Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion.
BACKGROUND
Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isolated rat hearts.


RESULTS
Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C.


CONCLUSIONS
Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia.
Liu
X
X
Cardiovascular Division, University of Connecticut School of Medicine, Farmington.
Engelman
R M
RM
Rousou
J A
JA
Flack
J E
JE
Deaton
D W
DW
Das
D K
DK
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002314:Cardioplegic Solutions; D006324:Heart Arrest, Induced / Q000379:methods*; D007036:Hypothermia, Induced; D008297:Male; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D013696:Temperature; D013997:Time Factors
D002314:Cardioplegic Solutions; D002118:Calcium