Mesenteric lymph duct ligation prevents trauma/hemorrhage shock-induced cardiac contractile dysfunction.
Mesenteric lymph duct ligation prevents trauma/hemorrhage shock-induced cardiac contractile dysfunction.
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DOI：
10.1152/japplphysiol.90937.2008
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发表时间：
2009
影响因子：
3.3
通讯作者：
J. Sambol;Marlon A. Lee;F. Caputo;Kentaro Kawai;C. Badami;T. Kawai;E. Deitch;A. Yatani
中科院分区：
文献类型：
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作者：
J. Sambol;Marlon A. Lee;F. Caputo;Kentaro Kawai;C. Badami;T. Kawai;E. Deitch;A. Yatani
临床和实验研究表明，创伤合并失血性休克(T/HS)与心肌收缩功能障碍有关。然而，引发心功能不全的最初事件还没有完全阐明。因此，我们测试了一种假说，即肠(肠系膜)淋巴中携带的因子在大鼠剖腹(T)加失血性休克(HS；平均动脉压30-40托，持续90分钟)后，有助于发挥负性肌力作用。在创伤加假休克(T/SS)或假休克(T/HS)后24 h，通过记录5组大鼠的左心室发展压(LVdP)和左心室发展压最大上升和下降速率(+/-dp/dt(Max))来评价左心功能：1)未加药组，2)T/SS组，3)T/HS组，4)T/SS+LDL组，5)T/HS+LDL组。来自幼稚、T/SS和T/SS+低密度脂蛋白大鼠的心脏功能相似。T/HS后LVdP和+/-dp/dt(Max)均显著降低。T/HS心脏对冠脉流量和Ca(2+)的增加也表现出钝性反应，这在T/HS之前被低密度脂蛋白阻止。虽然在生理条件下心电图正常，但当T/HS心脏灌流低钙(约0.5 mm)时，可观察到P-R间期延长和二度加文氏房室传导阻滞。对照组和T/HS+低密度脂蛋白组无此变化。T/HS的作用与Ca(2+)通道拮抗剂地尔硫卓相似，提示细胞内Ca(2+)调节功能障碍是T/HS所致心功能不全的原因之一。综上所述，肠系膜淋巴携带的肠源性因子是T/HS所致急性心功能不全的原因。
Clinical and experimental studies have shown that trauma combined with hemorrhage shock (T/HS) is associated with myocardial contractile dysfunction. However, the initial events triggering the cardiac dysfunction are not fully elucidated. Thus we tested the hypothesis that factors carried in intestinal (mesenteric) lymph contribute to negative inotropic effects in rats subjected to a laparotomy (T) plus hemorrhagic shock (HS; mean arterial blood pressure of 30-40 Torr for 90 min) using a Langendorff isolated heart preparation. Left ventricular (LV) function was assessed 24 h after trauma plus sham shock (T/SS) or T/HS by recording the LV developed pressure (LVDP) and the maximal rate of LVDP rise and fall ( +/- dP/dt(max)) in five groups of rats: 1) naive noninstrumented rats, 2) rats subjected to T/SS, 3) rats subjected to T/HS, 4) rats subjected to T/SS with mesenteric lymph duct ligation (T/SS+LDL), or 5) rats subjected to T/HS+LDL. Cardiac function was comparable in hearts from naive, T/SS, and T/SS+LDL rats. Both LVDP and +/- dP/dt(max) were significantly depressed after T/HS. The T/HS hearts also manifested a blunted responsiveness to increases in coronary flow rates and Ca(2+), and this was prevented by LDL preceding T/HS. Although electrocardiograms were normal under physiological conditions, when the T/HS hearts were perfused with low Ca(2+) levels ( approximately 0.5 mM), prolonged P-R intervals and second-degree plus Wenckebach-type atrioventricular blocks were observed. No such changes occurred in the control or T/HS+LDL hearts. The effects of T/HS were similar to those of the Ca(2+) channel antagonist diltiazem, indicating that an impairment of cellular Ca(2+) handling contributes to T/HS-induced cardiac dysfunction. In conclusion, gut-derived factors carried in mesenteric lymph are responsible for acute T/HS-induced cardiac dysfunction.