Purpose: Some of the neuroprotective effects of hydrogen sulfide (H(2)S) have been attributed to systemic hypometabolism and hypothermia. However, systemic metabolism may vary more dramatically than brain metabolism after cardiac arrest (CA). The authors investigated the effects of inhaled exogenous hydrogen sulfide on brain metabolism and neurological function in rabbits after CA and resuscitation.
Methods: Anesthetized rabbits were randomized into a sham group, a sham/H(2)S group, a CA group, and a CA/H(2)S group. Exogenous 80 ppm H(2)S was administered to the sham/H(2)S group and the CA/H(2)S group which suffered 3 min of untreated CA by asphyxia and resuscitation. Effects on brain metabolism (cerebral extraction of oxygen (CEO(2)), arterio-jugular venous difference of glucose [AJVD(glu)] and lactate clearance), S100B, viable neuron counts, neurological dysfunction score, and survival rate were evaluated.
Results: CEO(2), AJVD(glu), and lactate increased significantly after CA. Inhalation of 80 ppm H(2)S significantly increased CEO(2) (25.04 ± 7.11 vs. 16.72 ± 6.12 %) and decreased AJVD(glu) (0.77 ± 0.29 vs. 1.18 ± 0.38 mmol/L) and lactate (5.11 ± 0.43 vs. 6.01 ± 0.64 mmol/L) at 30 min after resuscitation when compared with the CA group (all P < 0.05). In addition, neurologic deficit scores, viable neuron counts, and survival rate were significantly better whereas S100B was decreased after H(2)S inhalation.
Conclusions: The present study reveals that inhalation of 80 ppm H(2)S reduced neurohistopathological damage and improves early neurological function after CA and resuscitation in rabbits. The increased CEO(2) and decreased AJVD(glu) and enhanced lactate clearance may be involved in the protective effects.