Display options
Cite
Strande JL, Routhu KV, Hsu A, et al. Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury. J Inflamm (Lond). 2009;6:34doi: 10.1186/1476-9255-6-34.
Strande, J. L., Routhu, K. V., Hsu, A., Nicolosi, A. C., & Baker, J. E. (2009). Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury. Journal of inflammation (London, England), 634. https://doi.org/10.1186/1476-9255-6-34
Strande, Jennifer L, et al. "Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury." Journal of inflammation (London, England) vol. 6 (2009): 34. doi: https://doi.org/10.1186/1476-9255-6-34
Strande JL, Routhu KV, Hsu A, Nicolosi AC, Baker JE. Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury. J Inflamm (Lond). 2009 Dec 10;6:34. doi: 10.1186/1476-9255-6-34. PMID: 20003243; PMCID: PMC2799407.
Copy Download .nbib Format: NLM
Share it on

J Inflamm (Lond). 2009 Dec 10;6:34. doi: 10.1186/1476-9255-6-34.

Gadolinium decreases inflammation related to myocardial ischemia and reperfusion injury.

Journal of inflammation (London, England)

Jennifer L Strande, Kasi V Routhu, Anna Hsu, Alfred C Nicolosi, John E Baker

Affiliations

  1. Division of Cardiovascular Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, USA. [email protected].

PMID: 20003243 PMCID: PMC2799407 DOI: 10.1186/1476-9255-6-34

Abstract

BACKGROUND: The lanthanide cation, gadolinium (GdCl3) protects the myocardium against infarction following ischemia and reperfusion. Neutrophils and macrophages are the main leukocytes responsible for infarct expansion after reperfusion. GdCl3 interferes with macrophage and neutrophil function in the liver by decreasing macrophage secretion of inflammatory cytokines and neutrophil infiltration. We hypothesized that GdCl3 protects against ischemia and reperfusion injury by decreasing inflammation. We determined the impact of GdCl3 treatment for reperfusion injury on 1) circulating monoctye and neutrophil counts, 2) secretion of inflammatory cytokines, and 3) influx of monocytes and neutrophils into the myocardium.

METHODS: Rats (n = 3-6/gp) were treated with saline or GdCl3 (20 mumol/kg) 15 min prior to a 30 min period of regional ischemia and 120 min reperfusion. Sham rats were not subject to ischemia. Blood was collected either after 30 min ischemia or 120 min reperfusion and hearts were harvested at 120 min reperfusion for tissue analysis. Blood was analyzed for leukocytes counts and cytokines. Tissue was analyzed for cytokines and markers of neutrophil and monocyte infiltration by measuring myeloperoxidase (MPO) and alpha-naphthyl acetate esterase (ANAE).

RESULTS: GdCl3 did not affect the number of circulating neutrophils prior to ischemia. Two hours reperfusion resulted in a 2- and 3- fold increase in circulating monocytes and neutrophils, respectively. GdCl3 decreased the number of circulating monocytes and neutrophils during reperfusion to levels below those present prior to ischemia. Furthermore, after 120 min of reperfusion, GdCl3 decreased ANAE and MPO activity in the myocardium by 1.9-fold and 6.5-fold respectively. GdCl3 decreased MPO activity to levels below those measured in the Sham group. Serum levels of the major neutrophil chemoattractant cytokine, IL-8 were increased from pre-ischemic levels during ischemia and reperfusion in both control and GdCl3 treated rats. Likewise, IL-8 levels increased throughout the 3 hour time period in the Sham group. There was no difference in IL-8 detected in the myocardium after 120 min reperfusion between groups. In contrast, after 120 min reperfusion GdCl3 decreased the myocardial tissue levels of macrophage secreted cytokines, GM-CSF and IL-1.

CONCLUSION: GdCl3 treatment prior to ischemia and reperfusion injury decreased circulating monocytes and neutrophils, macrophage secreted cytokines, and leukocyte infiltration into injured myocardium. These results suggest GdCl3 decreased monoctye and neutrophil migration and activation and may be a novel treatment for inflammation during ischemia and reperfusion.

References

  1. J Surg Res. 2001 Apr;96(2):204-10 - PubMed
  2. Am J Physiol Heart Circ Physiol. 2003 Apr;284(4):H1080-6 - PubMed
  3. J Pharmacol Exp Ther. 2008 Mar;324(3):1045-54 - PubMed
  4. Ann Thorac Surg. 2001 May;71(5):1596-602 - PubMed
  5. Am J Physiol Lung Cell Mol Physiol. 2004 Feb;286(2):L363-72 - PubMed
  6. Cardiovasc Res. 2002 Jan;53(1):31-47 - PubMed
  7. Toxicol Pathol. 1996 Sep-Oct;24(5):588-94 - PubMed
  8. J Clin Invest. 1995 Jan;95(1):134-41 - PubMed
  9. J Am Coll Cardiol. 1997 Nov 15;30(6):1554-61 - PubMed
  10. Shock. 1999 Jun;11(6):403-10 - PubMed
  11. Science. 2009 Jul 31;325(5940):612-6 - PubMed
  12. Am J Pathol. 2006 Feb;168(2):659-69 - PubMed
  13. Biochem Pharmacol. 2000 Feb 15;59(4):369-75 - PubMed
  14. Circulation. 1988 Dec;78(6):1449-58 - PubMed
  15. Circulation. 2005 Dec 20;112(25):3911-8 - PubMed
  16. J Mol Cell Cardiol. 2008 Feb;44(2):345-51 - PubMed
  17. J Pharmacol Exp Ther. 1984 Feb;228(2):510-22 - PubMed
  18. Am J Physiol. 1996 Jun;270(6 Pt 1):G909-18 - PubMed
  19. Hepatobiliary Pancreat Dis Int. 2006 Aug;5(3):436-42 - PubMed
  20. Circulation. 1983 May;67(5):1016-23 - PubMed
  21. Cytokine. 2005 Dec 7;32(5):199-205 - PubMed
  22. Am J Physiol. 1986 Aug;251(2 Pt 2):H314-23 - PubMed
  23. Br J Exp Pathol. 1980 Dec;61(6):624-30 - PubMed
  24. Eur J Pharmacol. 1994 Jan 3;270(1):45-51 - PubMed
  25. J Pharmacol Methods. 1990 Dec;24(4):285-95 - PubMed
  26. J Leukoc Biol. 1994 Jun;55(6):723-8 - PubMed
  27. Cardiovasc Res. 1999 Mar;41(3):722-30 - PubMed

Publication Types