Itzkowitz D, Mor L, Bomzon A, Oliven A
Department of Internal Medicine B, Bnai-Zion Medical Center, Haifa, Israel.
Biochem Mol Biol Int. 1994 Nov;34(5):1011-6.
Pulmonary emphysema would be expected to reduce angiotensin converting enzyme (ACE) activity due to diminished capillary bed. However, transpulmonary angiotensin conversion has been found to be unaffected or marginally reduced in emphysema. In the present study we examined the activity of ACE in an experimental model of emphysema. Vmax and Km of ACE were determined in lung homogenates of six hamsters with elastase-induced emphysema and seven control hamsters. In the emphysematous lungs, ACE activity was significantly elevated due to marked increase in Vmax (19.2 +/- 1.7 vs. 4.9 +/- 1.6 nmol/min/mg protein for emphysematous and control lungs, P < 0.01). The Km of ACE was unaffected by emphysema. We suggest that the increase in ACE activity may be an adaptive change to enable adequate metabolic activity in the face of progressive reduction in pulmonary capillary surface area in emphysema.
由于毛细血管床减少，预计肺气肿会降低血管紧张素转换酶（ACE）的活性。然而，已发现经肺血管紧张素转换在肺气肿中未受影响或略有降低。在本研究中，我们在肺气肿实验模型中检测了ACE的活性。测定了六只患有弹性蛋白酶诱导性肺气肿的仓鼠和七只对照仓鼠肺匀浆中ACE的Vmax和Km。在肺气肿肺中，由于Vmax显著增加，ACE活性显著升高（肺气肿肺和对照肺分别为19.2±1.7与4.9±1.6 nmol/min/mg蛋白质，P<0.01）。ACE的Km不受肺气肿影响。我们认为，ACE活性增加可能是一种适应性变化，以便在肺气肿患者肺毛细血管表面积逐渐减少的情况下仍能保持足够的代谢活性。
