Ischemic Preconditioning in Chronically Hypoxic Neonatal Rat Heart

Ošťádalová, I

doi:10.1203/01.pdr.0000030879.20888.5b

Cited by 25 publications

(27 citation statements)

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“…The improved recovery of cardiac contractile function in the hypoxic group confirms our previous observations (23), as well as those of others (4,41), indicating that the already high ischemic tolerance of the immature heart can be further increased by chronic hypoxia. Despite a certain recent progress in understanding this protective phenomenon, its detailed mechanism is still far from clear (15).…”

Section: Discussionsupporting

confidence: 90%

“…The extent of these adaptive responses to hypoxia was comparable with those of our previous studies using the same experimental model (23). Chronic treatment with AT 1 receptor blocker irbesartan during the same developmental period led to a proportional retardation of body and heart growths since the normalized mass of the two ventricles was not appreciably affected in the normoxic group.…”

Section: Discussionsupporting

confidence: 86%

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ANG II type 1 receptor antagonist irbesartan inhibits coronary angiogenesis stimulated by chronic intermittent hypoxia in neonatal rats

Rakusan¹,

Chvojkova²,

Oliviéro³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Rakusan K, Chvojkova Z, Oliviero P, Ostadalova I, Kolar F, Chassagne C, Samuel JL, Ostadal B. ANG II type 1 receptor antagonist irbesartan inhibits coronary angiogenesis stimulated by chronic intermittent hypoxia in neonatal rats. Am J Physiol Heart Circ Physiol 292: H1237-H1244, 2007. First published December 1, 2006; doi:10.1152/ajpheart.00965.2006.-Chronic hypoxia has been shown to stimulate myocardial microvascular growth and improve cardiac ischemic tolerance in young and adult rats. The aim of this study was to determine whether the ANG II type 1 receptor (AT1) pathway was involved in these processes. Newborn Wistar rats, exposed to chronic intermittent hypoxia (8 h/day) for 10 days, were simultaneously treated with AT1 receptor blocker irbesartan and compared with untreated animals. The major finding is that chronic hypoxia increased the capillary supply of myocardial tissue, which was even more pronounced in hypertrophied right ventricle, whereas increased arteriolar supply was found only in the left ventricle. This angiogenic response was completely prevented by irbesartan. Moreover, chronic hypoxia improved the postischemic recovery of cardiac contractile function during reperfusion, and this protective effect was also completely abolished by irbesartan. Chronic hypoxia increased the myocardial density of AT1 but not of ANG II type 2 receptor subtypes, whereas the effect of irbesartan was not significant. The expression of caveolin-1␣ markedly increased in response to chronic hypoxia, and irbesartan prevented this effect. Neither hypoxia nor irbesartan treatment altered the expression of nitric oxide synthase 3, heat shock protein 90, and VEGF. It is concluded that the AT1 receptor pathway plays an important role in coronary angiogenesis and improved cardiac ischemic tolerance induced in neonatal rats by chronic hypoxia.angiotensin II receptors; ischemia-reperfusion; caveolin-1 ADAPTATION TO CHRONIC HYPOXIA increases cardiac tolerance to all major deleterious consequences of acute oxygen deprivation in both adult and immature heart. In addition to the protective effect, chronic hypoxia may also induce other adaptive responses, including hypoxic pulmonary hypertension and right ventricular (RV) hypertrophy (22). This is a beneficial adaptation, allowing the RV to cope with an increased afterload and to maintain cardiac output. Although many potential factors have been proposed to play a role in the mechanisms of cardiac adaptation to chronic hypoxia, the available data are not sufficiently conclusive. Moreover, a substantial amount of information concerning the adaptive response was obtained from the adult myocardium, whereas much less is known about this process in the immature heart. However, clinical relevance of the developmental approach is obvious: chronic hypoxia is the main pathophysiological feature of hypoxemic congenital heart disease. Understanding the mechanisms by which these malformations modify the myocardium and how they impact on the adaptive mechanisms during ischemia may provide ins...

