Neutrophils-induced increase of adenosine triphosphate depletion in rat neonatal cardiac myocytes with impaired energy metabolism

Isolated, cultured rat neonatal cardiac myocytes were placed in medium suppled menfed with mitochondrial respiratory inhibitor potassium cyanide which caused a rapid adenosine triphosphate (ATP) depletion. These myocytes with the impaired energy metabolism (“hypoxia-like state”) were exposed to unstimulated human neutrophils. Effect of human neu rophils on the myocy es m the “hypoxia-like state” was quantified as a total change in the amount of ATP in cardiac cells. After 5 hours of incubation of neu rophils with the myocytes in the “hypoxia-like state” an additional decrease (of 50 per cent) in ATP content was observed. Since catalase (which destroys hydrogen peroxide) prevented the further decline in ATP level in the myocy es with impaired energy metabolism, it seem that hydrogen peroxide and possibly their products are responsible for this effect. These results suggest that unstimulated human neu rophils af er activation by the contact with injured cardiac cells caused further decrease of ATP level in target cells.