Low Ca2+ Reperfusion and Enhanced Susceptibility of the Postischemic Heart to the Calcium Paradox

• Published in: Circulation research Vol. 64; no. 6; pp. 1158 - 1164
• Main Authors: Kirkels, J Hans, Ruigrok, Tom J.C, Van Echteld, Cees J.A, Meijler, Frits L
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD American Heart Association, Inc 01.06.1989; Lippincott
• Subjects: Adenosine Triphosphate - metabolism; Animals; Antianginal agents. Coronary vasodilator agents; Biological and medical sciences; Calcium - administration & dosage; Calcium - adverse effects; Calcium - metabolism; Cardiovascular system; Coronary Circulation; Coronary Disease - metabolism; Coronary Disease - physiopathology; Hydrogen-Ion Concentration; In Vitro Techniques; Magnetic Resonance Spectroscopy; Male; Medical sciences; Myocardial Contraction; Myocardial Reperfusion; Myocardial Reperfusion Injury - prevention & control; Myocardium - metabolism; Pharmacology. Drug treatments; Phosphates - metabolism; Phosphocreatine - metabolism; Rats; Rats, Inbred Strains; Heart; Calcium; Rat; Rodentia; Cardiovascular disease; Coronary heart disease; Vertebrata; Chemotherapy; Experimental disease; Mammalia; Reperfusion; Treatment; Ischemia; Perfusion; Animal
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.64.6.1158

This study was designed to define the effect of postischemic low Ca perfusion on recovery of high-energy phosphates, intracellular pH, and contractile function in isolated rat hearts. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to follow creatine phosphate, adenosine triphosphate, intracellular inorganic phosphate, and intracellular 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 followed 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 impaired, and contracture developed without any rhythmic contractions. These observations indicated the occurrence of a calcium paradox rather than postponed ischemia reperfusion 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 metabolic 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.