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 86%

ANG II type 1 receptor antagonist irbesartan inhibits coronary angiogenesis stimulated by chronic intermittent hypoxia in neonatal rats

Rakusan¹,

Chvojkova²,

Oliviéro³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Different letters denote significant differences among groups. Several authors have used chronic maternal hypoxia to restrict fetal growth in rats previously and have demonstrated that across a range of oxygen reductions imposed at different times throughout gestation, this treatment results in reduced fetal or neonatal body weight and altered fetal organ growth (6,15,25,28,34,36,37,46,47). Decreased maternal food intake as a consequence of maternal hypoxia has also been reported previously (6,15,46).…”

Section: Discussionmentioning

confidence: 72%

“…Intermittent hypobaric hypoxia, either prenatally or postnatally, in rats also increased heart weight and proportion of body weight (34). It is interesting that several recent studies have demonstrated perturbations in heart development and function after chronic maternal hypoxia (25,47).…”

Section: Discussionmentioning

confidence: 98%

Differential effects of maternal hypoxia or nutrient restriction on carotid and femoral vascular function in neonatal rats

Williams

Campbell²,

McMillen³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

116

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“…Adult and neonatal rats exhibited diminished frequency of ischemia-induced, K ATP channel-dependent arrhythmias, smaller infarct size and better postischemic contractility recovery following IH exposure (12,153,161). Furthermore, effects of IH adaptation were abolished by administration of K ATP channel blockers (glibenclamide, 5-hydroxydecanoate) while K ATP channel openers diazoxide (mitochondrial-selective) and pinacidil (general) mimicked the beneficial effects of IH in control animals (12,274 (129,142,163); and 3) regulation of mitochondrial volume and respiratory chain activity (126).…”

Section: Circulatory Systemmentioning

confidence: 99%

Hypoxia. 4. Hypoxia and ion channel function

Shimoda

Polàk

2011

American Journal of Physiology-Cell Physiology

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The ability to sense and respond to oxygen deprivation is required for survival; thus, understanding the mechanisms by which changes in oxygen are linked to cell viability and function is of great importance. Ion channels play a critical role in regulating cell function in a wide variety of biological processes, including neuronal transmission, control of ventilation, cardiac contractility, and control of vasomotor tone. Since the 1988 discovery of oxygen-sensitive potassium channels in chemoreceptors, the effect of hypoxia on an assortment of ion channels has been studied in an array of cell types. In this review, we describe the effects of both acute and sustained hypoxia (continuous and intermittent) on mammalian ion channels in several tissues, the mode of action, and their contribution to diverse cellular processes. oxygen deprivation; mammalian ion channels; oxygen homeostasis SENSING and appropriately responding to changes in O 2 concentration is of paramount importance for the survival of all organisms. Over time, O 2 homeostasis has evolved into a complex system to regulate O 2 delivery and use. While the rapid response to acute reductions in O 2 concentration typically results from processes that alter preexisting proteins, such as phosphorylation, stabilization, dimerization, or degradation, durable adaptation to prolonged hypoxic insult requires a coordinated response at the level of gene transcription. Since a deficit in O 2 is an important component of various physiological processes and the pathogenesis of numerous diseases, understanding the mechanisms by which changes in O 2 are linked to cell function is of great interest.Ion channels play a critical role in regulating a wide variety of biological processes, including neuronal transmission; control of ventillation; contraction of cardiac, skeletal, and smooth muscle; transport of nutrients and ions across the epithelium; T-cell activation; and glucose metabolism and pancreatic ␤-cell insulin release. To date, over 300 types of ion channels, differing in their mode of activation (voltage-dependent or -independent, ligand-gated, mechanosensitive, pH) and their ionic permeability (K ϩ , Ca 2ϩ , Cl Ϫ , Na ϩ ), have been identified. This heterogeneity in ion channel populations provides an astonishing array of variable responses within and between cell types. In 1988, a report demonstrating that rabbit carotid body glomus cells express an O 2 -sensitive potassium channel ushered in a new era of research exploring whether ion channel activity could be regulated in response to changes in O 2 availability (131). Since that initial description of an O 2 -regulated ion channel, an abundance of work has been produced indicating that a variety of ion channels spread across the different ion channel families are O 2 sensitive and exhibit changes in channel activity with acute hypoxia and alterations in channel quantity with prolonged hypoxic challenge. Although a great amount of work has been devoted to the study of hypoxia and ion channels in reptiles, amp...

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Ischemic Preconditioning in Chronically Hypoxic Neonatal Rat Heart

Cited by 25 publications

References 0 publications

ANG II type 1 receptor antagonist irbesartan inhibits coronary angiogenesis stimulated by chronic intermittent hypoxia in neonatal rats

ANG II type 1 receptor antagonist irbesartan inhibits coronary angiogenesis stimulated by chronic intermittent hypoxia in neonatal rats

Differential effects of maternal hypoxia or nutrient restriction on carotid and femoral vascular function in neonatal rats

Hypoxia. 4. Hypoxia and ion channel function

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