| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Regular Articles |
From the Division of Cardiovascular and Respiratory Medicine,Department of Internal Medicine, Kobe University Graduate School ofMedicine, Kobe, Japan
Microvascular injury has been proposed to be a main cause of ischemia-reperfusion (I/R) injury. The roles of endothelial nitric oxide synthase (eNOS)-derived NO, a key regulator of vascular function, in I/R injury are incompletely understood. We used transgenic mice overexpressing eNOS in endothelial cells (eNOS-Tg) and their littermates wild-type mice (WT) to investigate the roles of eNOS in I/R injury in skeletal muscle. Superoxide levels in the affected muscles were reduced by approximately 50% in eNOS-Tg compared with WT during reperfusion. In WT, the disassembly of endothelial junctional proteins seen in the early period of reperfusion was recovered in the later phase. These findings were correlated with the increased vascular permeability in vivo. In contrast, eNOS-Tg maintained the endothelial junction assembly as well as vascular permeability during reperfusion. Leukocyte extravasation into tissue and up-regulated expression of adhesion molecules in the reperfused vessels were significantly inhibited in eNOS-Tg. Tissue viability of the affected muscle was decreased in WT time-dependently after reperfusion, whereas eNOS-Tg showed no significant reduction. NOS inhibition completely reversed these protective effects of eNOS overexpression in I/R injury. Thus, eNOS overexpression appears to prevent the I/R injury in skeletal muscle by maintaining vascular integrity.
Related articles in Am J Pathol:
This article has been cited by other articles:
 |
|
 |
|
  T. Nagayama, M. Zhang, S. Hsu, E. Takimoto, and D. A. Kass Sustained Soluble Guanylate Cyclase Stimulation Offsets Nitric-Oxide Synthase Inhibition to Restore Acute Cardiac Modulation by Sildenafil J. Pharmacol. Exp. Ther., August 1, 2008; 326(2): 380 - 387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. T. Hua, H. Albadawi, F. Entabi, M. Conrad, M. C. Stoner, B. T. Meriam, R. Sroufe, S. Houser, G. M. LaMuraglia, and M. T. Watkins Polyadenosine Diphosphate-Ribose Polymerase Inhibition Modulates Skeletal Muscle Injury Following Ischemia Reperfusion Arch Surg, April 1, 2005; 140(4): 344 - 351. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. K. Walsh, H. Huang, Z. Wang, J. Williams, R. de Crom, R. van Haperen, C. I. Thompson, D. J. Lefer, and T. H. Hintze Control of myocardial oxygen consumption in transgenic mice overexpressing vascular eNOS Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H2115 - H2121. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Tejedo, G. M. Cahuana, R. Ramirez, M. Esbert, J. Jimenez, F. Sobrino, and F. J. Bedoya Nitric Oxide Triggers the Phosphatidylinositol 3-Kinase/Akt Survival Pathway in Insulin-Producing RINm5F Cells by Arousing Src to Activate Insulin Receptor Substrate-1 Endocrinology, May 1, 2004; 145(5): 2319 - 2327. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. P. Jones, J. J. M. Greer, A. K. Kakkar, P. D. Ware, R. H. Turnage, M. Hicks, R. van Haperen, R. de Crom, S. Kawashima, M. Yokoyama, et al. Endothelial nitric oxide synthase overexpression attenuates myocardial reperfusion injury Am J Physiol Heart Circ Physiol, January 1, 2004; 286(1): H276 - H282. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. P. Chung, M. M. Monick, N. Y. Hamzeh, N. S. Butler, L. S. Powers, and G. W. Hunninghake Role of Repeated Lung Injury and Genetic Background in Bleomycin-Induced Fibrosis Am. J. Respir. Cell Mol. Biol., September 1, 2003; 29(3): 375 - 380. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
