Metabolic and functional consequences of barium-induced contracture in rabbit myocardium

Barium contracture tonically activates myocardium while preserving cellular integrity. We studied the metabolic and mechanical consequences of sustained Ba²⁺ contracture. We measured the time course of phosphocreatine (PCr), ATP, P(i), total phosphate, and intracellular pH via ³¹P nuclear magnetic resonance (NMR) in isolated, isovolumic rabbit hearts. For mechanical studies, we measured force transients and dynamic stiffness in excised rabbit right ventricular papillary muscles at different elapsed times in Ba²⁺ contracture. In the perfused hearts, PCr fell steadily to 20% of control after 60 min. ATP remained constant for ~25 min then fell to 25% by 60 min. P(i) rose to 200% within 15 min and then remained unchanged, whereas total phosphate dropped steadily to 50% of control by 60 min. Myocardial O₂ consumption remained near control for 30 min and then declined to 50% by 60 min. Consistent with ATP and O₂ consumption measurements, mechanical responses were unchanged for approximately the first half hour. Because of the elevated P(i), however, myofilament kinetics may have been accelerated compared with the control metabolic state. After the initial period of stable contracture, the gradual alteration of mechanical behavior exhibited a progressive trend toward more rigor-like characteristics. In summary, myocardium in Ba²⁺ contracture is metabolically and mechanically stable for ~30 min but begins to degrade thereafter. When compared with other tonic states of activation, Ba²⁺ contracture appears to be less demanding energetically.