Cellular and molecular aspects of myocardial dysfunction
| Autor: | David P. Nelson, Jodie Y. Duffy, Steven M. Schwartz, Jeffery M. Pearl |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
medicine.medical_specialty
Apoptosis Critical Care and Intensive Care Medicine law.invention Renin-Angiotensin System law medicine.artery Internal medicine Receptors Adrenergic beta medicine Cardiopulmonary bypass Animals Humans Child Heart Failure Inflammation Aorta business.industry fungi Infant Newborn food and beverages Myocardial Contraction Structure and function Cardiac surgery Surgery Acute Disease Chronic Disease Cardiology Cardiomyopathies business |
| Zdroj: | Critical Care Medicine. 29:S214-S219 |
| ISSN: | 0090-3493 |
| DOI: | 10.1097/00003246-200110001-00003 |
| Popis: | Disruption of any one of a large number of balanced systems that maintain cardiomyocyte structure and function can cause myocardial dysfunction. Such disruption can occur either in response to acute stresses such as cardiac surgery with cardiopulmonary bypass and cross-clamping of the aorta or because of more chronic stresses resulting from factors such as genetic abnormalities, infection, or chronic ischemia. Several currently available therapies such as beta-adrenergic receptor agonists and antagonists, phosphodiesterase inhibitors, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and other agents affect cardiomyocytes in ways that are more far reaching than initially appreciated when these agents were first introduced into clinical practice. As our knowledge and understanding of myocardial dysfunction increases, particularly in the neonatal and pediatric patient, we will be able to further target interventions to highly specific perturbations of cellular function and individual genetic variability. |
| Databáze: | OpenAIRE |
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