A Short History of Hydrogen Sulfide
From the sewers of Paris to physiological messenger
Investigations on the biological effects of hydrogen sulfide began around the turn of the 20th century. François Chaussier, François Magendie, Claude Bernard and Felix Hoppe-Seyler were among the well-known scientists of the day who labored in that vineyard.
In experiments with dogs, marked differences in the effects of hydrogen sulfide were noted with only small changes in its concentration in the air they were breathing. Fifty ppm, which was considered a minimally lethal concentration at the time, resulted in a slight progressive depression in the rate and depth of respirations. After many hours of exposure, the dogs died from a type of pulmonary edema, acute respiratory distress syndrome (ARDS). When that concentration was doubled to 100 ppm, death resulted in 15 to 20 minutes. In these cases the respiration was stimulated almost immediately, this progressed to a pronounced hyperpnea (deep breathing), and death in apnea followed. At 300 ppm, respiratory arrest occurred after a few violent gasps. The same effects on respiration, with the exception of ARDS, were known to occur with injected or inhaled hydrogen cyanide. Mice may be more resistant to the effects of hydrogen sulfide. In a 1964 experiment, they survived for 10 minutes in an atmosphere of 1,872 ppm and for 20 minutes at 985 ppm.
A more complete explanation of the respiratory stimulant effects of hydrogen cyanide and hydrogen sulfide had to await the discovery of the chemoreceptor function of the carotid body (shown at right), and the reflex effects that follow the activation of those receptors. The respiratory stimulant effects of cyanide and sulfide could be completely abolished by severing the sinus nerve and thus denervating the carotid sinus. In that case, larger doses of either chemical resulted only in respiratory depression, which was presumably mediated via the brainstem. Similarly, injections of sulfide or cyanide into the internal carotid or vertebral arteries also failed to stimulate respiration, since in those cases the chemicals reached the carotid sinus only after dilution in the general circulation. When innervation of the sinus was intact, the hyperpnea was accompanied by a fleeting rise in systemic blood pressure, and sometimes by a slowed heart rate (bradycardia). The cardiovascular effects varied with the injection site and the species and are still not adequately explained.