Bacillus anthracis edema but not lethal toxin challenge in rats is associated with depressed myocardial function in hearts isolated and tested in a Langendorff system.
Bacillus anthracis edema but not lethal toxin challenge in rats is associated with depressed myocardial function in hearts isolated and tested in a Langendorff system.
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大鼠中的炭疽杆菌水肿而非致死性毒素攻击与兰根多夫系统中分离和测试的心脏的心肌功能下降有关。
DOI：
10.1152/ajpheart.00851.2014
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Cui,Xizhong
中科院分区：
文献类型：
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作者：
Li,Yan;Abu-Asab,Mones;Su,Junwu;Qiu,Ping;Feng,Jing;Ohanjanian,Lernik;Kumar,HanishSampath;Fitz,Yvonne;Eichacker,PeterQ;Cui,Xizhong
尽管直接心肌抑制与炭疽芽孢杆菌致死毒素（LT）的致死作用有关，但在从健康大鼠心脏中分离出来并在恒压下灌注的情况下，典型致死浓度的LT或水肿毒素（ET）均未抑制心肌功能。在本研究中，我们用LT和ET刺激大鼠，并进行了体内和离体心脏测量。分别在8、24和48小时对Sprague-Dawley大鼠进行了24小时LT （n= 94）、ET （n= 99）或稀释液（对照组；n= 50）的研究。与对照组大鼠（全部存活）相比，LT（56.1%）和ET（37.3%）的存活率同样降低（P< 0.0001） （LT与ET的P= 0.66）。在12 ~ 20 h期间，LT降低平均动脉血压（P≤0.05），而ET在整个过程中逐渐降低平均动脉血压（P< 0.05）。超声心动图显示，LT在8和48 h时降低左室射血分数，但在24 h时升高，心输出量降低（时间相互作用或随时间平均P≤0.05）。ET降低24 h收缩期和舒张期容积，增加左室射血分数（P≤0.05）。在恒压下灌注120分钟的离体心脏中，LT在任何时间点都没有显著改变左室收缩压或发展压，而ET在24小时时降低了这两项（初始P< 0.0001）。ET而非LT使血浆肌酸激酶和心肌肌钙蛋白水平逐渐升高（P< 0.05）。综上所述，尽管超声心动图发生了变化，但在离体大鼠心脏中，体内致死性左心室浸润并没有产生心肌抑制的证据。虽然致死性ET刺激确实降低了孤立心功能，但这可能是由于先前的低血压和缺血造成的。
Although direct myocardial depression has been implicated in the lethal effects ofBacillus anthracislethal toxin (LT), in hearts isolated from healthy rats and perfused under constant pressure, neither LT or edema toxin (ET) in typically lethal concentrations depressed myocardial function. In the present study, we challenged rats with LT and ET and performed in vivo and ex vivo heart measures. Sprague-Dawley rats infused over 24 h with LT (n= 94), ET (n= 99), or diluent (controls;n= 50) were studied at 8, 24, or 48 h. Compared with control rats (all survived), survival rates with LT (56.1%) and ET (37.3%) were reduced (P< 0.0001) similarly (P= 0.66 for LT vs. ET). LT decreased mean arterial blood pressure from 12 to 20 h (P≤ 0.05), whereas ET decreased it progressively throughout (P< 0.05). On echocardiography, LT decreased left ventricular (LV) ejection fraction at 8 and 48 h but increased it at 24 h and decreased cardiac output (P≤ 0.05 for the time interaction or averaged over time). ET decreased systolic and diastolic volumes and increased LV ejection fraction at 24 h (P≤ 0.05). In isolated hearts perfused for 120 min under constant pressure, LT did not significantly alter LV systolic or developed pressures at any time point, whereas ET decreased both of these at 24 h (P< 0.0001 initially). ET but not LT progressively increased plasma creatine phosphokinase and cardiac troponin levels (P< 0.05). In conclusion, despite echocardiographic changes, in vivo lethal LT challenge did not produce evidence of myocardial depression in isolated rat hearts. While lethal ET challenge did depress isolated heart function, this may have resulted from prior hypotension and ischemia.