title: [Metallothionein involvement in the delayed protection after ischemic or anoxic preconditioning in myocardium or cultured cardiomyocytes].
abstract: OBJECTIVE
  To study whether metallothionein (MT) is an OH scavenger and plays a protective role in cardiac ischemic/reperfusion injury. MT involves in the delayed protection 24 hr after preconditioning (PC).
  
  
  METHODS
  MT contents in myocardium or cultured cardiomyocytes are assayed at the 0 hr, 12 hr, and 24 hr after PC on the model of rabbit heart in situ or that of the cultured cardiomyocytes. The myocardial infarct size, LDH release, cell viability, and the content of cellular MDA were measured with or without the intervention of PD098059, the inhibitor of mitogen-activated protein kinase in the models before PC and different time intervals after PC.
  
  
  RESULTS
  The MT contents were increased significantly at 2 hr (1406.2 +/- 112.2 vs 129.9 +/- 10.4 pmol/mg Pr., P < 0.01, in cardiomyocytes) and 24 hr (1032.7 +/- 199.1 vs 129.9 +/- 10.4 pmol/mg Pr., P < 0.01, in cardiomyocytes; 62.1 +/- 12.6 vs 27.2 +/- 3.7 pmol/mg Pr., P < 0.01, in myocardium) after PC compared with those in normal group. The infarct sizes (13.2 +/- 3.6% vs 32.3 +/- 5.7%, P < 0.05) and the rise of LDH release in plasma (1944 +/- 256 vs 2826 +/- 239 IU/L, P < 0.05) were greatly decreased in preconditioned myocardium after a long time ischemia-reperfusion than those in the unpreconditioned. Compared with the cardiomyocytes unconditioned, the number of viable cell (71.0 +/- 1.6 vs 48.2 +/- 2.2%, P < 0.01) was greatly increased, the cellular MDA contents (33.5 +/- 12.8 vs 103.5 +/- 15.0 nmol/mg Pr., P < 0.01) and the LDH release (850.0 +/- 139.1 vs 1552.0 +/- 102.6 IU/L, P < 0.01) were dramatically decreased in preconditioned ones. All the delayed protection at 24 hr after PC were completely disappeared with the inhibition of MT's production with PD098059 (P > 0.05).
  
  
  CONCLUSIONS
  The myocardium or cardiomyocytes at 24 hr after PC are offered more capacity to tolerate the I/R damage, and MT involves in the delayed protection.
authors.affiliation: First Hospital, Beijing Medical University.
authors.forename: K
authors.initials: K
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: C
authors.initials: C
authors.lastname: Ye
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D008668:Metallothionein / Q000378:metabolism*; D009203:Myocardial Infarction / Q000378:metabolism / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D011817:Rabbits
chemical_list: D008668:Metallothionein