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Effects of Hydrogen Sulfide on Circulation
Author(s) -
Sonobe Takashi,
Haouzi Philippe
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.640.1
Subject(s) - contractility , vasodilation , vascular resistance , cardiac output , medicine , hydrogen sulfide , blood pressure , saline , sodium hydrosulfide , chemistry , ventilation (architecture) , anesthesia , cardiology , endocrinology , mechanical engineering , sulfur , organic chemistry , engineering
Hydrogen sulfide (H 2 S) has been suggested to relax the vascular smooth muscles and produce a vasodilation. However, it remains unclear whether endogenous H 2 S produced in the vessels, if any, can produce a vasodilatory effect, which has a relevant physiological or clinical meaning, as concentrations of H 2 S used in vitro to produce these effects are within a toxic range. In urethane anesthetized mechanically ventilated rats, NaHS was intravenously infused in a stepwise manner to produce an increase in alveolar H 2 S partial pressure and thus arterial concentration of free H 2 S (CgH 2 S) from undetectable up to levels we have previously shown to depress breathing control. Compared to saline infusion, blood pressure started to decrease significantly along with the peripheral vascular resistance by ‐19 ± 5%, (P<0.01) when CgH 2 S reached ~ 1 microM. As soon as CgH 2 S exceeded these levels, cardiac output decreased with a decrease in ventricular pressure, along with a significant elevation of blood lactate. Whenever H 2 S exposure was maintained at a higher level, above 3‐4 microM of CgH 2 S, a profound inhibition of cardiac contractility occurred leading to cardiac arrest by a pulseless electrical activity. In conclusion, a small reduction in peripheral vascular resistance was found in the rat at relatively low H 2 S concentrations. These changes were extremely modest with an alarming overlap with the levels of H 2 S altering cardiac contractility.