Sonobe Takashi, Haouzi Philippe
Division of Pulmonary and Critical Care Medicine, Department of Medicine, Pennsylvania State University, College of Medicine, 500 University Drive, H041, Hershey, PA, 17033, USA.
Cardiovasc Toxicol. 2016 Jan;16(1):67-78. doi: 10.1007/s12012-015-9309-z.
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 μM. As CgH2S exceeded 2-3 μM, parameters of ventricular contractility diminished with no further reduction in peripheral resistance. Whenever H2S exposure was maintained at a higher level (CgH2S over 7 μM), a severe depression 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.
硫化氢（H₂S）中毒会导致快速的心循环衰竭，进而引发心脏骤停。在非致命性的硫化物暴露形式中，循环性休克的存在与长期神经后遗症有关。我们的目的是阐明H₂S诱导循环衰竭的机制。在麻醉、麻痹并进行机械通气的大鼠中，在输注硫氢化钠（NaHS）以将可溶性H₂S的动脉浓度（CgH₂S）从检测不到的水平提高到导致循环衰竭的水平时，测定心输出量、动脉压和心室压力。与对照/输注生理盐水相比，当CgH₂S达到约1 μM时，血压开始显著下降，同时外周血管阻力适度下降（-19±5%，P<0.01）。当CgH₂S超过2 - 3 μM时，心室收缩性参数降低，而外周阻力没有进一步降低。每当H₂S暴露维持在较高水平（CgH₂S超过7 μM）时，会观察到心脏收缩性严重抑制，数分钟内导致心搏停止，但没有外周血管麻痹的证据。H₂S暴露后特异性对抗硫化物诱导的心脏收缩性抑制的即时和长期神经效应仍有待研究。
