Ventricular hypertrophy blocked delayed anesthetic cardioprotection in rats by alteration of iNOS/COX-2 signaling.
Ventricular hypertrophy blocked delayed anesthetic cardioprotection in rats by alteration of iNOS/COX-2 signaling.
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心室肥大通过改变 iNOS/COX-2 信号传导阻断大鼠延迟麻醉心脏保护作用。
DOI：
10.1038/srep07071
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发表时间：
2014-11-17
影响因子：
4.6
通讯作者：
Sun R
中科院分区：
文献类型：
--
作者：
Ma L;Kong F;Ge H;Liu J;Gong F;Xu L;Hu B;Sun R
本研究的目的是确定心室肥厚是否影响延迟异氟醚预处理对心肌缺血-再灌注（IR）损伤的保护作用。对雄性Sprague-Dawley大鼠进行横向主动脉缩窄（TAC）以诱导左心室（LV）肥大，然后对假手术或肥大大鼠心脏进行异氟烷预处理（2.1% v/v，1 h）。 暴露后24 h，分离心脏并通过Langendorff逆行灌注30 min（平衡），随后缺血40 min，然后再灌注120 min。 检测血流动力学、心肌梗死面积、细胞凋亡、一氧化氮合酶（NOS）、环氧合酶2（考克斯2）、半胱天冬酶3（Caspase 3）活性及NO生成。结果发现，异氟醚延迟预处理可明显改善假手术大鼠再灌注期的血流动力学参数，减少心肌梗死面积和细胞凋亡。然而，在肥厚心脏中未观察到延迟异氟烷预处理诱导的心脏改善。异氟醚延迟预处理可显著增强假手术大鼠海马iNOS、考克斯-2和NO的表达，抑制Caspase-3的活性，而异氟醚预处理的TAC对照组则无此现象。我们的研究结果表明，心室肥厚通过改变iNOS/考克斯-2通路而取消了异氟醚诱导的延迟性心脏保护作用。
The aim of the current study was to determine whether ventricular hypertrophy affects the delayed isoflurane preconditioning against myocardial ischemia-reperfusion (IR) injury. Transverse aortic constriction (TAC) was performed on male Sprague-Dawley rats to induce left ventricular (LV) hypertrophy, then sham-operated or hypertrophied rat hearts were subjected to isoflurane preconditioning (2.1% v/v, 1 h). 24 h after exposure, the hearts were isolated and perfused retrogradely by the Langendorff for 30 min (equilibration) followed by 40 min of ischemia and then 120 min of reperfusion. The hemodynamics, infarct size, apoptosis, nitric oxide synthase (NOS), cyclooxygenase-2 (COX-2), Cleaved Caspase-3 and production of NO were determined. We found that the hemodynamic parameters were all markedly improved during the reperfusion period and the myocardial infarct size and apoptosis was significantly reduced by delayed isoflurane preconditioning in sham-operated rats. However, such cardiac improvement induced by delayed isoflurane preconditioning was not observed in hypertrophied hearts. The expression of iNOS, COX-2 and NO was markedly enhanced, whereas Cleaved Caspase-3 activity was inhibited by delayed isoflurane preconditioning in sham-operated rats, a phenomenon was not found in TAC-control groups pretreated with isoflurane. Our results demonstrated that ventricular hypertrophy abrogated isoflurane-induced delayed cardioprotection by alteration of iNOS/COX-2 pathway.
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DOI：
10.1152/ajpheart.00484.2009
发表时间：
2009-11-01
影响因子：
4.8
作者：
Kupai, Krisztina;Csonka, Csaba;Ferdinandy, Peter
通讯作者：
Ferdinandy, Peter
影响因子：
3.1
作者：
Chen, Chen Hsiu;Chuang, Jiin Haur;Chan, Julie Y. H.
通讯作者：
Chan, Julie Y. H.
影响因子：
9.5
作者：
Tang, XL;Stein, AB;Bolli, R
通讯作者：
Bolli, R
影响因子：
37.8
作者：
EHRING, T;BAUMGART, D;HEUSCH, G
通讯作者：
HEUSCH, G
影响因子：
3.2
作者：
Labat-Moleur, F;Guillermet, C;Negoescu, A
通讯作者：
Negoescu, A