MYOCARDIAL PROTECTIVE EFFECT AND ITS MECHANISM OF LEUKOCYTE-DEPLETED REPERFUSION IN NEONATAL RABBIT HEARTS

Citation
Y. Sawa et al., MYOCARDIAL PROTECTIVE EFFECT AND ITS MECHANISM OF LEUKOCYTE-DEPLETED REPERFUSION IN NEONATAL RABBIT HEARTS, The Annals of thoracic surgery, 58(5), 1994, pp. 1386-1390
Citations number
21
Categorie Soggetti
Surgery
ISSN journal
00034975
Volume
58
Issue
5
Year of publication
1994
Pages
1386 - 1390
Database
ISI
SICI code
0003-4975(1994)58:5<1386:MPEAIM>2.0.ZU;2-T
Abstract
Thirty-six isolated blood-perfused hearts from newborn rabbits (age ra nge, birth to 2 days) were subjected to 2 hours of cold global ischemi a (15 degrees C), with an initial infusion of cold crystalloid cardiop legic solution, followed by 30 minutes of reperfusion (37 degrees C). The hearts were divided into two groups: those reperfused with whole b lood (n = 18) and those reperfused with leukocyte-depleted blood (n = 18) obtained by the passage of blood through a leukocyte removal filte r. At 30 minutes of reperfusion, the group of hearts reperfused with l eukocyte-depleted blood showed significantly higher percentages of rec overy in terms of the left ventricular developed pressure, the maximum rate of increase of left ventricular pressure, the rate pressure prod uct, coronary sinus flow and the adenosine triphosphate content in myo cardium than did the group of hearts reperfused with whole blood. The hearts reperfused with leukocyte-depleted blood also showed significan tly lower levels of malondialdehyde, chemiluminescence in the coronary sinus effluent, and counts of intracapillary neutrophils in myocardiu m than did the group of hearts reperfused with whole blood. The ultras tructural semiquantitative assessment in the myocardium showed that th e mitochondrial and endothelial cell damages after 30 minutes of reper fusion were significantly less in the hearts reperfused with leukocyte -depleted blood than those in the hearts reperfused with whole blood. These results suggest that reperfusion with leukocyte-depleted blood p revents reperfusion injury in neonatal hearts, with possible attenuati on of endothelial cellular injury and a subsequent no-reflow phenomeno n.