Adaptation to High Altitude Hypoxia Protects the Rat Heart Against Ischemia-induced Arrhythmias. Involvement of Mitochondrial KATPChannel

Asemu, Girma; Papoušek, F; Ošťádal, B; Kolář, František

doi:10.1006/jmcc.1999.1013

Cited by 101 publications

(90 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous investigators have shown that intermittent hypoxia could protect against ischemia/ reperfusion injury [4][5][6]11], but no measure of apoptosis has been reported. Another finding in our study is that the antiapoptotic effect of intermittent hypoxia was due to regulate expression of Bcl-2/Bax protein.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies showed that intermittent hypoxia might have the cardioprotective effects similar to those observed in ischemic preconditioning [2][3][4][5][6][7][8]. A number of studies have attempted to define the mechanisms of this phenomenon and several potential factors have been proposed to be involved in the protective mechanism afforded by intermittent hypoxia [3,[5][6][7][9][10][11], however, the precise mechanisms underlying the protective effects of intermittent hypoxia on ischemic hearts are far from clear.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

et al. 2003

View full text Add to dashboard Cite

Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury. Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion. Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins, Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion, enhanced recovery of cardiac function was observed in intermittent hypoxia hearts compared with normoxia group. Ischemia/ reperfusion-induced apoptosis, as evidenced by TUNEL-positive nuclei and DNA fragmentation, was significantly reduced in intermittent hypoxia group compared with normoxia group. After ischemia/reperfusion, expression of Bax in both cytosolic and membrane fractions was decreased in intermittent hypoxia hearts compared with normoxia group. Although ischemia/reperfusion did not induce changes in the level of Bcl-2 expression in cytosolic fraction between intermittent hypoxia and normoxia groups, the expression of Bcl-2 in membrane fraction was upregulated in intermittent hypoxia group compared with normoxia group. These results indicated that the cardioprotection of intermittent hypoxia against ischemia/reperfusion injury appears to be in part due to reduce myocardial apoptosis. Intermittent hypoxia attenuated ischemia/reperfusion-induced apoptosis via increasing the ratio of Bcl-2/Bax, especially in membrane fraction.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

et al. 2003

View full text Add to dashboard Cite

show abstract

“…Activation of mitochondrial K ATP channels initiates ischemic pre-conditioning and prevents the mitochondrial dysfunction associated with Ca 2+ overload during ischemic reperfusion in the heart [116][117][118] . In adult animals, application of mitochondrial K ATP openers, such as diazoxide or BMS-191095, reduces neuronal death (rats: [116,[119][120][121] ; mice: [122] ), whereas a selective mitochondrial K ATP channel blocker, 5-hydroxydecanoate, prevents preconditioning-induced neuronal protection in middle cerebral artery occlusion (MCAO) focal cerebral ischemia [123] .…”

Section: K Atp Channels and Their Neuroprotective Role In Cerebral Ismentioning

confidence: 99%

“…In adult animals, application of mitochondrial K ATP openers, such as diazoxide or BMS-191095, reduces neuronal death (rats: [116,[119][120][121] ; mice: [122] ), whereas a selective mitochondrial K ATP channel blocker, 5-hydroxydecanoate, prevents preconditioning-induced neuronal protection in middle cerebral artery occlusion (MCAO) focal cerebral ischemia [123] . In contrast, xenon-induced preconditioning is not associated with the mitochondrial channels, but rather, is mediated by plasmalemma K ATP channels [124] .…”

Section: K Atp Channels and Their Neuroprotective Role In Cerebral Ismentioning

confidence: 99%

Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia

Sun

Feng

2012

Acta Pharmacol Sin

View full text Add to dashboard Cite

ATP-sensitive potassium (K ATP ) channels are weak, inward rectifiers that couple metabolic status to cell membrane electrical activity, thus modulating many cellular functions. An increase in the ADP/ATP ratio opens K ATP channels, leading to membrane hyperpolarization. K ATP channels are ubiquitously expressed in neurons located in different regions of the brain, including the hippocampus and cortex. Brief hypoxia triggers membrane hyperpolarization in these central neurons. In vivo animal studies confirmed that knocking out the Kir6.2 subunit of the K ATP channels increases ischemic infarction, and overexpression of the Kir6.2 subunit reduces neuronal injury from ischemic insults. These findings provide the basis for a practical strategy whereby activation of endogenous K ATP channels reduces cellular damage resulting from cerebral ischemic stroke. K ATP channel modulators may prove to be clinically useful as part of a combination therapy for stroke management in the future.

show abstract

“…It has been reported that the hearts of animals adapted to long-term HAH develop better functional recovery following ischemia and produce smaller cardiac infarction. In addition, it has also been reported that adaptation to HAH could protect the heart against ischemia-induced arrhythmias [38]. However, the cardioprotective effect of adaptation to HAH is age-dependent.…”

Section: Cardiac Systemmentioning

confidence: 99%

Cardiovascular Adaptation to High-Altitude Hypoxia

Ji¹,

Wang²,

Xiao³

2017

Hypoxia and Human Diseases

View full text Add to dashboard Cite

High-altitude exposure has been well recognized as a hypoxia exposure that significantly affects cardiovascular function. However, the pathophysiologic adaptation of cardiovascular system to high-altitude hypoxia (HAH) varies remarkably. It may depend on the exposed time and oxygen partial pressure in the altitude place. In short-term HAH, cardiovascular adaptation is mainly characterized by functional alteration, including cardiac functional adjustments, pulmonary vascular constriction, transient pulmonary hypertension, and changes in cerebral blood flow (CBF). These changes may be explained mainly by ventilatory acclimatization and variation of autonomic nervous activity. In long-term HAH, cardiovascular adaptation is mainly characterized by both functional and structural alterations. These changes include right ventricle (RV) hypertrophy, persistent pulmonary hypertension, lower CBF and reduced uteroplacental and fetal volumetric blood flows.

show abstract

Adaptation to High Altitude Hypoxia Protects the Rat Heart Against Ischemia-induced Arrhythmias. Involvement of Mitochondrial KATPChannel

Cited by 101 publications

References 40 publications

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia

Cardiovascular Adaptation to High-Altitude Hypoxia

Contact Info

Product

Resources

About