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首页> 外文期刊>Physiological Reports >Apnea causes microvascular perfusion maldistribution in isolated rat lungs
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Apnea causes microvascular perfusion maldistribution in isolated rat lungs

机译：呼吸暂停会导致离体大鼠肺微血管灌注异常

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Obstructive sleep apnea is associated with significant cardiovascular disease, yet little is known about the effects of OSA on pulmonary microvascular perfusion. In a recent report, we showed that pulmonary microvascular perfusion was significantly mal‐distributed in anesthetized, spontaneously breathing rats exposed to five episodes of obstructive apnea. We quantified microvascular perfusion by analyzing trapping patterns of 4? μ m diameter fluorescent latex particles infused into the pulmonary circulation after the last episode. We could not determine if the perfusion maldistribution was due to the effects of large subatmospheric intrapleural pressures during apnea, or to precapillary OSA hypoxic vasoconstriction. To address this, we repeated these studies using isolated, buffer‐perfused rat lungs ( P pulm art , 10?cm H 2 O) ventilated in a chamber (?5 to ?15?cm H 2 O, 25?breaths/min; P trachea ?=?0). We simulated apnea by clamping the trachea and cycling the chamber pressures between ?25 and ?35?cm H 2 O for five breaths. After five apnea episodes, we infused 4? μ m diam. fluorescent latex particles into the pulmonary artery. The number of particles recovered from the venous effluent was 74% greater in nonapneic isolated lungs compared to apneic lungs ( P ?≤?0.05). Apneic lungs also had perfusion maldistributions that were 73% greater than those without apnea ( P ?≤?0.05). We conclude that simulated apnea in isolated, perfused rat lungs produces significantly greater particle trapping and microvascular perfusion maldistribution than in nonapneic isolated lungs. We believe these effects are due to the large, negative intrapleural pressures produced during apnea, and are not due to hypoxia.
机译：阻塞性睡眠呼吸暂停与严重的心血管疾病有关，但对OSA对肺微血管灌注的影响知之甚少。在最近的一份报告中，我们发现暴露于五次阻塞性呼吸暂停的麻醉，自发呼吸的大鼠中肺微血管灌注明显分布不均。我们通过分析4？的捕获模式来量化微血管灌注。最后一次发作后，将直径为μm的荧光乳胶颗粒注入肺循环。我们无法确定灌注不均是由于呼吸暂停期间大气压下胸膜内压的作用还是毛细血管前OSA缺氧性血管收缩所致。为了解决这个问题，我们使用隔离的，缓冲液灌注的大鼠肺（P纸艺术，10？cm H 2 O）在一个小室中通风（？5至？15？cm H 2 O，每分钟呼吸25次）进行重复这些研究。 P气管θ＝θ0）。我们通过夹住气管并使腔室压力在？25和？35？cm H 2 O之间循环五次呼吸来模拟呼吸暂停。在发生五次呼吸暂停事件后，我们输注了4次？直径μm荧光乳胶颗粒进入肺动脉。在非窒息性隔离肺中，从静脉流出物中回收的颗粒数量比窒息性肺高74％（P≤≤0.05）。呼吸暂停肺部的灌注分布不均比无呼吸暂停者高73％（P≤0.05）。我们得出的结论是，与非窒息性分离肺相比，离体，灌注大鼠肺中的模拟呼吸暂停产生的颗粒捕集和微血管灌注分布不均明显更大。我们认为这些影响是由于呼吸暂停期间产生的较大的负胸膜内压所致，而不是由于低氧所致。

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