Zhang S, Yang J H, Yu F, Zhao J, Jiang P, Chang L, Tang C, Xu J
National Laboratory of Biomacromolecule, Center for Molecular Biology, Institute of Biophysics, Chinese Academy of Science, Beijing, China.
Transplant Proc. 2006 Jun;38(5):1247-52. doi: 10.1016/j.transproceed.2006.02.061.
Cardiac ischemia/reperfusion (I/R) injury, a necessary consequence of transplantation, is probably related to the formation of reactive oxygen species (ROS). The ROS burst within the first moments of reperfusion is associated with injury, continuously generate O2- at about 3% to 5% of total O2 consumption owing to electron leak by mitochondrial oxidoreductases, especially complexes I and III. 3-nitro-N-methyl-salicylamide (NNMS) displays inhibitory effects on succinate-cytochrome C reductase, but also reduces effects on creation of O2- radical and H2O2 by isolated rat mitochondria. Presumably NNMS inhibits electron leakage from the mitochondrial respiratory chain. We investigated effect of NNMS on heart protection after hypothermic ischemia.
A Langendorff-prepared rat heart model was employed after the heart had been preserved for 4 hours under hypothermic conditions of ischemia with subsequent reperfusion/rewarming for 60 minutes.
The group of hearts treated with NNMS showed increased recovery of heart function compared with a group of mEC. The lactate dehydrogenase (LDH) activity in coronary flow (CF) by hearts treated with NNMS was lower than that with mECs, as was the content of malonedialdehyde (MDA) and conjugated diene (CD).
NNMS improved heart physiology after reperfusion following 4 hours of hypothermic ischemia.
心脏缺血/再灌注（I/R）损伤是移植的必然结果，可能与活性氧（ROS）的形成有关。再灌注最初时刻的ROS爆发与损伤相关，由于线粒体氧化还原酶尤其是复合物I和III的电子泄漏，在线粒体总耗氧量的约3%至5%时持续产生超氧阴离子（O2-）。3-硝基-N-甲基水杨酰胺（NNMS）对琥珀酸-细胞色素C还原酶有抑制作用，同时也降低离体大鼠线粒体产生超氧阴离子自由基和过氧化氢（H2O2）的作用。据推测，NNMS抑制线粒体呼吸链的电子泄漏。我们研究了NNMS对低温缺血后心脏保护的作用。
采用Langendorff制备的大鼠心脏模型，心脏在低温缺血条件下保存4小时，随后再灌注/复温60分钟。
与mEC组相比，用NNMS处理的心脏组心功能恢复增加。用NNMS处理的心脏的冠状动脉血流（CF）中的乳酸脱氢酶（LDH）活性低于mEC组，丙二醛（MDA）和共轭二烯（CD）的含量也是如此。
NNMS改善了低温缺血4小时后再灌注时的心脏生理功能。
