Broccard A F, Shapiro R S, Schmitz L L, Ravenscraft S A, Marini J J
Department of Pulmonary and Critical Care Medicine, University of Minnesota, St. Paul-Ramsey Medical Center 55191-2595, USA.
Crit Care Med. 1997 Jan;25(1):16-27. doi: 10.1097/00003246-199701000-00007.
To evaluate the influence of body position on the extent and distribution of experimental lung damage in an oleic acid canine model of acute respiratory distress syndrome, using mechanical ventilation with high tidal volumes and positive end-expiratory pressure (PEEP).
Prospective, randomized study.
Experimental animal laboratory.
Twelve anesthetized and paralyzed dogs.
Ninety minutes after lung injury was induced by injection of oleic acid, 12 animals were randomized to be ventilated for 4 hrs, in either the supine (supine group, n = 6) or prone (prone group, n = 6) positions, using the same ventilatory pattern (F10(2) 0.6, PEEP > or = 10 cm H2O, and a tidal volume that generated a peak transpulmonary pressure of 35 cm H2O when implemented in the supine position). Regardless of randomization to position, the tidal volumes, F10(2), and PEEP were kept constant and the pulmonary artery occlusion pressure was maintained between 4 and 6 mm Hg for the duration of the study.
At the end of the protocol, the lungs were excised for gravimetric determination (wet/dry weight ratio) and histologic examination (histologic score). Changes over time in the static pressure-volume curve of the lungs (obtained in the supine position) were also used as end-point variables. At baseline, hemodynamic and respiratory variables did not differ between groups. Just before randomization to position (90 mins after oleic acid injection), both groups presented similar lung static pressure-volume curves. Pulmonary artery occlusion pressure (4.3 +/- 1.9 vs. 4.8 +/- 1.3 mm Hg [supine vs. prone group]), cardiac output (4.1 +/- 0.4 vs. 5.2 +/- 1.3 L/min [supine vs. prone group]), and venous admixture (36.7 +/- 20.7% vs. 28.3 +/- 19.4% [supine vs. prone group]) were also not significantly (p > .05) different when measured in the supine position. At the end of the experiment, lung gravimetric data in the two experimental groups were not statistically different, suggesting a similar extent of edema. Histologic abnormalities, however, were less in the prone group than in the supine group (p < .01), due primarily to marked differences in extent and severity in the dependent regions of the lungs. Static lung compliance improved over time in the prone group (34 +/- 9 to 46 +/- 19 mL/cm H2O)(p = .02), but not in the supine group (34 +/- 6 to 36 +/- 6 mL/cm H2O).
After oleic acid-induced lung injury, animals ventilated with high tidal volume and PEEP undergo less extensive histologic change in the prone position than in the supine position. The prone position alters the distribution of histologic abnormalities.
在使用高潮气量和呼气末正压（PEEP）进行机械通气的油酸诱导的犬急性呼吸窘迫综合征模型中，评估体位对实验性肺损伤范围和分布的影响。
前瞻性随机研究。
实验动物实验室。
12只麻醉并麻痹的犬。
在注射油酸诱导肺损伤90分钟后，12只动物被随机分为两组，分别采用相同的通气模式（F10(2) 0.6，PEEP≥10 cm H2O，在仰卧位时潮气量产生的跨肺压峰值为35 cm H2O），在仰卧位（仰卧组，n = 6）或俯卧位（俯卧组，n = 6）通气4小时。无论随机分配到何种体位，在研究期间潮气量、F10(2)和PEEP保持恒定，肺动脉闭塞压维持在4至6 mmHg之间。
实验结束时，切除肺组织进行重量测定（湿/干重比）和组织学检查（组织学评分）。肺静态压力-容积曲线随时间的变化（在仰卧位获得）也用作终点变量。基线时，两组的血流动力学和呼吸变量无差异。在随机分配体位前（注射油酸后90分钟），两组的肺静态压力-容积曲线相似。仰卧位测量时，肺动脉闭塞压（仰卧组4.3±1.9 vs. 俯卧组4.8±1.3 mmHg）、心输出量（仰卧组4.1±0.4 vs.俯卧组5.2±1.3 L/min）和静脉混合血（仰卧组36.7±20.7% vs.俯卧组28.3±19.4%）也无显著差异（p>.05）。实验结束时，两个实验组的肺重量数据无统计学差异，提示水肿程度相似。然而，俯卧组的组织学异常比仰卧组少（p<.01），主要是由于肺依赖区的范围和严重程度存在显著差异。俯卧组肺静态顺应性随时间改善（34±9至46±19 mL/cm H2O）（p =.02），而仰卧组无改善（34±6至36±6 mL/cm H2O）。
油酸诱导肺损伤后，采用高潮气量和PEEP通气的动物，俯卧位时的组织学改变比仰卧位时少。俯卧位改变了组织学异常的分布。
