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重症休克
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  severe hemorrhagic shock
     Characteristic Changes of ATP sensitive Potassium Channels in Arteriolar Smooth Muscle Cells During Severe Hemorrhagic Shock
     重症休克时细动脉平滑肌细胞膜ATP敏感钾通道的变化
短句来源
     Role of Calcium Kinetic Changes in Vascular Hyporeactivity during Severe Hemorrhagic Shock
     钙动力学变化在重症休克血管反应性低下发生中的作用
短句来源
     Using a ratio fluorescent approach to study the role of the kinetic changes of calcium in vascular hyporeactivity of severe hemorrhagic shock.
     使用荧光比率方法研究血管平滑肌细胞钙动力学变化在重症休克血管反应性降低中的作用.
短句来源
     The Detection of Calcium Kinetic Changes for Vascular Smooth Muscle Cells in Severe Hemorrhagic Shock
     重症休克时平滑肌细胞内的钙动力学变化
短句来源
     Objective: To establish a ratio fluorescent approach to detect the kinetic changes of calcium in vascular smooth muscle cells and study its role in vascular hyporeactivity in severe hemorrhagic shock.
     目的建立一种荧光比率方法来测量细胞内钙离子的动力学变化,并研究血管平滑肌细胞钙动力学变化在重症休克血管反应性降低中的作用。
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  “重症休克”译为未确定词的双语例句
     Results Single K ATP channel conductance increased from (111±6.5) ps in normal to (129±9.5) ps in HS.
     结果重症休克使通道电导由正常的(111±6.5)ps增大到(129±9.5)ps;
短句来源
     The Inhibition of L-Ca in ASMCs Involves in the Pathogenesis of Vascular Hyporeactivity in Severe Shock
     血管平滑肌L型钙通道抑制参与重症休克血管低反应性的发生
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     Observations on curative effects of acupuncture combined with phentolamine and alamine on
     针灸联用酚妥拉明和阿拉明纠正重症休克46例疗效观察
短句来源
     Peroxynitrite involves in the pathogenesis of vascular hyporeactivity during severe shock
     过氧化亚硝酸根参与重症休克血管反应性低下的发生
短句来源
     The changes of mesentery lymph microcirculation in serious hemorrhagic shock rat
     重症休克淋巴微循环的变化
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  相似匹配句对
     Shock
     休克
短句来源
     The changes of mesentery lymph microcirculation in serious hemorrhagic shock rat
     重症休克淋巴微循环的变化
短句来源
     Emergency Treatment of Grave Anaphylactic Shock
     重症过敏性休克临床抢救探讨
短句来源
     shock;
     ②休克;
短句来源
     Diagnosis and treatment of severe breast hyperplasia
     重症乳腺增生症的诊治
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  severe hemorrhagic shock
Methods: A model of rat with severe hemorrhagic shock and active bleeding was established in 32 SD (Sprague-Dawley) rats.
      
In 42 cases, one case died of severe hemorrhagic shock, and the remaining 41 cases (97.6%) were cured (including 40 cases receiving surgical operation and one case receiving the conservative treatment).
      
In severe hemorrhagic shock, definite control of bleeding is the most important goal.
      
Aggressive fluid resuscitation, hyperventilation, and excessive ventilation pressure may impair outcome in severe hemorrhagic shock.
      
The hepatic micro-circulation was investigated by intravital fluorescence microscopy in female Sprague-Dawley rats undergoing severe hemorrhagic shock for 60 min and subsequent resuscitation.
      
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Aim: To study the role of calcium kinetic changes in vascular hyporeactivity in severe hemorrhagic shock (HS). Methods: HS model was made and the response of arterioles in spinotrapezius muscles to norepinephrine (NE) in HS was tested. The calcium kinetic changes were measured with confocal microscopy, and the effect of glibenclamide, a specific inhibitor for ATP sensitive potassium (KATP) channel, on vascular reactivity and the concentration of intracellular calcium ions ([Ca2+]i) were studied. Results:...

