Cardiac adaptation to chronic high-altitude hypoxia: Beneficial and adverse effects

Ošťádal, B; Kolář, František

doi:10.1016/j.resp.2007.03.005

Cited by 109 publications

(69 citation statements)

References 111 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hearts of hypoxia-acclimated cod were better able to maintain Q max during severe hypoxia and showed significantly enhanced recovery following 30min of reperfusion with oxygenated saline (Figs3 and 4, Table4). These results suggest that acclimation to chronic hypoxia increases myocardial hypoxia tolerance, and are consistent with the substantial body of research that has been conducted on chronically hypoxic mammals (for a review, see Ostadal and Kolar, 2007). Furthermore, they are in agreement with those of Driedzic et al (Driedzic et al, 1985) who showed that hearts from hypoxia-acclimated (4-6weeks; P O2 , 4-4.7kPa) eelpout were better able to sustain peak tension development during anoxia in the presence of elevated levels of Ca 2+ in the bathing media.…”

Section: Maximum Cardiac Function: Hypoxia and Reperfusionsupporting

confidence: 85%

“…Finally, there are several other mechanisms that have been reported to confer hypoxia tolerance on the mammalian L. H. Petersen and A. K. Gamperl heart during periods of prolonged oxygen deprivation. Amongst these are ATP-sensitive potassium (K ATP ) channels [both sarcolemmal (sK ATP ) and mitochondrial (mK ATP )], nitric oxide (NO), HIF-1a, and various protein kinases (including PKC) (Kolar and Ostadal, 2004;Ostadal and Kolar, 2007). However, research on the importance of these mechanisms in conferring cardioprotection in fishes is still in its infancy, and is often contradictory (see MacCormack and Driedzic, 2002;Chen et al, 2005;Rissanen et al, 2006;Marques et al, 2008).…”

Section: Maximum Cardiac Function: Hypoxia and Reperfusionmentioning

confidence: 99%

See 1 more Smart Citation

In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Petersen

Gamperl

2010

Journal of Experimental Biology

View full text Add to dashboard Cite

SUMMARYRecent in vivo experiments on Atlantic cod (Gadus morhua) acclimated to chronic hypoxia (6-12weeks at 10°C; PW O2~8 -9kPa) revealed a considerable decrease in the pumping capacity of the heart. To examine whether this diminished cardiac performance was due to the direct effects of chronic moderate hypoxia on the myocardium (as opposed to alterations in neural and/or hormonal control), we measured the resting and maximum in situ function of hearts from normoxia-and hypoxia-acclimated cod:(1) when initially perfused with oxygenated saline; (2) at the end of a 15min exposure to severe hypoxia (P O2~0 .6kPa); and (3) 30min after the hearts had been reperfused with oxygenated saline. Acclimation to hypoxia did not influence resting (basal) in situ cardiac performance during oxygenated or hypoxic conditions. However, it caused a decrease in maximum cardiac output (Q max ) under oxygenated conditions (from 49.5 to 40.3mlmin , yet, the hearts of hypoxiaacclimated fish were better able to sustain this level of Q under hypoxia, and the recovery of Q max (as compared with initial values under oxygenated conditions) was significantly improved (94% vs 83%). These data show that acclimation to hypoxia has a direct effect on cod myocardial function and/or physiology, and suggest that the cod heart shows some adaptations to prolonged hypoxia.

show abstract

Section: Maximum Cardiac Function: Hypoxia and Reperfusionsupporting

confidence: 85%

Section: Maximum Cardiac Function: Hypoxia and Reperfusionmentioning

confidence: 99%

In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Petersen

Gamperl

2010

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

“…While severe oxygen deprivation may cause myocardial injury and ultimately heart failure, adaptation to moderate chronic hypoxia leads to complex adaptive changes [38] including metabolic remodeling due to ROS-sensitive induction of a fetal gene program that restores the balance between energy supply and demand [39]. Several studies reported rather diverse and inconclusive results regarding the effects of chronic hypoxia on myocardial energy transfer system [13,14,40], which likely reflects differences in hypoxic challenge and animal species.…”

Section: Introductionmentioning

confidence: 99%

Chronic Hypoxia Enhances Expression and Activity of Mitochondrial Creatine Kinase and Hexokinase in the Rat Ventricular Myocardium

