Effect of elastase-induced emphysema on the force-generating ability of the diaphragm.
Effect of elastase-induced emphysema on the force-generating ability of the diaphragm.
复制标题
弹性蛋白酶诱导的肺气肿对膈肌产生力的能力的影响。
DOI：
10.1172/jci110709
复制
发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Kelsen,SG
中科院分区：
文献类型：
--
作者：
Supinski,GS;Kelsen,SG
肺气肿对横膈膜产生力的能力的影响是在10只金黄色仓鼠的肋横膈膜肌条中检查的，这些仓鼠在腹膜内注射胰腺弹性蛋白酶后18个月被杀死，该剂量产生过度充气（平均总肺容量[TLC] =对照的163%）和全身性全腺泡肺气肿。13只注射生理盐水的正常动物作为对照。等长张力的时间过程和肌纤维和肌节长度的变化对强直电刺激产生的等长张力（T）的影响（长度-张力[L-T]关系）进行了检查。给予弹性蛋白酶会导致原位测量的横隔肌厚度增加和肋横隔肌纤维长度减少。由于肥大，肺气肿显着增加了最大强直张力。然而，肺气肿（E）和对照（C）动物中，针对肌肉横截面积（T/cm 2）增加校正的最大张力相同。肺气肿也改变了横膈膜的肌纤维L-T曲线，但控制肌肉比目鱼肌的L-T曲线却没有变短。与E对膈肌纤维L-T曲线的影响相反，E和C的肌节L-T曲线相同。由于张力最大时的长度与肌节数密切相关（r= 0.94;P< 0.001），肺气肿动物肌肉中串联肌节数的减少似乎可以解释肌纤维L-T曲线的移动。我们的结论是，在弹性蛋白酶诱导的肺气肿适应性的变化，在隔膜的横截面积和肌节数增加的力量产生能力的隔膜。我们推测，肌节数量的变化补偿了胸部慢性过度充气导致的肌纤维长度的改变，而膈肌肥大代表了对呼吸负荷和/或膈肌构型变化的反应（拉普拉斯关系）。图片
The effect of emphysema on the ability of the diaphragm to generate force was examined in costal diaphragm muscle strips from 10 Golden hamsters killed 18 mo after intratracheal injection of pancreatic elastase in a dose producing hyperinflation (mean total lung capacity [TLC] = 163% of control) and generalized panacinar emphysema. 13 saline-injected normal animals served as controls. The time course of isometric tension and the effect of alterations in muscle fiber and sarcomere length on the isometric tension (T) generated in response to tetanizing electrical stimuli (length-tension [L-T] relationship) were examined. Elastase administration caused an increase in diaphragm muscle thickness and reduction in the length of costal diaphragm muscle fibers measuredin situ.Emphysema significantly increased the maximum tetanic tension as a result of hypertrophy. Maximal tension corrected for increases in muscle cross-sectional area (T/cm2), however, was the same in emphysematous (E) and control (C) animals. Emphysema also shifted the muscle fiber L-T curve of the diaphragm but not of a control muscle, the soleus, toward shorter lengths. In contrast to the effects of E on the diaphragm muscle fiber L-T curve, the sarcomere L-T curve was the same in E and C. Since the length at which tension was maximal correlated closely with sarcomere number (r= 0.94;P< 0.001) reduction in the number of sarcomeres in series in muscles from emphysematous animals appeared to explain the shift in the muscle fiber L-T curve. We conclude that in elastase-induced emphysema adaptive changes both in diaphragm cross-sectional area and sarcomere number augment the force-generating ability of the diaphragm. We speculate that changes in sarcomere number compensate for alterations in muscle fiber length resulting from chronic hyperinflation of the thorax, while diaphragmatic muscle hypertrophy represents a response to changes in respiratory load and/or diaphragm configuration (LaPlace relationship).Images