Chiappe de Mon L E, Chiappe de Cingolani G E, Cingolani H E
Arch Int Physiol Biochim. 1978 May;86(2):277-87. doi: 10.3109/13813457809069905.
The effect of acidosis on cAMP-dependent protein kinase activity in perfused hearts from normal and reserpinized rats has been investigated. The results were compared to the effect of acidosis on myocardial contractility under the same conditions. The results showed that acidosis increases the cAMP-dependent protein kinase activity in normal hearts. This increase was abolished when the hearts were depleted of norepinephrine by previous treatment with reserpine. As regards myocardial contractility, there was a similar decrease by acidosis either in normal hearts with increased cAMP-dependent protein kinase activity or in reserpinized hearts in which the increase in protein kinase activity was prevented. Two alternative hypotheses are suggested: (1) a dissociation between contractility and cAMP levels, or (2) a "blockade" by acidosis of the mechanical effect of increasing cAMP-dependent protein kinase activity.
研究了酸中毒对正常大鼠和利血平化大鼠灌注心脏中依赖环磷酸腺苷(cAMP)的蛋白激酶活性的影响。将这些结果与相同条件下酸中毒对心肌收缩性的影响进行了比较。结果表明,酸中毒会增加正常心脏中依赖cAMP的蛋白激酶活性。当通过先前用利血平处理使心脏去甲肾上腺素耗竭时,这种增加就会被消除。至于心肌收缩性,在依赖cAMP的蛋白激酶活性增加的正常心脏或蛋白激酶活性增加被阻止的利血平化心脏中,酸中毒都会导致类似的收缩性降低。提出了两种替代假说:(1)收缩性与cAMP水平之间的解离,或(2)酸中毒对增加依赖cAMP的蛋白激酶活性的机械效应的“阻断”。