PULMONARY VENTILATION AND MECHANICS IN MORBIDLY OBESE ZUCKER RATS
PULMONARY VENTILATION AND MECHANICS IN MORBIDLY OBESE ZUCKER RATS
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DOI：
10.1164/ajrccm.150.2.8049815
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发表时间：
1994-08-01
影响因子：
24.7
通讯作者：
SCHLENKER, EH
中科院分区：
文献类型：
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作者：
FARKAS, GA;SCHLENKER, EH
肥胖的Zucker大鼠是肥胖的常染色体遗传模型，代表了相对较早发病的人类肥胖的良好模型。虽然与新陈代谢和体温调节相关的因素在这些动物中已经得到了广泛的研究，但肺力学和通气性尚未被记录在案，也没有形成本研究的基础。研究人员对16只肥胖和18只瘦弱雌性仔猪进行了研究(698+/-79vs304+/-24g，p<；0.001)。在仰卧位麻醉的动物中评估肺功能，包括肺容量和呼吸系统顺应性。除残气量外，所有其他肺容量，包括功能残气量、总肺活量、呼气储备量和吸气量，在肥胖组与瘦子组相比均显著降低(p<；0.05或更高)。还测定了完整呼吸系统和切除肺的压力-容量关系。虽然两种表型的肺顺应性相似，但肥胖大鼠的呼吸系统顺应性显著降低(0.85+/-0.06比0.67+/-0.09ml/cmH2O，p<；0.01)。呼吸室内空气表型的耗氧量和呼吸机参数(包括呼吸频率、潮气量、分钟通气量、吸气时间和呼气时间)相似，两组对低氧反应的分钟通气量相似。与此形成鲜明对比的是，肥胖动物对高碳酸血症的呼吸反应迟钝(221+/-38对135+/-44毫升/分钟，p<；0.01)。总而言之，这项研究中确定的许多观察结果在定性上类似于先前在病态肥胖人类受试者中描述的观察结果，因此肥胖的Zucker大鼠可能被证明是人类受试者单纯性肥胖的有用动物模型。
The obese Zucker rat, an autosomally genetic model of obesity, represents a good model of relatively early onset human obesity. Although factors associated with the control of metabolism and thermoregulation have been studied extensively in these animals, pulmonary mechanics and ventilation have not been documented and form the basis of this investigation. Studies were carried out in 16 obese and 18 lean female littermates (698 +/- 79 versus 304 +/- 24 g, p < 0.001). Pulmonary function, including lung volumes and respiratory system compliance, was evaluated in supine anesthetized animals. With the exception of residual volume, all other lung volumes, including function residual capacity, total lung capacity, expiratory reserve volume, and inspiratory capacity, were significantly reduced (p < 0.05 or better) in the obese phenotype compared with volumes in the lean littermates. Pressure-volume relationships of the intact respiratory system and the excised lung were also determined. Although lung compliance was similar between the phenotypes, respiratory system compliance was significantly lower (0.85 +/- 0.06 versus 0.67 +/- 0.09 ml/cm H2O, p < 0.01) in the obese rats. Oxygen consumption and ventilatory parameters (including respiratory rate, tidal volume, minute ventilation, inspiratory time, and expiratory time) were similar between phenotypes breathing room air, and the minute ventilation in response to hypoxia was similar in both groups. In marked contrast, obese animals exhibited a blunted ventilatory response to hypercapnia (221 +/- 38 versus 135 +/- 44 ml/min, p < 0.01). In conclusion, many of the observations determined in this study are qualitatively similar to those previously described in morbidly obese human subjects, and therefore the obese Zucker rat may prove to be a useful animal model of simple obesity in human subjects.