Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of Kentucky, Lexington, KY, United States.
Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, University of Kentucky, Lexington, KY, United States.
Respir Physiol Neurobiol. 2020 Jan;271:103289. doi: 10.1016/j.resp.2019.103289. Epub 2019 Sep 7.
Infection induced diaphragm weakness is a major contributor to death and prolonged mechanical ventilation in critically ill patients. Infection induced muscle dysfunction is associated with activation of muscle proteolytic enzymes, and taurine is known to suppress proteolysis. We therefore postulated that taurine administration may prevent infection induced diaphragm dysfunction. The purpose of this study was to test this hypothesis using a clinically relevant animal model of infection, i.e. cecal ligation puncture induced sepsis (CLP). Studies were performed on (n = 5-7 mice/group): (a) sham operated controls, (b) animals with sepsis induced by CLP, (c) sham operated animals given taurine (75 mg/kg/d, intraperitoneally), and (d) CLP animals given taurine. At intervals after surgery animals were euthanized, diaphragm force generation measured in vitro, and diaphragm calpain, caspase and proteasomal activity determined. CLP elicited a large reduction in diaphragm specific force generation at 24 h (1-150 Hz, p < 0.001) and taurine significantly attenuated CLP induced diaphragm weakness at all stimulation frequencies (p < 0.001). CLP induced significant increases in diaphragm calpain, caspase and proteasomal activity; taurine administration prevented increases in the activity of all three pathways. In additional time course experiments, diaphragm force generation remained at control levels over 72 h in CLP animals treated with daily taurine administration, while CLP animals demonstrated severe, sustained reductions in diaphragm strength (p < 0.01 for all time points). Our results indicate that taurine administration prevents infection induced diaphragm weakness and reduces activation of three major proteolytic pathways. Because this agent is has been shown to be safe, non-toxic when administered to humans, taurine may have a role in treating infection induced diaphragm weakness. Future clinical studies will be needed to assess this possibility.
感染引起的膈肌无力是导致危重病患者死亡和延长机械通气时间的主要原因。感染引起的肌肉功能障碍与肌肉蛋白水解酶的激活有关,而牛磺酸已知可抑制蛋白水解。因此,我们假设牛磺酸的给药可能预防感染引起的膈肌功能障碍。本研究的目的是使用一种临床相关的感染动物模型,即盲肠结扎穿孔诱导的脓毒症(CLP)来检验这一假设。在以下情况下进行了研究(n=5-7 只/组):(a)假手术对照;(b)CLP 诱导的败血症动物;(c)接受牛磺酸(75mg/kg/d,腹腔内)治疗的假手术动物;(d)接受牛磺酸治疗的 CLP 动物。手术后间隔一定时间,处死动物,在体外测量膈肌肌力,测定膈肌钙蛋白酶、半胱天冬酶和蛋白酶体活性。CLP 在 24 小时(1-150Hz,p<0.001)引起膈肌特定肌力产生明显下降,牛磺酸显著减弱 CLP 诱导的膈肌无力,在所有刺激频率下(p<0.001)。CLP 引起膈肌钙蛋白酶、半胱天冬酶和蛋白酶体活性显著增加;牛磺酸给药可防止这三种途径的活性增加。在进一步的时间过程实验中,CLP 动物接受每日牛磺酸治疗后,膈肌肌力在 72 小时内保持在对照水平,而 CLP 动物则表现出严重、持续的膈肌强度下降(所有时间点均为 p<0.01)。我们的结果表明,牛磺酸给药可预防感染引起的膈肌无力,并减少三种主要蛋白水解途径的激活。由于该药物已被证明在给人类给药时是安全、无毒的,因此牛磺酸可能在治疗感染引起的膈肌无力方面发挥作用。需要进一步的临床研究来评估这种可能性。