Dataset Information

[The Effect of Short-Term Intermittent Hypoxia Exposure on Mouse Myocardial Oxidative Stress and Cardiac Function].

ABSTRACT:

Objective

To investigate the effect of short-term intermittent hypoxia (IH) on the structure and function of mouse myocardium.

Methods

Thirty male C57BL6/J mice were randomly assigned to two groups, a control (Con) group and an IH group exposed to hypoxic treatment at atmospheric pressure. The IH group received 10% oxygen pretreatment for 8 hours per day on 14 consecutive days, while the Con group was exposed to normoxia environment and all the other treatment the group received were identical to those given to the IH group, The body mass of the mice was monitored daily during the treatment. The exercise tolerance and the cardiac function of isolated heart were assessed at the end of IH exposure. Additionally, analysis was conducted regarding myocardial enzymology, histology, and other indicators relevant to oxidative stress, including protein carbonylation and lipid peroxidation.

Results

There was no significant difference in the exercise tolerance between the two groups. Nevertheless, IH mice showed enhanced cardiac function during isolated heart perfusion ( P<0.05). As compared to the control group, prominent alterations of myocardial structure were detected by transmission electron microscopy of the IH heart, accompanied by elevated creatine kinase-MB levels ( P<0.05). The levels of myocardial reactive oxygen species, protein carbonylation and lipid peroxidation were all significantly upregulated in the IH group as compared to the control group ( P<0.05).

Conclusion

IH exposure induced myocardial oxidative stress damage and myofibrillar structural alteration in mice, but did not impair the exercise tolerance of the mice or the contractile function of the isolated heart.

SUBMITTER: Ou W

PROVIDER: S-EPMC10408848 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature

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Publications

[The Effect of Short-Term Intermittent Hypoxia Exposure on Mouse Myocardial Oxidative Stress and Cardiac Function].

Ou Wei W Liang Yu Y Qing Yu Y Deng Yan Y Wu Wei W Li Tao T

Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 20220101 1

<h4>Objective</h4>To investigate the effect of short-term intermittent hypoxia (IH) on the structure and function of mouse myocardium.<h4>Methods</h4>Thirty male C57BL6/J mice were randomly assigned to two groups, a control (Con) group and an IH group exposed to hypoxic treatment at atmospheric pressure. The IH group received 10% oxygen pretreatment for 8 hours per day on 14 consecutive days, while the Con group was exposed to normoxia environment and all the other treatment the group received w ...[more]

PMID: 35048607

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Project description:BackgroundShort-term intermittent hypoxia (IH) is common in patients with acute respiratory disorders. Although prolonged exposure to hypoxia induces atrophy and increased fatigability of skeletal muscle, the response to short-term IH is less well known. We hypothesized that the diaphragm and limb muscles would adapt differently to short-term IH given that hypoxia stimulates ventilation and triggers a superimposed exercise stimulus in the diaphragm.MethodsWe determined the structural, metabolic, and contractile properties of the mouse diaphragm after 4 days of IH (8 hours per day, 30 episodes per hour to a FiO2 nadir=6%), and compared responses in the diaphragm to a commonly studied reference limb muscle, the tibialis anterior. Outcome measures included muscle fiber size, assays of muscle proteolysis (calpain, ubiquitin-proteasome, and autophagy pathways), markers of oxidative stress and mitochondrial function, quantification of intramyocellular lipid and lipid metabolism genes, type I myosin heavy chain (MyHC) expression, and in vitro contractile properties.ResultsAfter 4 days of IH, the diaphragm alone demonstrated significant atrophy (30% decrease of myofiber size) together with increased LC3B-II protein (2.4-fold) and mRNA markers of the autophagy pathway (LC3B, Gabarapl1, Bnip3), whereas active calpain and E3 ubiquitin ligases (MuRF1, atrogin-1) were unaffected in both muscles. Succinate dehydrogenase activity was significantly reduced by IH in both muscles. However, only the diaphragm exhibited increased intramyocellular lipid droplets (2.5-fold) after IH, along with upregulation of genes linked to activated lipid metabolism. In addition, although the diaphragm showed evidence for acute fatigue immediately following IH, it underwent an adaptive fiber type switch toward slow type I MyHC-expressing fibers, associated with greater intrinsic endurance of the muscle during repetitive stimulation in vitro.ConclusionsShort-term IH induces preferential atrophy in the mouse diaphragm together with increased autophagy and a rapid compensatory metabolic adaptation associated with enhanced fatigue resistance.

Project description:More than 140 million people live and works (in a chronic or intermittent form) above 2500 m worldwide and 35 million live in the Andean Mountains. Furthermore, in Chile, it is estimated that 55,000 persons work in high altitude shifts, where stays at lowlands and interspersed with working stays at highlands. Acute exposure to high altitude has been shown to induce oxidative stress in healthy human lowlanders, due to an increase in free radical formation and a decrease in antioxidant capacity. However, in animal models, intermittent hypoxia (IH) induce preconditioning, like responses and cardioprotection. Here, we aimed to describe in a rat model the responses on cardiac and vascular function to 4 cycles of intermittent hypobaric hypoxia (IHH). Twelve adult Wistar rats were randomly divided into two equal groups, a four-cycle of IHH, and a normobaric hypoxic control. Intermittent hypoxia was induced in a hypobaric chamber in four continuous cycles (1 cycle = 4 days hypoxia + 4 days normoxia), reaching a barometric pressure equivalent to 4600 m of altitude (428 Torr). At the end of the first and fourth cycle, cardiac structural, and functional variables were determined by echocardiography. Thereafter, ex vivo vascular function and biomechanical properties were determined in femoral arteries by wire myography. We further measured cardiac oxidative stress biomarkers (4-Hydroxy-nonenal, HNE; nytrotirosine, NT), reactive oxygen species (ROS) sources (NADPH and mitochondrial), and antioxidant enzymes activity (catalase, CAT; glutathione peroxidase, GPx, and superoxide dismutase, SOD). Our results show a higher ejection and shortening fraction of the left ventricle function by the end of the 4th cycle. Further, femoral vessels showed an improvement of vasodilator capacity and diminished stiffening. Cardiac tissue presented a higher expression of antioxidant enzymes and mitochondrial ROS formation in IHH, as compared with normobaric hypoxic controls. IHH exposure determines a preconditioning effect on the heart and femoral artery, both at structural and functional levels, associated with the induction of antioxidant defence mechanisms. However, mitochondrial ROS generation was increased in cardiac tissue. These findings suggest that initial states of IHH are beneficial for cardiovascular function and protection.

Dataset Information

[The Effect of Short-Term Intermittent Hypoxia Exposure on Mouse Myocardial Oxidative Stress and Cardiac Function].

Objective

Methods

Results

Conclusion

Publications

[The Effect of Short-Term Intermittent Hypoxia Exposure on Mouse Myocardial Oxidative Stress and Cardiac Function].

Similar Datasets

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