Ischemic preconditioning in chronically hypoxic neonatal rat heart
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Hematocrit MeSH
- Hydroxy Acids pharmacology MeSH
- Hypoxia physiopathology MeSH
- Rats MeSH
- Decanoic Acids pharmacology MeSH
- NG-Nitroarginine Methyl Ester pharmacology MeSH
- Animals, Newborn * MeSH
- Rats, Wistar MeSH
- Ischemic Preconditioning * MeSH
- Heart drug effects physiopathology MeSH
- Body Weight MeSH
- Organ Size MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 5-hydroxydecanoic acid MeSH Browser
- Hydroxy Acids MeSH
- Decanoic Acids MeSH
- NG-Nitroarginine Methyl Ester MeSH
Rat hearts isolated on d 1, 4, 7, and 10 of postnatal life were perfused (in Langendorff mode) with Krebs-Henseleit solution at constant pressure, temperature, and stimulation rate. Recovery of the contractile function after global ischemia was measured by an isometric force transducer and analyzed using an online computer. Ischemic preconditioning (IP) was induced by three 3-min periods of global ischemia, each separated by a 5-min period of reperfusion. Prenatal hypoxia was induced by exposure of pregnant mothers to intermittent high altitude (IHA), simulated in a barochamber (8 h/d, 5000 m) from d 15 to 20 of pregnancy. Postnatal hypoxia was simulated by the identical procedure from postnatal d 1 to 6 and 9. Prenatal exposure to IHA failed to improve ischemic tolerance on d 1, but postnatal exposure to IHA improved recovery of the developed force after ischemia on d 7 (33 +/- 3% versus 43 +/- 4%) and 10 (39 +/- 2% versus 54 +/- 2%). Combination of IHA and IP induced higher protective effects in all age groups, including postnatal d 1 (48 +/- 2% versus 56 +/- 3%), whereas IHA and IP applied separately failed to improve ischemic tolerance. Neither the mitochondrial K(ATP) channel blocker 5-hydroxydecanoate nor the nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester abolished protection by IP in normoxic animals, but they decreased significantly protection by IHA hypoxia. The final recovery was even lower than the corresponding normoxic values. It seems likely that mitochondrial K(ATP) channels and nitric oxide may be involved in the protective mechanisms of adaptation to chronic hypoxia but not to that of IP, at least in neonates.
References provided by Crossref.org
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
Neonatal cardiac mitochondria and ischemia/reperfusion injury
Selenium protects the immature rat heart against ischemia/reperfusion injury
Myocardial ischemic injury and protection