Aim: To study the role of calcium kinetic changes in vascular hyporeactivity in severe hemorrhagic shock (HS). Methods: HS model was made and the response of arterioles in spinotrapezius muscles to norepinephrine (NE) in HS was tested. The calcium kinetic changes were measured with confocal microscopy, and the effect of glibenclamide, a specific inhibitor for ATP sensitive potassium (KATP) channel, on vascular reactivity and the concentration of intracellular calcium ions ([Ca2+]i) were studied. Results: HS for 1 ̄2 hours caused a reduction of vasoreactivity to NE and on the effect of NE making [Ca2+]i rise in arteriolar smooth muscle cells. The reduction of [Ca2+]i rise was largely caused by the decrease of Ca2+ entry from extracellular sources. Glibenclamide could improve NE effect on、 [Ca2+]i as well as vasoreactivity. Conclusion: Vascular hyporeactivity in HS was partly due to the reduction of membrane Ca2+entry which was induced by activation of KATP channel and membrane hyperpolarization. Glybenclamide can increase vasoreactivity, which may be a new way to the treatment of hemorrhagic shock.

目的:研究血管平滑肌钙动力学变化在重症休克血管反应性降低中的作用.方法:复制大鼠失血性休克模型,测定脊斜肌细动脉对去甲肾上腺素(NE)反应性;用激光共聚焦显微镜测定单个平滑肌细胞钙动力学变化;观察ATP敏感钾通道(KATP)阻滞剂优降糖对血管反应性和钙动力学影响.结果:大鼠失血休克后1~2小时细动脉对NE反应性显著下降,NE升高细胞内钙离子浓度的作用明显减弱,以外钙内流减弱最为明显.优降糖明显提高休克时NE对平滑肌细胞内钙离子的升高作用,改善细动脉对NE反应性.结论:重症失血性休克血管反应性低下与KATP通道开放导致细胞外钙内流减少有关.优降糖能提高血管反应性为临床治疗休克提出了一种新的途径

Abstract Aim To elucidate the characteristic changes of ATP sensitive potassium (K ATP ) channels when vascular hyporeactivity occurred during severe hemorrhagic shock (HS). Methods Single channel current was studied on cell attached and inside out patches of enzymatically isolated arteriolar smooth muscle cells. Results Single K ATP channel conductance increased from (111±6.5) ps in normal to (129±9.5) ps in HS. The channels kinetics also changed in HS, which included the increase of mean open...

Abstract Aim To elucidate the characteristic changes of ATP sensitive potassium (K ATP ) channels when vascular hyporeactivity occurred during severe hemorrhagic shock (HS). Methods Single channel current was studied on cell attached and inside out patches of enzymatically isolated arteriolar smooth muscle cells. Results Single K ATP channel conductance increased from (111±6.5) ps in normal to (129±9.5) ps in HS. The channels kinetics also changed in HS, which included the increase of mean open time and open probability. HS elicited multichannel activities in some patches, too. Conclusion K ATP channels are activated during HS, which induces membrane hyperpolarization of smooth muscle cells and involves in the pathogenesis of vascular hyporeactivity.

目的探讨重症休克血管反应性降低时细动脉平滑肌ATP敏感钾通道(KATP通道)特性的改变。方法酶性分离正常及休克大鼠肠系膜细动脉平滑肌细胞,用膜片钳技术(细胞贴附式和内面向外式)记录KATP通道特性。结果重症休克使通道电导由正常的(111±6.5)ps增大到(129±9.5)ps;通道动力学也发生了改变,其中通道平均开放时间延长,通道开放时间常数τ01,τ02达1.88ms、13.12ms,通道开放概率明显增大,并诱导通道多级开放。结论重症休克时细动脉平滑肌细胞膜KATP通道开放,带来细胞膜超极化,参与低血管反应性的发生

Objective :With glybenclamide

目的:通过在体局部和全身给予ATP敏感钾通道特异性阻滞剂优降糖和碳酸氢钠治疗,探讨重症休克时低血管反应性的发生机制,以寻找有效的治疗措施。方法:对33只SD大鼠制作脊斜肌微循环观察标本,复制重症低血容量性休克模型。实验分局部治疗组〔在脊斜肌表面滴加优降糖和(或)碳酸氢钠〕和全身治疗组(通过股静脉注射优降糖和碳酸氢钠),分别观察药物对休克大鼠血管反应性、血压、微动脉血流量和24小时存活率的影响。结果:局部治疗后,休克大鼠血管反应性明显升高,以优降糖和碳酸氢钠联合应用效果最为显著。全身治疗后,休克大鼠血压、微动脉血流量和24小时存活率显著提高。结论:重症休克引起ATP敏感钾通道激活以及酸中毒参与了低血管反应性的发生,优降糖与碳酸氢钠联合应用对重症低血容量性休克具有较好的治疗作用。

 
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