Omlor G, Niehaus G D, Maron M B
Department of Pediatrics, Northeastern Ohio Universities College of Medicine, Rootstown 44272.
J Appl Physiol (1985). 1993 Jun;74(6):3068-72. doi: 10.1152/jappl.1993.74.6.3068.
Positive inspiratory pressure- (PIP) ventilated, isolated rat lungs become edematous when perfused at rates approximately the normal cardiac output. The study was conducted to test the hypothesis that high peak inspiratory pressures contribute to the edema development. Five isolated lungs were perfused at a rate of 24.4 +/- 2.2 ml.min-1.100 g body wt-1 with 40% whole blood (diluted with saline containing 4.0 g/100 ml bovine serum albumin) and ventilated with peak pressures ranging from 0 to 20 mmHg. The lungs exhibited edema at PIP values > 9.3 mmHg. The stable pulmonary vascular pressure and resistance suggested that the edema may have resulted from a PIP-induced increase in microvascular permeability. In a second study, the stability of the preparation was evaluated during a 3-h test period. Seven lungs were ventilated at a peak inspiratory pressure of 8.0 mmHg and perfused at 26.8 +- 1.7 ml.min-1 x 100 g body wt-1. Microvascular integrity was maintained for approximately 2 h as indicated by filtration coefficient measurements of 0.175 +/- 0.068, 0.197 +/- 0.066, and 0.169 +/- 0.067 g.min-1 x mmHg-1 x 100 g-1 at 25, 70, and 115 min, respectively, after initiation of the study. The results suggest that isolated rat lungs perfused at rates that parallel normal rat cardiac output and ventilated at low peak inspiratory pressures provide a viable mechanism for evaluation of the pathophysiology of microvascular injury.
当以大约正常心输出量的速率进行灌注时，接受正压吸气压力（PIP）通气的离体大鼠肺会出现水肿。本研究旨在检验高峰吸气压力会促使水肿形成这一假说。五只离体肺以24.4±2.2毫升·分钟⁻¹·100克体重⁻¹的速率用40%全血（用含4.0克/100毫升牛血清白蛋白的盐水稀释）进行灌注，并用0至20毫米汞柱的峰值压力进行通气。当PIP值>9.3毫米汞柱时，肺出现水肿。稳定的肺血管压力和阻力表明，水肿可能是由PIP引起的微血管通透性增加所致。在第二项研究中，在3小时的测试期内评估了制备物的稳定性。七只肺在8.0毫米汞柱的高峰吸气压力下进行通气，并以26.8±1.7毫升·分钟⁻¹·100克体重⁻¹的速率进行灌注。研究开始后，分别在25、70和115分钟时，滤过系数测量值为0.175±0.068、0.197±0.066和0.169±0.067克·分钟⁻¹·毫米汞柱⁻¹·100克⁻¹，这表明微血管完整性维持了约2小时。结果表明，以与正常大鼠心输出量相当的速率进行灌注并在低高峰吸气压力下进行通气的离体大鼠肺，为评估微血管损伤的病理生理学提供了一种可行的机制。
