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  • 1995-1999  (2)
  • Ischemic preconditioning  (1)
  • Key words Free radicals – N-2-mercaptopropionyl glycine – myocardial infarction – preconditioning – triphenyltetrazolium chloride  (1)
  • 1
    Electronic Resource
    Electronic Resource
    The mechanism of protection from 5 (N-ethyl-N-isopropyl)amiloride differs from that of ischemic preconditioning in rabbit heart (1997)
    Springer
    Basic research in cardiology 92 (1997), S. 339-350 
    Details
    ISSN: 1435-1803
    Keywords: Ischemic preconditioning ; Na+/H+ exchange ; 5-(N-ethyl-N-isopropyl)amiloride (EIPA) ; protein kinase C
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of 5-(N-ethyl-N-isopropyl)amiloride (EIPA) on infarction in isolated rabbit hearts and cardiomyocytes. Thirty min of regional ischemia caused 29.6±2.8% of the risk zone to infarct in untreated Krebs buffer-perfused hearts. Treatment with EIPA (1 μM) for 20 min starting either 15 min before ischemia or 15 min after the onset of ischemia significantly reduced infarction to 5.4±2.0% and 7.0±1.0%, respectively (p〈0.01 versus untreated hearts). In both cases salvage was very similar to that seen with ischemic preconditioning (PC) (7.1±1.5% infarction). Unlike the case with ischemic preconditioning, however, protection from EIPA was not blocked by 50μM polymyxin B, a PKC inhibitor, or 1μM glibenclamide, a KATP channel blocker. Forty-five min of regional ischemia caused 51.0±2.9% infarction in untreated hearts. Ischemic preconditioning reduced infarction to 23.4±3.1% (p〈0.001 versus untreated hearts). In these hearts with longer periods of ischemia pretreatment with EIPA reduced infarction similarly to 28.8±2.1% (p〈0.01 versus untreated hearts). However, when EIPA was combined with ischemic PC, no further reduction in infarction was seen (23.8±3.5% infarction). To further elucidate the mechanism of EIPA's cardioprotective effect, this agent was also examined in isolated rabbit cardiomyocytes. Preconditioning caused a delay of about 30 min in the progressive increase in osmotic fragility that occurs during simulated ischemia. In contrast, EIPA had no effect on the time course of ischemia-induced osmotic fragility. Furthermore, EIPA treatment did not alter the salutary effect of ischemic preconditioning when the two were combined in this model. We conclude that Na+/H+ exchange inhibition limits myocardial infarction in the isolated rabbit heart by a mechanism which is quite different from that of ischemic preconditioning. Despite the apparently divergent mechanisms, EIPA's cardioprotective effect could not be added to that of ischemic or metabolic preconditioning in these models.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00788946
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Failure of N-2-mercaptopropionyl glycine to reduce myocardial infarction after 3 days of reperfusion in rabbits (1999)
    Springer
    Basic research in cardiology 94 (1999), S. 180-187 
    Details
    ISSN: 1435-1803
    Keywords: Key words Free radicals – N-2-mercaptopropionyl glycine – myocardial infarction – preconditioning – triphenyltetrazolium chloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have repoarted that prolonged infusion of N-2-mercaptopropionyl glycine (MPG), a diffusible antioxidant, could limit infarct size in dogs. However, there are no comparable studies testing this agent in other species. We examined the efficacy of MPG in a rabbit model of infarction. Rabbit hearts were subjected to a 30-min coronary artery occlusion. Infarct size expressed as a percentage of risk zone was determined by either triphenyltetrazolium chloride (TTC) staining after 3 h of reperfusion (study 1) or by histology after 72 h of reperfusion (study 2). In study 1, 37 ± 2.6 % of the risk zone infarcted in the control group. Intravenous MPG at a rate of 100 mg/kg/h starting 15 min after the onset of ischemia and continuing until 1 h after reperfusion had no effect on infarct size (35.4 ± 3.4 % infarction). However, infusion of MPG until the end of reperfusion significantly reduced infarct size as measured with TTC to 17.2 ± 2.5 % (p 〈 0.01 vs. control group). In study 2, 48.6 ± 4.0 % of the risk zone infarcted in the control group. In the treatment group MPG was started as above and was continued for 4 h of reperfusion followed by an intramuscular injection at the termination of the intravenous infusion. No protection was seen after 72 h of reperfusion (43.8 ± 2.1 % infarction). These findings reveal that MPG at a dose and schedule that appeared to protect the dog heart could not effect sustained protection in the rabbit heart. TTC staining revealed that MPG appeared to have preserved viability for up to 3 h of reperfusion suggesting that failure may have been due to early withdrawal of the drug. Alternatively, early TTC staining may yield spurious results under conditions in which protection is dependent upon antioxidant or free radical scavenger treatment as has previously been suggested. It is concluded that MPG as administered in the previous canine studies does not limit infarct size in all species, thus raising a concern about MPG's potential efficacy in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003950050141
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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