Development of cardiac sensitivity to oxygen deficiency: comparative and ontogenetic aspects
Language English Country United States Media print
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't, Review
- MeSH
- Hypoxia physiopathology MeSH
- Myocardial Ischemia physiopathology MeSH
- Cardiomyopathies physiopathology MeSH
- Humans MeSH
- Disease Susceptibility MeSH
- Ischemic Preconditioning MeSH
- Aging physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Comparative Study MeSH
Hypoxic states of the cardiovascular system are undoubtedly associated with the most frequent diseases of modern times. They originate as a result of disproportion between the amount of oxygen supplied to the cardiac cell and the amount actually required by the cell. The degree of hypoxic injury depends not only on the intensity and duration of the hypoxic stimulus, but also on the level of cardiac tolerance to oxygen deprivation. This variable changes significantly during phylogenetic and ontogenetic development. The heart of an adult poikilotherm is significantly more resistant as compared with that of the homeotherms. Similarly, the immature homeothermic heart is more resistant than the adult, possibly as a consequence of its greater capability for anaerobic glycolysis. Tolerance of the adult myocardium to oxygen deprivation may be increased by pharmacological intervention, adaptation to chronic hypoxia, or preconditioning. Because the immature heart is significantly more dependent on transsarcolemmal calcium entry to support contraction, the pharmacological protection achieved with drugs that interfere with calcium handling is markedly altered. Developing hearts demonstrated a greater sensitivity to calcium channel antagonists; a dose that induces only a small negative inotropic effect in adult rats stops the neonatal heart completely. Adaptation to chronic hypoxia results in similarly enhanced cardiac resistance in animals exposed to hypoxia either immediately after birth or in adulthood. Moreover, decreasing tolerance to ischemia during early postnatal life is counteracted by the development of endogenous protection; preconditioning failed to improve ischemic tolerance just after birth, but it developed during the early postnatal period. Basic knowledge of the possible improvements of immature heart tolerance to oxygen deprivation may contribute to the design of therapeutic strategies for both pediatric cardiology and cardiac surgery.
References provided by Crossref.org
Sex Differences in Cardiac Tolerance to Oxygen Deprivation - 40 Years of Cardiovascular Research
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
Developmental Aspects of Cardiac Adaptation to Increased Workload
Sex-based differences in cardiac ischaemic injury and protection: therapeutic implications
Neonatal cardiac mitochondria and ischemia/reperfusion injury
Selenium protects the immature rat heart against ischemia/reperfusion injury
Postnatal development of phospholipids and their fatty acid profile in rat heart
Myocardial ischemic injury and protection