Abstract

Hydrogen sulfide (H2S) has been suggested to relax the vascular smooth muscles and produce a vasodilation. However, it remains unclear whether endogenous H2S produced in the vessels, if any, can produce a vasodilatory effect, which has a relevant physiological or clinical meaning, as concentrations of H2S 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 H2S partial pressure and thus arterial concentration of free H2S (CgH2S) 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 CgH2S reached ~ 1 microM. As soon as CgH2S exceeded these levels, cardiac output decreased with a decrease in ventricular pressure, along with a significant elevation of blood lactate. Whenever H2S exposure was maintained at a higher level, above 3‐4 microM of CgH2S, 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 H2S concentrations. These changes were extremely modest with an alarming overlap with the levels of H2S altering cardiac contractility.

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