Pulmonary perfusion heterogeneity is increased by sustained, heavy exercise in humans
Pulmonary perfusion heterogeneity is increased by sustained, heavy exercise in humans
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DOI：
10.1152/japplphysiol.00491.2009
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发表时间：
2009-11-01
影响因子：
3.3
通讯作者：
Hopkins, S. R.
中科院分区：
文献类型：
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作者：
Burnham, K. J.;Arai, T. J.;Hopkins, S. R.
Burnham KJ、Arai TJ、Dubowitz DJ、Henderson AC、Holverda S、Buxton RB、Prisk GK、Hopkins SR。人类持续的剧烈运动会增加肺灌注的不均匀性。 J Appl Physiol 107: 1559-1568, 2009。首次发表于 2009 年 9 月 10 日； doi:10.1152/japplphyol.00491.2009.-运动会给肺系统带来相当大的压力，并且通气-灌注（(V) 超过 dotA/(Q) 超过 dot）异质性随着运动而增加，影响气体交换的效率。特别是，已知长时间的剧烈运动和最大运动会增加 (V) 超过 dotA/(Q) 超过 dot 异质性，并且这些变化持续到恢复。我们假设长时间运动后肺灌注的空间异质性也会同样升高。为了测试这一点，运动受试者（n = 6，(V) over dotO(2max) = 61 ml.kg(-1).min(-1)）在之前通过多重惰性气体消除技术 (MIGET) 表征的 (V) over dotA/(Q) over dot 异质性上进行了 45 分钟的循环运动，强度类似于 70% (V) over dotO(2max)。在运动前和运动后（运动后 20、40、60 分钟）获取肺灌注的 MRI 动脉自旋标记测量值，以量化等重力（冠状）和重力依赖（矢状）平面的空间分布。区域质子密度测量允许灌注密度标准化并以毫升每分钟每克量化。运动后任一平面的平均肺密度均无显着变化（P = 0.19）。运动后矢状面的密度归一化灌注增加（P = 0.18），可能是由于灌注重新分布和血管募集。运动后冠状面的密度归一化灌注没有变化 (P = 0.66)，然而，通过相对离散度 [RD，运动前 0.62(0.07)，运动后 0.82(0.21)，P < 0.0001] 和几何标准差 [GSD，运动前 1.74(0.14)，运动后] 测量，灌注异质性显着增加。 2.30（0.56），P <0.005]。这些异质性变化与运动引起的通气分布对数标准差的变化有关，MIGET 指数为 (V) 超过 dotA/(Q) 超过点异质性（R R-2 = 0.68，P < 0.05，GSD，R-2 = 0.55，P = 0.09）。这些数据与间质性肺水肿一致，但不能证明其是运动引起的空间灌注异质性和（V）点A/（Q）点异质性增加的机制。
Burnham KJ, Arai TJ, Dubowitz DJ, Henderson AC, Holverda S, Buxton RB, Prisk GK, Hopkins SR. Pulmonary perfusion heterogeneity is increased by sustained, heavy exercise in humans. J Appl Physiol 107: 1559-1568, 2009. First published September 10, 2009; doi:10.1152/japplphysiol.00491.2009.-Exercise presents a considerable stress to the pulmonary system and ventilation-perfusion ((V) over dotA/(Q) over dot) heterogeneity increases with exercise, affecting the efficiency of gas exchange. In particular, prolonged heavy exercise and maximal exercise are known to increase (V) over dotA/(Q) over dot heterogeneity and these changes persist into recovery. We hypothesized that the spatial heterogeneity of pulmonary perfusion would be similarly elevated after prolonged exercise. To test this, athletic subjects (n = 6, (V) over dotO(2max) = 61 ml.kg(-1).min(-1)) with exercising (V) over dotA/(Q) over dot heterogeneity previously characterized by the multiple inert gas elimination technique (MIGET), performed 45 min of cycle exercise at similar to 70% (V) over dotO(2max). MRI arterial spin labeling measures of pulmonary perfusion were acquired pre- and postexercise (at 20, 40, 60 min post) to quantify the spatial distribution in isogravitational (coronal) and gravitationally dependent (sagittal) planes. Regional proton density measurements allowed perfusion to be normalized for density and quantified in milliliters per minute per gram. Mean lung density did not change significantly in either plane after exercise (P = 0.19). Density-normalized perfusion increased in the sagittal plane postexercise (P = 0.18), likely because of perfusion redistribution and vascular recruitment. Density-normalized perfusion was unchanged in the coronal plane postexercise (P = 0.66), however, perfusion heterogeneity was significantly increased as measured by the relative dispersion [RD, pre 0.62(0.07), post 0.82(0.21), P < 0.0001] and geometric standard deviation [GSD, pre 1.74(0.14), post 2.30(0.56), P < 0.005]. These changes in heterogeneity were related to the exercise-induced changes of the log standard deviation of the ventilation distribution, an MIGET index of (V) over dotA/(Q) over dot heterogeneity (RD R-2 = 0.68, P < 0.05, GSD, R-2 = 0.55, P = 0.09). These data are consistent with but not proof of interstitial pulmonary edema as the mechanism underlying exercise-induced increases in both spatial perfusion heterogeneity and (V) over dotA/(Q) over dot heterogeneity.