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Ann Thorac Surg 2000;69:228-232
© 2000 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, College of Physicians and Surgeons, Columbia University, New York, New York USA
b Department of Physiology, College of Physicians and Surgeons, Columbia University, New York, New York, USA
c Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York, USA
Address reprint requests to Dr Vural, N. Tandogan cad. 5/6 Kavaklidere, 06540 Ankara, Turkey
e-mail: kvural{at}tr-net.net.tr
Background. The aim of this study was to test the hypothesis that agents which stabilize the mast cell membrane may modulate the phenotype of the vascular wall in a lung ischemia-reperfusion model, including altering expression of endothelial and leukocyte adhesion receptors and the inducible nitric oxide synthase (NOS-2).
Methods. Three sets of rats were given either intravenous saline (group A), ketotifen (group B), or cromolyn (group C), respectively. The left pulmonary artery was ligated temporarily and reopened after 2 hours of ischemia. Then, after a 2-hour period of reperfusion, the left lung was excised. ICAM-1 and NOS-2 were measured at the protein level by Western blotting, and cGMP levels were measured by enzyme-linked immunosorbent assay in the lung tissue specimens for each drug group.
Results. ICAM-1 expressions, determined as the intensity of a given band on the Western blot, were 197 ± 59 in group B and 195 ± 83 in group C versus 369 ± 114 in group A (p = 0.002 for analysis of variance). In contrast with ICAM-1, NOS-2 expression was increased by ketotifen or cromolyn treatment (464 ± 82 in group B and 507 ± 93 in group C, compared with 377 ± 44 for group A, p = 0.007). The finding of increased NOS-2 expression in groups B and C is consistent with the observed increase in tissue cGMP levels in the same groups (1.92 ± 0.9 pmol/mL for group A versus 7.8 ± 3.5 pmol/mL for group B, and 12.4 ± 5.8 pmol/mL for group C, p = 0.0004).
Conclusions. These data establish that mast cell stabilizing agents modulate the vascular phenotype in the setting of pulmonary ischemia and reperfusion by decreasing ICAM-1 expression, augmenting expression of NOS-2, and increasing tissue cGMP levels. As decreasing ICAM-1 expression and increasing cGMP levels have proven useful to limit proinflammatory mechanisms of tissue injury, mast cell stabilizing agents may provide a new therapeutic option to improve organ function in the setting of reperfusion.
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 K. M. Vural and M. C. Oz Endothelial adhesivity, pulmonary hemodynamics and nitric oxide synthesis in ischemia-reperfusion Eur. J. Cardiothorac. Surg., September 1, 2000; 18(3): 348 - 352. [Abstract] [Full Text] [PDF]
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