Mesenteric lymph from rats with trauma-hemorrhagic shock causes abnormal cardiac myocyte function and induces myocardial contractile dysfunction.
Mesenteric lymph from rats with trauma-hemorrhagic shock causes abnormal cardiac myocyte function and induces myocardial contractile dysfunction.
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创伤失血性休克大鼠的肠系膜淋巴液导致心肌细胞功能异常，诱发心肌收缩功能障碍。
DOI：
10.1152/japplphysiol.00100.2011
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发表时间：
2011
期刊：
影响因子：
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通讯作者：
Yatani,Atsuko
中科院分区：
文献类型：
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作者：
Sambol,JustinT;Lee,MarlonA;Jiang,Mingshan;Dosi,Garima;Dong,Wei;Deitch,EdwinA;Yatani,Atsuko
创伤失血性休克（T/HS）后出现心肌收缩功能障碍。我们以前已经表明，在大鼠固定压力模型的T/HS（平均动脉压30-35毫米汞柱，90分钟），肠系膜淋巴管结扎之前T/HS防止T/HS诱导的心肌收缩抑制。为了确定T/HS淋巴液是否直接改变心肌收缩力，我们研究了生理相关浓度的肠系膜淋巴液收集从大鼠进行创伤假休克（T/SS）或T/HS对分离的心肌细胞和Langendorff灌注的整个心脏的功能影响。急性应用T/HS淋巴液（0.1-2%），而不是T/SS淋巴液，诱导对心肌细胞的双重变力作用，细胞缩短幅度立即增加（1.4 ± 0.1倍），随后完全阻断收缩。同样，T/HS淋巴引起双重，积极和消极的影响，对细胞的Ca 2+瞬变。这些效应与心肌细胞电生理特性的变化有关; T/HS淋巴液最初延长了动作电位时程（90%复极化时的动作电位时程，3.3 ± 0.4倍），随后是平台电位和膜去极化的降低。此外，静脉输注T/HS淋巴液，而不是T/SS淋巴液，在注射后24 h引起心肌收缩功能障碍，这类似于实际T/HS引起的变化：左心室发展压（LVDP）和LVDP的最大上升和下降速率（±dP/dtmax）降低，对Ca 2+的正性肌力反应减弱。然而，在T/HS淋巴灌注的心脏中，对β-肾上腺素能受体刺激的收缩反应性保持不变。这些结果表明，T/HS淋巴直接导致负性肌力作用的心肌和T/HS淋巴细胞诱导的心肌细胞功能的变化可能有助于T/HS诱导的心肌功能障碍的发展。
Myocardial contractile dysfunction develops following trauma-hemorrhagic shock (T/HS). We have previously shown that, in a rat fixed pressure model of T/HS (mean arterial pressure of 30–35 mmHg for 90 min), mesenteric lymph duct ligation before T/HS prevented T/HS-induced myocardial contractile depression. To determine whether T/HS lymph directly alters myocardial contractility, we examined the functional effects of physiologically relevant concentrations of mesenteric lymph collected from rats undergoing trauma-sham shock (T/SS) or T/HS on both isolated cardiac myocytes and Langendorff-perfused whole hearts. Acute application of T/HS lymph (0.1–2%), but not T/SS lymph, induced dual inotropic effects on myocytes with an immediate increase in the amplitude of cell shortening (1.4 ± 0.1-fold) followed by a complete block of contraction. Similarly, T/HS lymph caused dual, positive and negative effects on cellular Ca2+transients. These effects were associated with changes in the electrophysiological properties of cardiac myocytes; T/HS lymph initially prolonged the action potential duration (action potential duration at 90% repolarization, 3.3 ± 0.4-fold), and this was followed by a decrease in the plateau potential and membrane depolarization. Furthermore, intravenous infusion of T/HS lymph, but not T/SS lymph, caused myocardial contractile dysfunction at 24 h after injection, which mimicked actual T/HS-induced changes; left ventricular developed pressure (LVDP) and the maximal rate of LVDP rise and fall (±dP/dtmax) were decreased and inotropic response to Ca2+was blunted. However, the contractile responsiveness to β-adrenergic receptor stimulation in the T/HS lymph-infused hearts remained unchanged. These results suggest that T/HS lymph directly causes negative inotropic effects on the myocardium and that T/HS lymph-induced changes in myocyte function are likely to contribute to the development of T/HS-induced myocardial dysfunction.