Ivanova T N, Poliakova E D, Ivanov A I
Vopr Med Khim. 1990 Nov-Dec;36(6):28-32.
Activity of lysosomal enzymes and lipid peroxidation as well as effects of dibutyryl-cAMP and isoproterenol, which increased the intracellular content of cAMP, on the state of lysosomal membranes were studied in isolated perfused rat heart under conditions of reversible ischemia and subsequent reperfusion. The ischemia and especially postischemic reperfusion led to activation of acid hydrolases in sarcoplasmic reticulum and of lipid peroxidation: content of malonic dialdehyde was increased in heart tissue. Addition of dibutyryl-cAMP or isoproterenol into the perfusion solution at concentrations not affecting the heart systole caused a decrease in activity of lysosomal enzymes in sarcoplasm as well as in the rate of lipid peroxidation. A decrease in the lysosomal membranes lability and in the rate of lipid peroxidation appear to prevent the irreversible impairments of cardiomyocytes in ischemia particularly within the first minutes of postischemic reperfusion. Possible mechanisms of lysosomal membranes stabilization under conditions of reversible ischemia and postischemic reperfusion are discussed.
在可逆性缺血及随后再灌注的条件下,研究了离体灌流大鼠心脏中溶酶体酶活性、脂质过氧化作用,以及增加细胞内cAMP含量的二丁酰-cAMP和异丙肾上腺素对溶酶体膜状态的影响。缺血尤其是缺血后再灌注导致肌浆网中酸性水解酶活化及脂质过氧化作用:心脏组织中丙二醛含量增加。在不影响心脏收缩的浓度下,向灌流液中加入二丁酰-cAMP或异丙肾上腺素,可使肌浆中溶酶体酶活性及脂质过氧化速率降低。溶酶体膜稳定性降低和脂质过氧化速率降低似乎可预防缺血时心肌细胞的不可逆损伤,尤其是在缺血后再灌注的最初几分钟内。讨论了可逆性缺血和缺血后再灌注条件下溶酶体膜稳定的可能机制。