Waskova-Arnostova

Kasparova

Elsnicová

et al. 2014

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Creatine kinase (CK) and hexokinase (HK) play a key role in myocardial energy homeostasis. We aimed to determine CK and HK expression and enzyme activity in the left (LV) and right (RV) ventricles of rats adapted for 3 weeks to normobaric hypoxia (10 % O₂) either continuously (CNH) or intermittently with 1-h or 16-h normoxic episode per day. Methods: The Real-Time RT-PCR, Western blot, and enzyme-coupled assays were used. In addition, the effect of CNH on the HK co-localization with mitochondria, which can inhibit apoptosis, was assessed using immunofluorescence techniques. Results: CK and HK activities increased in the LV during all hypoxic adaptations, which was consistent with elevated protein levels of mitochondrial mtCKs, cytosolic CKB, HK1, and HK2 isoforms. Enzyme activities also increased in the hypoxic RV, but only CKB protein was elevated. No effect of CNH on HK1 or HK2 co-localization with mitochondria was observed. Conclusion: Up-regulation of mtCKs and HK isoforms may stimulate the respiratory chain and help to maintain energy homeostasis of chronically hypoxic myocardium and prevent oxidative stress. In this way, CK and HK enzymes can possibly participate in the establishment of ischemia-resistant phenotype of chronically hypoxic hearts.

show abstract

“…This pathological situation induces complex structural, hormonal, and biochemical modifications that affect both energy-producing and energy-consuming processes in heart cells (see Refs. 20,33). Concerning energy-producing modifications, an important reduction in the mitochondrial mass has been observed, associated with the reduction of the activities of respiratory chain complexes (29).…”

mentioning

confidence: 99%

Modular control analysis of effects of chronic hypoxia on mouse heart

Calmettes

Deschodt-Arsac²,

Thiaudière³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

R13-R19, 2007) was applied here on perfused hearts to describe the modifications of the regulation of heart energetics induced in mice exposed to 3-wk chronic hypoxia. MoCA combines 31 P-NMR spectroscopy and modular (top down) control analysis to describe the integrative regulation of energy metabolism in the intact beating heart, on the basis of two modules [ATP/phosphocreatine (PCr) production and ATP/PCr consumption] connected by the energetic intermediates. In contrast with previous results in rat heart, in which all control of contraction was on ATP demand, mouse heart energetics presented a shared control of contraction between ATP/PCr-producing and -consuming modules. In chronic hypoxic mice, the decrease in heart contractile activity and PCr-to-ATP ratio was surprisingly associated with an important and significant higher response of ATP/PCr production (elasticity) to PCr changes compared with control hearts (Ϫ10.4 vs. Ϫ2.46). By contrast, no changes were observed in ATP/PCr consumption since comparable elasticities were observed. Since elasticities determine the regulation of energetics of heart contraction, the present results show that this new parameter may be used to uncover the origin of the observed dysfunctions under chronic hypoxia conditions. Considering the decrease in mitochondrial content reported after exposure to chronic hypoxia, it appears that the improvement of ATP/PCr production response to ATP demand may be viewed as a positive adaptative mechanism. It now appears crucial to understand the very processes responsible for ATP/PCr producer elasticity toward the energetic intermediates, as well as their regulation. perfused mouse heart; systems biology; 31 P-labeled magnetic resonance spectroscopy CHRONIC HYPOXIA (CH) induces numerous adaptative changes in heart physiology, including remodeling. Indeed, in addition to the effect of lowered oxygen availability on oxidative cardiac metabolism, the heart is submitted to an increased workload as a result of the hypoxia-induced pulmonary hypertension (21,22). This pathological situation induces complex structural, hormonal, and biochemical modifications that affect both energy-producing and energy-consuming processes in heart cells (see Refs. 20,33). Concerning energy-producing modifications, an important reduction in the mitochondrial mass has been observed, associated with the reduction of the activities of respiratory chain complexes (29). In parallel, several studies reported a metabolic switch from fatty acid to carbohydrate utilization after CH (13,25,28,36,37). In regard to energyconsuming processes, one of the early mechanisms observed in isolated mammalian cardiomyocytes submitted to acute hypoxia is a downregulation of protein and RNA synthesis (9, 34). Moreover, biochemical investigations under CH also revealed a modification of the contractile apparatus itself, characterized by an increase in ␤-myosin heavy chain expression in both ventricles (35). These modifications of ATP/phosphocreatine (PCr) production and consumption proces...

show abstract

Cardiac adaptation to chronic high-altitude hypoxia: Beneficial and adverse effects

Cited by 109 publications

References 111 publications

In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Chronic Hypoxia Enhances Expression and Activity of Mitochondrial Creatine Kinase and Hexokinase in the Rat Ventricular Myocardium

Modular control analysis of effects of chronic hypoxia on mouse heart

Contact Info

Product

Resources

About