Point: Exercise-induced intrapulmonary shunting is imaginary.
Point: Exercise-induced intrapulmonary shunting is imaginary.
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观点：运动引起的肺内分流是想象出来的。
DOI：
10.1152/japplphysiol.91489.2008
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Wagner,PeterD
中科院分区：
文献类型：
--
作者：
Hopkins,SusanR;Olfert,IMark;Wagner,PeterD
人类和其他物种的肺气体交换效率都会随着运动而恶化，从而增加肺泡动脉 PO2 差异 (AaDO2)(2)。造成这种情况的潜在因素是通气-灌注不平衡、肺泡-毛细血管扩散限制和分流 (20)。这些已经在不同的运动条件下得到了充分的记录，包括常氧、缺氧和高氧，特别是通过多重惰性气体消除技术（MIGET）（19）。可以测量不同溶解度的惰性气体的肺泡、动脉和混合静脉浓度，并用于量化通气灌注不均、肺泡毛细血管扩散限制（加上任何肺后静脉混合物）和肺内分流。由此，可以确定它们对 AaDO2 的个体贡献 (4, 19)，而肺内分流始终是三者中最不重要的。最近，肺内分流，即混合静脉血通过肺循环而不与肺部通气区域接触的通道 (20)，作为运动气体交换障碍的潜在原因再次引起人们的关注 (3,7,15)。这是因为运动期间的搅动盐水对比超声心动图显示静脉注射微泡的跨肺通道，但在休息时则不然 (3,7,15)。三到五个心动周期后左心房出现微泡被认为是肺内分流的证据。此外，有人认为这些是运动期间肺部气体交换的重要决定因素 (3,7,15)。尽管我们不认为跨肺气泡传播是想象出来的，但我们还是想起了 Theodore Geisel 的《Horton Hears A Who》一书（《苏斯博士》；14）。在这部儿童经典作品中，大象霍顿听到一粒灰尘发出声音，而这片灰尘是被称为“谁”的小居民的家园。这本书强化了“人就是人，无论多小”的道德观念。虽然可以说“分流就是分流，无论多小”，但应该考虑几个重要的点，特别是在评估微泡传输对肺气体交换的影响时。首先，传输的气泡的大小仍然未知，并且有几个假设可能会影响数据的解释，最近在通过未闭卵圆孔检测心内分流的背景下进行了审查（21）。该技术假设在盐水中搅动空气产生的大多数气泡都大于肺毛细血管，因此被肺循环捕获。尽管微泡的大小并不均匀，但运动过程中小于肺毛细血管直径 (10 m) 的气泡被认为在通过肺循环后会降解到如此小的尺寸，以致无法再检测到 (21)。大约 28 年前，使用 M 型超声心动图实验证明了这一点 (10)；然而，这些实验从未使用更灵敏的现代回波技术重复过（21）。因此，在左心检测到的气泡尺寸可能比假设的要小，并且一些气泡可能穿过正常的肺部。
Pulmonary gas exchange efficiency deteriorates with exercise in both humans and other species, increasing the alveolararterial PO2 difference (AaDO2)(2). The potential contributors to this are ventilation-perfusion inequality, alveolar-capillary diffusion limitation, and shunt (20). These have been well documented under varying exercise conditions including normoxia, hypoxia, and hyperoxia, in particular by the multiple inert gas elimination technique (MIGET)(19). Alveolar, arterial, and mixed venous concentrations of inert gases of differing solubility can be measured and used to quantify ventilationperfusion inequality, alveolar-capillary diffusion limitation (plus any post-pulmonary venous admixture), and intrapulmonary shunt. From this, their individual contributions to AaDO2 can be determined (4, 19), and intrapulmonary shunt has consistently been the least important of the three. Recently, intrapulmonary shunting, the passage of mixed venous blood through the pulmonary circulation without contact with ventilated regions of the lung (20), has attracted renewed attention as a potential cause of exercising gas exchange impairment (3, 7, 15). This is because of transpulmonary passage of intravenously injected microbubbles demonstrated by agitated saline contrast echocardiography during exercise, but not at rest (3, 7, 15). The appearance of the microbubbles in the left atrium after three to five cardiac cycles is held as evidence of intrapulmonary shunts. Furthermore, it is suggested that these are important determinants of pulmonary gas exchange during exercise (3, 7, 15). Although we do not think transpulmonary bubble transmission is imaginary, we are reminded of the book Horton Hears A Who by Theodore Geisel (“Dr. Seuss”; 14). In this children’s classic, Horton the Elephant hears a sound from a speck of dust, which is home to tiny inhabitants known as Whos. The book reinforces the moral that “a person’sa person, no matter how small.” While it can be argued that a “shunt is a shunt, no matter how small,” several important points should be considered, especially when evaluating what microbubble transmission implies for exercising pulmonary gas exchange.First, the size of transmitted bubbles remains unknown and there are several assumptions that potentially affect the interpretation of the data, reviewed recently in the context of detecting intracardiac shunting via a patent foramen ovale (21). The technique assumes that most bubbles induced by agitating air in saline are larger than pulmonary capillaries and therefore are trapped by the pulmonary circulation. Although the size of the microbubbles is not uniform, the bubbles that are less than the diameter of a pulmonary capillary during exercise (10 m) are argued to degrade to such a small size after transit through the pulmonary circulation that they are no longer detectable (21). This was shown experimentally some 28 years ago using M-mode echocardiography (10); however, these experiments have never been repeated using more sensitive modern echo techniques (21). Consequently the size of the bubbles detected in the left heart may be smaller than is assumed, and some bubbles may traverse a normal pulmonary