Significant progress has been made in determining the action of sulfide on the primary target organs. It is reasonably clear that sulfide causes both K(+)-channel-mediated hyperpolarization of neurons and potentiation of other inhibitory mechanisms. It is not clear whether these processes are similar to those that occur in anoxia. Changes in perinatal and adult brain neurotransmitter content and release may be related to clinical impairment of cognition. H2S exposures at concentrations below the current occupational limits cause physiological changes in pulmonary function, thus suggesting that asthmatics are at risk. Studies of fetal and neonatal brain tissue have shown an abnormal development, and the long-term consequences of these neuronal changes have not yet been assessed. Finally, new approaches to therapy are required, such as the use of agents that actively remove sulfide from its sites of action. This may prove more useful in preventing some of the long-term adverse sequelae than the use of nitrites and hyperbaric O2, although the latter should be used in cases of pulmonary edema.

An analytical method for the determination of sulfide in human and rat brain is described. It utilizes a continuous flow gas dialysis pretreatment and quantitation by ion chromatography with electrochemical detection. Rat brain sulfide levels were reliably measured after fatal intoxication by intraperitoneal injection of NaHS. By expeditious analysis of samples it was possible to demonstrate the presence of endogenous levels of sulfide in both rat and human brain as well as to measure elevated brain levels of sulfide after intoxication. In postmortem rat brain tissue, elevated sulfide levels could still be reliably demonstrated 96 h after death if the bodies had been refrigerated at 4 degrees C. Two case studies of human hydrogen sulfide inhalation fatalities are presented. The described method was able to measure significantly elevated sulfide levels in both cases.

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In rats under urethane anaesthesia, changes in the extracellular activities of K+ and Ca2+ (alpha K and alpha Ca) evoked by fimbrial or entorhinal stimulation and recorded in area CA3 with ion-selective microelectrodes are maximal in the pyramidal cell layers. With 10/s stimulation, alpha K increases by 6--9 mM whereas alpha Ca falls by 0.5--1.0 mM. In contrast with the increase in alpha K, which is distributed over a wide range of depth, the reduction in alpha Ca is particularly sharply limited to the level of pyramidal cell bodies. It is regularly associated with a negative aferpotential in the extracellular field, which presumably reflects a large postsynaptic Ca2+ inward current, apparently predominant in the cell bodies. Repetitive stimulation sometimes evokes spreading depressionlike swings in potential, which are seen only near the pyramidal stratum and are accompanied by massive increases in alpha K (to 30--40 mM) and falls in alpha Ca (to < 0.1 mM). A large Ca2+ influx into pyramidal cells may be of significance for "plastic" aspects of hippocampal function and when excessive, as during repetitive convulsive activity, may be responsible for the necrosis of CA3 neurons.