Effect of reperfusion with leukocyte-depleted blood on the expression of myocardial vascular cell adhesion molecule-1 ( VCAM-1 ) and myocardial function in isolated working heart perfusion model / 대한흉부외과학회지

BACKGROUND: Adhesion of leukocytes to myocardium or vascular endothelium has been known as an importation initial step in the ischemia-reperfusion injury which may affect the cardiac function. Therefore, leukocyte-depleted reperfusion may inhibit ischemia-reperfusion induced functional and ultrastructural deterioration. In this study, we quantified the time-dependent expression of the vascular cell adhesion molecule-1(VCMA-1) on piglet myocardium and demonstrated its relation to functional recovery using isolated piglet heart perfusion model. MATERIAL AND METHOD: Neonatal(1 to 3 day old) piglet heart was harvested with 4C degrees University of Wisconsin solution (UWS) and presrved in the same solution for 12 hours. Ex vivo model of an isolated working neonatal piglet heart perfusion consisting of membrane oxygenator and roller-pump was used (Fig. 1). Hearts were grouped into leukocyte-non-depleted (group A, n=8) and leukocyte-depleted group(group B, n=8). In group B, hearts were reperfused with leukocyte-depleted blood using a leukocyte filter (Sepacell R, Asahi Medical, Japan). Segments of right atrium were taken before and after 1, 2, 3, and 4 hours of reperfusion for the evaluation of expression of VCAM-1. The intensity of immunohistochyemical satining of the VCAM-1 on the myocardium were graded semiquantitatively (0 to 4). For the evaluation of myocardial stroke work indices were calculated as well at the same time-points. RESULT: Mean expressins of VCAM-1 on the myocardium at 0, 1, 2, 3, adn 4 hours of reperfusion were 0.63, 1.44, 1.64, 2.65, and 3.34 in group A, while 0.56, 1.40, 1.50, 1.88 and 2.14 in group B (Fig. 3). Mean stroke work indices at 0.5, 1, 2, 3, and 4 hours after reperfusion were 1.35x104, 1.32x104, 1.14x104, 0.81x104, 0.68x104 erg/gm in group A, while 1.40x104, 1.43x104, 1.43x104, 1.28x104, and 1.12x104 erg/em in group B(Fig. 4). CONCLUSION: In this study, we demonstrated that leukocyte-depletion attenuated the expression of VCAM-1 during reperfusion and the time-dependent functional deterioration of the myocardium was well correlated with the degree of VCAM-1 expression.

Time-dependent expression of ICAM-1 & VCAM-1 on coronaries of the heterotopically transplanted mouse heart

To investigate the pathogenesis of accelerated graft atherosclerosis after rdiac transplantation, a genetically well-defined and reproducible animal del is required. We performed heterotopic intraabdominal heart transplantation tween the two inbred strains of mice. Forty hearts from B10.A mice were ansplanted into B10.BR mice. Recipients were sacrificed at 1, 3, 5, 7, 14, 28, d 42 days after implantation. The specimens from both donor and recipient were amined with fluorescent immunohistochemistry and the serial histopathologic anges were evaluated. In the donor hearts, ICAM-1 and VCAM-1 expressions were nimal at day 1 and they gradually increased, reaching their peaks on day 5 or and remained unchanged by day 42. However, there were very little expressions the recipients' hearts. Mean percent areas of intima in the donor coronaries vealed progressive increase by day 42. However, those in the recipients cupied consistently less than 5% of the lumen. In conclusion, we demonstrated at a heterotopic murine heart transplantation model was a useful tool to oduce transplantation coronary artery disease and that adhesion molecules on e cardiac allografts were activated very early and remained elevated at all me-points, nonetheless the arterial lesion was detected after day 28 and its ogression was accelerated thereafter.