Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility.
Sulfide Intoxication-Induced Circulatory Failure is Mediated by a Depression in Cardiac Contractility.
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DOI：
10.1007/s12012-015-9309-z
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发表时间：
2016-01
影响因子：
3.2
通讯作者：
Haouzi P
中科院分区：
文献类型：
--
作者：
Sonobe T;Haouzi P
硫化氢(H_2S)中毒会引起快速的心循环衰竭，导致心脏骤停。在非致命形式的硫化物暴露中，循环系统休克的存在与长期的神经后遗症有关。我们的目的是阐明硫化氢引起循环衰竭的机制。在麻醉、麻痹和机械通气的大鼠上，测定心输出量、动脉压和心室压，同时输注NaHS使动脉中的可溶性H_2S(CgH_2S)浓度从检测不到的水平增加到导致循环衰竭的水平。与对照组/生理盐水输注相比，当CgH2S达到约1微米时，血压开始显著下降，外周血管阻力略有下降(-19±5%，P<；0.01)。当CgH_2S超过2-3微米时，心肌收缩功能参数降低，外周阻力无进一步降低。当H_2S暴露维持在较高水平(CgH_2S超过7微米)时，可以观察到明显的心脏收缩抑制，导致几分钟内停止搏动，但没有外周血管麻痹的证据。特异地对抗硫化氢暴露后引起的心肌收缩能力抑制的即刻和长期神经效应仍有待研究。
Hydrogen sulfide (H2S) intoxication produces a rapid cardio-circulatory failure leading to cardiac arrest. In non-lethal forms of sulfide exposure, the presence of a circulatory shock is associated with long-term neurological sequelae. Our aim was to clarify the mechanisms of H2S-induced circulatory failure. In anesthetized paralyzed and mechanically ventilated rats, cardiac output, arterial pressure and ventricular pressures were determined while NaHS was infused to increase arterial concentration of soluble H2S (CgH2S) from undetectable to levels leading to circulatory failure. Compared to control/saline infusion, blood pressure started to decrease significantly along with a modest drop in peripheral vascular resistance (-19 ± 5%, P<0.01), when CgH2S reached about 1 microM. As CgH2S exceeded 2-3 microM, parameters of ventricular contractility diminished with no further reduction in peripheral resistance. Whenever H2S exposure was maintained at a higher level (CgH2S over 7 microM), a clear inhibition of cardiac contractility was observed, leading to asystole within minutes, but with no evidence of peripheral vasoplegia. The immediate and long-term neurological effects of specifically counteracting sulfide induced cardiac contractility depression following H2S exposure remain to be investigated.