂停后10分钟或24小时接受乳胶颗粒的大鼠的平均logDI值分别为0.97(SD 0.31)和0.84(SD 0.38)(不显著)。我们的研究结果表明,第一次,一些呼吸暂停事件产生显着的,但暂时的,肺微循环内的灌注分布不均。睡眠呼吸暂停在几个月和几年内的重复夜间发作可以解释为什么OSA患者比没有OSA的人患心血管疾病的程度要高。
Obstructive sleep apnea (OSA) is associated with significant cardiovascular consequences, including pulmonary hypertension, yet little is known about its effects on pulmonary microvascular perfusion. To investigate effects of OSA on pulmonary microvascular perfusion, we clamped the tracheal cannulas of anesthetized, spontaneously breathing rats to simulate obstructive apnea. The clamp remained in place for 10 breaths before it was released to allow the animals to again breathe spontaneously. We repeated this protocol every 20 s until the rat experienced a total of five apneic episodes of 10 breaths each. We then infused into a femoral vein 108fluorescent latex particles (4 µm diameter), which became trapped within the pulmonary microcirculation. We removed the lungs, allowed them to air-dry, and quantified the particle distributions in sections of the lungs using dispersion index (DI) analysis, a method we developed previously. The log of the DI (logDI) is a measure of perfusion maldistribution. Greater log(DI) values correspond to greater maldistribution. Apneic lungs had average logDI values of 1.28 (SD 0.24). Rats not subjected to apnea had average logDI values of 0.85 (SD 0.08) (P≤ 0.05). Rats that received latex particles 10 min or 24 h after apnea had average logDI values of 0.97 (SD 0.31) and 0.84  (SD 0.38), respectively (not significant). Our results demonstrate, for the first time, that a few apneic events produced significant, but temporary, perfusion maldistribution within the pulmonary microcirculation. Repeated nightly episodes of apnea over months and years may explain why human patients with OSA suffer from significantly greater cardiovascular disease than those without OSA.