The Annals of Thoracic Surgery, Vol 37, 309-313, Copyright © 1984 by The Society of Thoracic Surgeons
Effects of delay in administration of potassium cardioplegia to the isolated rat heart
BM Freedman, MK Pasque, GL Pellom, DW Deaton, JR Frame and AS Wechsler
Ischemic injury to the heart in the period between aortic cross- clamping
and administration of cardioplegic solution was evaluated in the
normothermic rat heart model. After isolation and control perfusion with
oxygenated Krebs-Henseleit bicarbonate buffer, the hearts were given
lactated Ringer's cardioplegic solution (30 mEq of K+ per liter) for 2
minutes at three different intervals following aortic clamping: no delay,
2-minute delay, and 5-minute delay. Thereafter, the hearts were left
unperfused and the time to initiation of ischemic contracture was recorded.
Adenosine triphosphate (ATP) and creatine phosphate levels were measured in
all groups prior to and at the conclusion of cardioplegia administration. A
2-minute delay in the administration of cardioplegic solution resulted in
significantly lower (p less than 0.001) ATP levels that were restored after
2 minutes of cardioplegia administration. Contracture times were not
significantly altered. A 5- minute delay resulted in significantly shorter
(p less than 0.001) contracture times and significantly lower (p less than
0.001) ATP levels that were not restored to preischemic levels by 2 minutes
of cardioplegia administration. The fate of the myocardium may be
insensitive to events that occur during the earliest moments of ischemia
provided that rapid administration of oxygenated potassium cardioplegia
follows the ischemic period and restores preischemic high- energy phosphate
stores. However, there is a critical ischemic time during the initial
interval before cardioplegia that is associated with an impaired ability of
the myocardium to tolerate subsequent ischemia.
