Low Ca Reperfusion and Enhanced Susceptibility of the Postischemic Heart to the Calcium Paradox

This study was designed to define the effect of postischemic low Ca perfusion on recovery of high-energy phosphates, intraceUular pH, and contractile function in isolated rat hearts. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow creatine phosphate, adenosine triphosphate, intraceUular inorganic phosphate, and intraceUular pH during control perfusion (15 minutes), total ischemia (30 minutes), and reperfusion (30 minutes). In Group I the perfusate [Ca] was 1.3 mmol/1 throughout the experiment, whereas in Group II the perfusate [Ca] was reduced to 0.05 mmol/1 during the first 10 minutes of reperfusion. Hearts from Group III were not made ischemic but were subjected to 10 minutes of low Ca perfusion foUowed by 20 minutes of normal Ca perfusion. During low Ca reperfusion (Group II) recovery of high-energy phosphates and pH was significantly better than in controls (Group I). However, after reexposure to normal Ca, metabolic recovery was largely abolished, coronary flow was suddenly unpaired, and contracture developed without any rhythmic contractions. These observations indicated the occurrence of a calcium paradox rather than postponed ischemiareperfusion damage. On the other hand, normoxic hearts (Group III) tolerated temporary perfusion with 0.05 mmol/1 Ca very well with respect to left ventricular developed pressure, coronary flow, and metaboUc parameters. In conclusion, postischemic low Ca (0.05 mmol/1) perfusion may reduce reperfusion damage, but at the same time ischemia appears to enhance the susceptibility of the heart to the calcium paradox. (Circulation Research 1989;64:1158-1164)