Ischemic tolerance of rat hearts in acute and chronic phases of experimental diabetes
Language English Country Netherlands Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Diabetes Mellitus, Experimental complications physiopathology MeSH
- Myocardial Infarction physiopathology MeSH
- Myocardial Ischemia physiopathology MeSH
- Rats MeSH
- Disease Susceptibility MeSH
- Rats, Wistar MeSH
- Heart physiopathology MeSH
- Arrhythmias, Cardiac physiopathology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
UNLABELLED: Different from clinical studies of diabetes mellitus (DM), experimental data reveal both, higher and lower vulnerability of the heart to ischemic injury. We have previously demonstrated an enhanced resistance to ischemia-induced arrhythmias in isolated rat hearts in the acute phase of DM. Our objectives were thus to extend our knowledge to the effects of DM of different duration on myocardial infarction, in conjunction with susceptibility to arrhythmias, in the in vivo model. DM was induced by streptozotocin (45 mg/kg, i.v.) and following 1 week (acute phase) and 8 weeks (chronic phase), anesthetized open-chest diabetic and age-matched control rats were subjected to 30-min regional ischemia (occlusion of LAD coronary artery) followed by 4-h reperfusion for the evaluation of the infarct size (tetrazolium staining). In the control rats, ventricular tachycardia (VT) represented 45.4% of total arrhythmias and occurred in 90% of the animals. In the acute phase of DM, arrhythmia profile was similar to that in the control animals, and the incidence and severity of arrhythmias were not enhanced. On the other hand, the size of infarct area normalized to the size of area at risk was significantly smaller in the diabetics than in the controls (47.2 +/- 2.8 vs. 70.2 +/- 2.1%, respectively; p < 0.05). In the chronic phase, only 17.7% of arrhythmias occurred as VT in 44% of the diabetics (p < 0.05 vs. controls). Severity of arrhythmias was also lower (arrhythmia score: 2.1 +/- 0.3 vs. 2.9 +/- 0.3 in the controls, respectively; p < 0.05). This effect was not due to a smaller infarct size, since the latter did not differ from that in the controls. IN CONCLUSION: diabetic rat hearts exhibit rather lower, than higher sensitivity to ischemia. In acute phase of DM, diabetic hearts are more resistant to irreversible cell damage, whereas in the chronic phase they exhibit reduced susceptibility to arrhythmias; these discrepancies might reflect different pathogenesis of arrhythmias and myocardial infarction.
See more in PubMed
Cardiovasc Res. 1993 Nov;27(11):1908-12 PubMed
Cardiovasc Res. 1992 May;26(5):487-95 PubMed
Cardiovasc Res. 1996 Apr;31(4):526-36 PubMed
Cardiovasc Res. 1998 Nov;40(2):239-47 PubMed
Mol Cell Biochem. 1996 May 10;158(1):43-51 PubMed
Circulation. 1993 Sep;88(3):1273-8 PubMed
Cardiovasc Res. 1993 Apr;27(4):644-51 PubMed
Circulation. 1979 Jan;59(1):8-13 PubMed
Cardiovasc Res. 1993 Apr;27(4):608-11 PubMed
J Mol Cell Cardiol. 1998 Sep;30(9):1869-75 PubMed
Basic Res Cardiol. 2001 Apr;96(2):160-8 PubMed
Nature. 1983 Sep 8-14;305(5930):147-8 PubMed
Basic Res Cardiol. 2002 Mar;97(2):161-7 PubMed
J Mol Cell Cardiol. 1989 Jan;21(1):21-40 PubMed
J Mol Cell Cardiol. 1995 Sep;27(9):1883-94 PubMed
J Thorac Cardiovasc Surg. 1996 Sep;112(3):778-86 PubMed
Cardiovasc Res. 1997 Apr;34(1):113-20 PubMed
Basic Res Cardiol. 1982 Mar-Apr;77(2):117-39 PubMed
Circ Res. 1997 Dec;81(6):1027-33 PubMed
Jpn J Physiol. 1999 Oct;49(5):409-15 PubMed
Am J Physiol. 1983 Jun;244(6):E528-35 PubMed
Cardiovasc Res. 1988 Jul;22(7):447-55 PubMed
J Mol Cell Cardiol. 1995 Apr;27(4):969-79 PubMed
J Physiol. 1995 Nov 1;488 ( Pt 3):673-88 PubMed
Cardiovasc Res. 1998 Jul;39(1):194-215 PubMed
Mol Cell Biochem. 2000 Jul;210(1-2):143-51 PubMed
J Mol Cell Cardiol. 1995 Jan;27(1):169-79 PubMed
Circ Res. 1991 Apr;68(4):1127-37 PubMed
Am J Physiol. 1990 Jan;258(1 Pt 2):H255-61 PubMed
Life Sci. 1985 Aug 12;37(6):547-51 PubMed
Cardiovasc Res. 1990 Nov;24(11):873-8 PubMed
Circ Res. 1988 May;62(5):931-40 PubMed
J Am Coll Cardiol. 1999 Jan;33(1):119-24 PubMed
Circulation. 1986 Nov;74(5):1124-36 PubMed
J Mol Cell Cardiol. 1992 Apr;24(4):411-21 PubMed
Eur Heart J. 1988 Mar;9(3):259-64 PubMed
Circ Res. 1995 Jan;76(1):73-81 PubMed
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
