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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The role of K+ATP channels in the control of pre- and post-ischemic left ventricular developed pressure in septic rat hearts.
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The role of K+ATP channels in the control of pre- and post-ischemic left ventricular developed pressure in septic rat hearts.

机译:K + ATP通道在化脓性大鼠心脏缺血前和缺血后左心室发育压力控制中的作用。

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摘要

Myocardial function is impaired 24 h after the induction of sepsis, however, recovery of left ventricular (LV) function after 35 min of global ischemia is complete. The mechanisms by which this protection occurs are unknown. Ischemic preconditioning, another form of myocardial protection from ischemia/reperfusion (I/R) injury, has been shown to be modulated by ATP-sensitive potassium (K+ATP) channels. To investigate the role of K+ATP channels in the regulation of coronary flow (CF) and protection from I/R injury in septic rat hearts, we assessed the effects of the K+ATP channel antagonist glibenclamide (GLIB) and the agonist cromakalim (CROM) on pre- and post-ischemic CF and left ventricular developed pressure (LVDP). Although GLIB decreased pre-ischemic CF in both control and septic rat hearts, LVDP was unaffected. After I/R, CF was decreased in GLIB-treated control and septic rat hearts and LVDP was more severely depressed in control rat hearts than in septic rat hearts. CROM increased pre-ischemic CF in the septic group although LVDP was unaltered in both groups. After I/R, control rat heart CF was depressed but LVDP completely recovered. Post-ischemic CF in septic rat hearts was elevated compared with vehicle-treated septic rat hearts, but the recovery of LVDP was not improved. These results suggest that K+ATP channels modulate CF in septic rat hearts, but do not mediate cardioprotection as observed in control rat hearts.
机译:脓毒症诱发后24小时,心肌功能受损,但是,局部缺血35分钟后,左心室(LV)功能恢复完全。发生此保护的机制尚不清楚。缺血预处理是保护心肌免受缺血/再灌注(I / R)伤害的另一种形式,已被ATP敏感性钾(K + ATP)通道调节。为了研究脓毒症大鼠心脏中K + ATP通道在调节冠状动脉血流(CF)和防止I / R损伤中的作用,我们评估了K + ATP通道拮抗剂格列本脲(GLIB)和激动剂cromakalim(缺血前和后CF和左心室发育压力(LVDP)的CROM)。尽管GLIB降低了对照组和脓毒性大鼠心脏的缺血前CF,但LVDP并未受到影响。 I / R后,与脓毒性大鼠心脏相比,GLIB治疗的对照组和脓毒性大鼠心脏的CF降低,而对照大鼠心脏的LVDP严重降低。尽管两组的LVDP均未改变,但脓毒症组的CROM增加了缺血前的CF。 I / R后,对照大鼠心脏CF降低,但LVDP完全恢复。与用赋形剂处理的脓毒性大鼠心脏相比,脓毒性大鼠心脏缺血后的CF升高,但是LVDP的恢复没有改善。这些结果表明,K + ATP通道可调节败血症大鼠心脏中的CF,但不像对照大鼠心脏中那样介导心脏保护作用。

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