| First Author | Palazzo AJ | Year | 1998 |
| Journal | Am J Physiol | Volume | 275 |
| Issue | 6 Pt 2 | Pages | H2300-7 |
| PubMed ID | 9843832 | Mgi Jnum | J:52319 |
| Mgi Id | MGI:1328860 | Doi | 10.1152/ajpheart.1998.275.6.H2300 |
| Citation | Palazzo AJ, et al. (1998) Myocardial ischemia-reperfusion injury in CD18- and ICAM-1-deficient mice. Am J Physiol 275(6 Pt 2):H2300-7 |
| abstractText | Previous studies have demonstrated that circulating neutrophils (PMNs) contribute to the pathophysiology of myocardial ischemia-reperfusion (MYR) injury. PMN- endothelial cell interactions are highly regulated by adhesive interactions between PMN CD11/ CD18 and coronary endothelial cell intercellular adhesion molecule-1 (ICAM- 1). We investigated the effects of MI/R in wild-type, CD18- , and ICAM-1-deficient (-/-) mice. Wildtype (n = 6), CD18 - /- (n. = 6), and ICAM-1 -/- (n = 6) mice were subjected to 30 min of myocardial ischemia and 120 min of reperfusion to determine the extent of PMN infiltration and myocardial cell necrosis. Myocardial infarction (% of the area at risk) was 45.1 +/- 5.9 in wild-type mouse hearts. In contrast, the extent of myocardial infarction was significantly (P < 0.05) reduced in the CD18 (19.3 +/- 5.1%)- and ICAM-1 (17.9 +/- 3.2%)-deficient mice. Similarly, PMN infiltration into the ischemic-reperfused myocardium was attenuated by 54% in the CD18 -/- mice and by 32% in ICAM-1 -/- mice compared with wild-type hearts. Deficiency in either CD18 or ICAM-1 expression results in a marked reduction in PMN accumulation and myocardial necrosis after acute MI/R. |
