Reperfusion with 1.25 mM calcium after 5 minutes of Ca2+-free perfusion produced a marked rise in resting tension, no recovery of contractile force, and a 63% depression in microsomal Ca2+ uptake.
Does reperfusion after Ca2+-free perfusion alter contractile force, resting tension, and microsomal Ca2+ uptake in isolated rat hearts?
Reperfusion-induced contracture and intracellular calcium overload in the calcium paradox may be partly due to a defect in the sarcoplasmic reticulum's ability to regulate calcium.
This study was designed to investigate changes in contractile force, resting tension, and microsomal Ca2+ uptake in isolated rat hearts perfused under conditions associated with reversible and irreversible stages of the calcium paradox phenomenon. Five minutes of reperfusion with normal medium containing 1.25 mM calcium after 5 minutes of Ca2+-free perfusion produced a marked rise in resting tension, no recovery of contractile force, and a 63% depression in microsomal Ca2+ uptake. When reperfusion was carried out after 5 minutes of perfusion with 0.025 mM or greater concentrations of Ca2+, after less than 5 minutes of Ca2+-free exposure or after 5 minutes of varying degrees of hypothermic Ca2+-free perfusion, the increase in resting tension and decrease in contractile force development as well as microsomal Ca2+ accumulation were either absent or reduced. Furthermore, reperfusion-induced increases in resting tension and decreases in microsomal Ca2+ uptake also were found to be dependent on the duration of reperfusion as well as on the calcium concentration of the reperfusion medium. Microsomes isolated from control, Ca2+-free perfused or reperfused hearts were found to have similar phospholipid composition, protein profiles (SDS-polyacrylamide gel electrophoresis), and electron microscopic appearance. Whereas Ca2+-free perfusion alone had no effect on any of the parameters studied, reperfusion also depressed microsomal Ca2+-binding, Mg2+-ATPase, and Ca2+-stimulated ATPase activities. Changes in microsomal Ca2+ uptake exhibited sigmoidal relationships with the ability of Ca2+-depleted hearts to recover their contractile force or increase their resting tension upon reperfusion. Our findings suggest that reperfusion-induced contracture and intracellular calcium overload may be associated in part with a defect in the ability of sarcoplasmic reticulum to regulate calcium.
Alto et al. (1981) studied Calcium paradox phenomenon. Reperfusion with normal medium containing 1.25 mM calcium after 5 minutes of Ca2+-free perfusion vs. Control, Ca2+-free perfused hearts, or reperfusion after perfusion with ≥0.025 mM Ca2+ was evaluated on Contractile force, resting tension, and microsomal Ca2+ uptake. Reperfusion with 1.25 mM calcium after 5 minutes of Ca2+-free perfusion produced a marked rise in resting tension, no recovery of contractile force, and a 63% depression in microsomal Ca2+ uptake.