AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 279: H2824-H2828, 2000;
0363-6135/00 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (28)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hoffmeyer, M. R.
Right arrow Articles by Lefer, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoffmeyer, M. R.
Right arrow Articles by Lefer, D. J.
Vol. 279, Issue 6, H2824-H2828, December 2000

PR-39, a potent neutrophil inhibitor, attenuates myocardial ischemia-reperfusion injury in mice

Michaela R. Hoffmeyer1, Rosario Scalia2, Chris R. Ross3, Steven P. Jones1, and David J. Lefer1

1 Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130; 2 Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107; and 3 Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas 66506

We investigated the effects of PR-39, a recently discovered neutrophil inhibitor, in a murine model of myocardial ischemia-reperfusion injury. Mice were given an intravenous injection of vehicle (n = 12) or PR-39 (n = 9) and subjected to 30 min of coronary artery occlusion followed by 24 h of reperfusion. In addition, the effects of PR-39 on leukocyte rolling and adhesion were studied utilizing intravital microscopy of the rat mesentery. The area-at-risk per left ventricle was similar in vehicle- and PR-39-treated mice. However, myocardial infarct per risk area was significantly (P < 0.01) reduced in PR-39 treated hearts (21.0 ± 3.8%) compared with vehicle (47.1 ± 4.8%). Histological analysis of ischemic reperfused myocardium demonstrated a significant (P < 0.01) reduction in polymorphonuclear neutrophil (PMN) accumulation in PR-39-treated hearts (n = 6, 34.3 ± 1.7 PMN/mm2) compared with vehicle-treated myocardium (n = 6, 59.7 ± 3.1 PMN/mm2). In addition, PR-39 significantly (P < 0.05) attenuated leukocyte rolling and adherence in rat inflamed mesentery. These results indicate that PR-39 inhibits leukocyte recruitment into inflamed tissue and attenuated myocardial reperfusion injury in a murine model of myocardial ischemia-reperfusion.

intravital microscopy; reactive oxygen species; myocardial injury; leukocyte accumulation


This article has been cited by other articles:


Home page
 Eur. J. Cardiothorac. Surg.Home page
J. Zhu, Y. Qiu, Q. Wang, Y. Zhu, S. Hu, L. Zheng, L. Wang, and Y. Zhang
Low dose cyclophosphamide rescues myocardial function from ischemia-reperfusion in rats
Eur. J. Cardiothorac. Surg., September 1, 2008; 34(3): 661 - 666.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
Q. Wang, R. V. Donthi, J. Wang, A. J. Lange, L. J. Watson, S. P. Jones, and P. N. Epstein
Cardiac phosphatase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase increases glycolysis, hypertrophy, and myocyte resistance to hypoxia
Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2889 - H2897.
[Abstract] [Full Text] [PDF]

Home page
 Vet PatholHome page
B. Grubor, D. K. Meyerholz, and M. R. Ackermann
Collectins and cationic antimicrobial peptides of the respiratory epithelia.
Vet. Pathol., September 1, 2006; 43(5): 595 - 612.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
A. K. Thukkani, B. D. Martinson, C. J. Albert, G. A. Vogler, and D. A. Ford
Neutrophil-mediated accumulation of 2-ClHDA during myocardial infarction: 2-ClHDA-mediated myocardial injury
Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2955 - H2964.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
D. Li, V. Williams, L. Liu, H. Chen, T. Sawamura, T. Antakli, and J. L. Mehta
LOX-1 inhibition in myocardial ischemia-reperfusion injury: modulation of MMP-1 and inflammation
Am J Physiol Heart Circ Physiol, November 1, 2002; 283(5): H1795 - H1801.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
J. Bao, K. Sato, M. Li, Y. Gao, R. Abid, W. Aird, M. Simons, and M. J. Post
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated Ikappa Balpha degradation
Am J Physiol Heart Circ Physiol, December 1, 2001; 281(6): H2612 - H2618.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
S. Sanada, M. Kitakaze, K. Node, S. Takashima, A. Ogai, H. Asanuma, Y. Sakata, M. Asakura, H. Ogita, Y. Liao, et al.
Differential Subcellular Actions of ACE Inhibitors and AT1 Receptor Antagonists on Cardiac Remodeling Induced by Chronic Inhibition of NO Synthesis in Rats
Hypertension, September 1, 2001; 38(3): 404 - 411.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online