地塞米松阻断败血症对心脏缺血再灌注损伤的保护作用。

A. Spanier, K. Mcdonough
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引用次数: 12

摘要

先前的研究表明,败血症在引起心功能障碍的同时,可以保护心脏免受缺血再灌注损伤。脓毒症诱导的保护可能是由于在脓毒症期间对细胞因子释放的反应中产生的一氧化氮合酶的诱导形式产生的一氧化氮。糖皮质激素地塞米松已被证明可以抑制诱导型一氧化氮合酶(iNOS)的合成。本研究的目的是确定地塞米松是否可以预防败血症引起的心功能障碍和败血症引起的心脏缺血再灌注损伤保护。在本实验中,通过在大鼠背部皮下间隙注射大肠杆菌使其脓毒症。对照组大鼠注射无菌生理盐水。手术时,部分对照组和脓毒症动物腹腔注射地塞米松(3mg /kg)。第二天,注射第一剂大肠杆菌后24-26小时,麻醉动物,取心,在等容跳动心脏制备中进行研究。左室舒张末期压设为5mmhg,在整个方案中持续测量左室压。左室发育压(LVDP)作为左室功能的指标。稳定后,使心脏全面缺血35分钟,然后再灌注25分钟。如前所示,脓毒症抑制LVDP,但也保护心脏免受缺血再灌注进一步抑制LVDP。地塞米松既能预防败血症引起的心功能障碍,又能保护心脏免受缺血再灌注损伤。此外,接受地塞米松治疗的脓毒症大鼠的血浆亚硝酸盐/硝酸盐水平与对照水平没有差异,而脓毒症动物的血浆亚硝酸盐/硝酸盐水平升高。地塞米松介导的消除败血症引起的心功能障碍和保护缺血再灌注损伤可能是由于抑制一氧化氮的产生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dexamethasone blocks sepsis-induced protection of the heart from ischemia reperfusion injury.
Previous investigations have shown that sepsis, while causing cardiac dysfunction, can protect the heart from ischemia-reperfusion injury. Sepsis-induced protection may be due to nitric oxide produced by an inducible form of nitric oxide synthase generated in response to cytokines released during sepsis. The glucocorticoid dexamethasone has been shown to inhibit the synthesis of the inducible form of nitric oxide synthase (iNOS). The goals of this study were to determine if dexamethasone would prevent sepsis-induced cardiac dysfunction and sepsis-induced protection of the heart from ischemia-reperfusion injury. In this experiment, rats were made septic by injecting Escherichia coli into the dorsal subcutaneous space. Control rats were injected with sterile saline. At the time of surgery, some of the control and septic animals were injected intraperitoneally with dexamethasone (3 mg/kg). The next day, 24-26 hr after injection of the first dose of E. coli, animals were anesthetized, and hearts were removed and studied in the isovolumic beating-heart preparation. Left ventricular end diastolic pressure was set to 5 mmHg, and left ventricular pressure was measured continuously throughout the protocol. Left ventricular developed pressure (LVDP) was used as an index of LV function. After stabilization, hearts were made globally ischemic for 35 min and then reperfused for 25 min. As has been shown previously, sepsis depressed LVDP but also protected the heart from further depression of LVDP by ischemia and reperfusion. Dexamethasone prevented both sepsis-induced cardiac dysfunction and sepsis-induced protection of the heart from ischemia-reperfusion injury. In addition plasma nitrite/nitrate levels were not different from control levels in the dexamethasone-treated septic rats whereas levels were elevated in the septic animals. The dexamethasone mediated abrogation of sepsis-induced cardiac dysfunction and protection during ischemia-reperfusion injury may be due to suppression of nitric oxide production.
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