Ohe M, Mimata T, Haneda T, Takishima T
Respir Physiol. 1986 Feb;63(2):177-86. doi: 10.1016/0034-5687(86)90112-x.
To examine the effect of hypoxia on pulmonary vascular smooth muscle, rabbit lobar pulmonary artery was suspended in a glucose free solution and both chronologic changes in tension and ATP content were determined together at 30 min intervals after repeated hypoxic challenge (PO2 = 11 +/- 2 mm Hg). The pulmonary artery contracted and its ATP content decreased with hypoxia. This contraction was not inhibited by nifedipine, Ca++ -free EGTA, procaine, phentolamine, isoproterenol, diphenhydramine, prostaglandin E1, atropine or nitroglycerin. Upon reoxygenation (PO2 = 104 +/- 3 mm Hg), the elevated resting tension decreased in a biphasic fashion and the ATP content of the lobar pulmonary artery increased. When hypoxic challenges were repeated, the rate of constriction on hypoxia increased, while the relaxation rate on reoxygenation, tension developed by 30 min of hypoxia and the total amount of ATP decreased. These results suggest that the ATP content in the lobar pulmonary artery is very sensitive to in vitro acute hypoxia and that the Ca++ transport process is more easily impaired by reduction in ATP levels than is the contractile machinery.
为研究缺氧对肺血管平滑肌的影响,将兔叶肺动脉悬于无糖溶液中,在反复缺氧刺激(PO2 = 11±2 mmHg)后每隔30分钟同时测定张力的时间变化和ATP含量。随着缺氧,肺动脉收缩,其ATP含量降低。硝苯地平、无钙EGTA、普鲁卡因、酚妥拉明、异丙肾上腺素、苯海拉明、前列腺素E1、阿托品或硝酸甘油均不能抑制这种收缩。复氧(PO2 = 104±3 mmHg)后,升高的静息张力呈双相下降,叶肺动脉的ATP含量增加。当重复缺氧刺激时,缺氧时的收缩速率增加,而复氧时的舒张速率、缺氧30分钟时产生的张力和ATP总量均降低。这些结果表明,叶肺动脉中的ATP含量对体外急性缺氧非常敏感,并且与收缩机制相比,ATP水平降低更容易损害Ca++转运过程。