Differences in left ventricular cardiomyocyte loss induced by chronic intermittent hypoxia between spontaneously hypertensive and Wistar-Kyoto rats.
Summary of "Differences in left ventricular cardiomyocyte loss induced by chronic intermittent hypoxia between spontaneously hypertensive and Wistar-Kyoto rats."
Chronic intermittent hypoxia (CIH) is thought to induce several cardiovascular effects in patients with obstructive sleep apnoea (OSA). However, the effects of CIH on patients with long-standing hypertension are unknown.
This prospective study aimed to investigate the influence of combined OSA and hypertension on cardiomyocyte death.
Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were exposed to repetitive hypoxia-reoxygenation cycles (30 s of 5% O(2); 45 s of 21% O(2)) or room air for 6 h/day during the light phase (10 a.m.-4 p.m.) for 10, 20, or 30 days, and the levels of necrosis and apoptosis induced in their left ventricular cardiomyocyte were examined.
CIH increased the accumulation of reactive oxygen species, which induced cardiomyocyte necrosis in WKY and SHR (both p < 0.05). Cardiomyocyte oxidative stress levels by CIH were higher in SHR than in WKY (p < 0.05); therefore, cardiomyocyte necrosis was amplified (p < 0.05). Notably, if a superoxide-scavenging agent is injected beforehand, cardiomyocyte necrosis can be effectively inhibited (p < 0.05). When WKY and SHR are exposed to CIH, increases in mitochondria-released cytochrome c and activation of caspase-3 are found in the cytosolic fraction only in WKY.
CIH causes cardiomyocyte loss in SHR mainly through cardiomyocyte necrosis. In WKY however, CIH simultaneously induces apoptosis and necrosis of cardiomyocytes.
Institute of Medical Sciences, College of Medicine, Tzu Chi University, Hualien, Taiwan.
This article was published in the following journal.
Name: Sleep & breathing = Schlaf & Atmung
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/21136300
- DOI: http://dx.doi.org/10.1007/s11325-010-0448-y
Medical and Biotech [MESH] Definitions
A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).
Isolated Noncompaction Of The Ventricular Myocardium
Rare congenital cardiomyopathies characterized by the lack of left ventricular myocardium compaction. The noncompaction results in numerous prominent trabeculations and a loose myocardial meshwork (spongy myocardium) in the LEFT VENTRICLE. Heterogeneous clinical features include diminished systolic function sometimes associated with left ventricular dilation, that presents either neonatally or progressively. Often, the RIGHT VENTRICLE is also affected. CONGESTIVE HEART FAILURE; PULMONARY EMBOLISM; and ventricular ARRHYTHMIA are commonly seen.
Absence of the orifice between the RIGHT ATRIUM and RIGHT VENTRICLE, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR) because the right ventricle is absent or not functional.
Ventricular Dysfunction, Left
A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.
Hypertrophy, Left Ventricular
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.
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