The anti-arrhythmic effect of chronic intermittent hypobaric hypoxia in rats with metabolic syndrome induced with fructose

2015 ◽  
Vol 93 (4) ◽  
pp. 227-232 ◽  
Author(s):  
Jing-Jing Zhou ◽  
Hui-Jie Ma ◽  
Yan Liu ◽  
Yue Guan ◽  
Leonid N. Maslov ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Hypobaric Hypoxia ◽  
Ischemia Reperfusion ◽  
Resting Potential ◽  
Sprague Dawley ◽  
Cellular Mechanisms ◽  
Intermittent Hypobaric Hypoxia ◽  
Sprague Dawley Rats ◽  
Phase 0 ◽  
Hypoxia Treatment

This study investigated the anti-arrhythmic effects from chronic intermittent hypobaric hypoxia (CIHH) and the cellular mechanisms in rats with metabolic syndrome. Male Sprague–Dawley rats were randomly distributed among the control, fructose-fed (fed with 10% fructose in the drinking water to induce metabolic syndrome), CIHH (42 days of hypobaric hypoxia treatment simulating an altitude of 5000 m a.s.l.: PB = 404 mm Hg, PO2 = 84 mm Hg, 6 h per day), and the CIHH plus fructose (CIHH-F) groups. In anesthetized rats, the arrhythmia score was determined after 30 min of cardiac ischemia followed by 120 min of reperfusion. Action potentials (AP) were recorded from isolated ventricular papillary muscles. The arrhythmia score was much lower in CIHH-F rats than in the fructose-fed rats. Under basic conditions, AP duration (APD) was significantly shortened in fructose-fed rats, but obviously prolonged in CIHH rats compared with that of the control rats. During ischemia, the AP amplitude, the maximal rate of rise of phase 0, APD, and resting potential, were lower in the control, fructose-fed, and CIHH-F groups, but were not changed in the CIHH rats. The lower AP during ischemia did not recover after washout for the fructose-fed rats. In conclusion, CIHH protects the heart against ischemia–reperfusion induced arrhythmia in rats with metabolic syndrome. This effect of CIHH is possibly related to baseline prolongation of the AP and attenuation of AP reduction during ischemia–reperfusion.

scholarly journals PGC-1α Participates in the Protective Effect of Chronic Intermittent Hypobaric Hypoxia on Cardiomyocytes

2018 ◽  
Vol 50 (5) ◽  
pp. 1891-1902 ◽  
Author(s):  
Shuo Gu ◽  
Hong Hua ◽  
Xinqi Guo ◽  
Zhanfeng Jia ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Protein Expression ◽  
Protein Level ◽  
Hypobaric Hypoxia ◽  
Molecular Mechanisms ◽  
Ventricular Myocytes ◽  
Ischemia Reperfusion ◽  
Sprague Dawley ◽  
Knock Down ◽  
Intermittent Hypobaric Hypoxia

Background/Aims: Myocardial ischemia/reperfusion (I/R) or hypoxia/reoxygenation (H/R) injury is always characterized by Ca2+ overload, energy metabolism disorder and necrocytosis of cardiomyocytes. We showed previously that chronic intermittent hypobaric hypoxia (CIHH) improves cardiac function during I/R through improving cardiac glucose metabolism. However, the underlying cellular and molecular mechanisms of CIHH treatment improving energy metabolism in cardiomyocytes are still unclear. In this study, we determined whether and how CIHH protects cardiomyocytes from Ca2+ overload and necrocytosis through energy regulating pathway. Methods: Adult male Sprague-Dawley rats were randomly divided into two groups: control (CON) and CIHH group. CIHH rats received a hypobaric hypoxia simulating 5,000-m altitude for 28 days, 6 hours each day, in hypobaric chamber. Rat ventricular myocytes were obtained by enzymatic dissociation. The intracellular calcium concentration ([Ca2+]i) and cTnI protein expression were used to evaluate the degree of cardiomyocytes injury during and after H/R. The mRNA and protein expressions involved in cardiac energy metabolism were determined using quantitative PCR and Western blot techniques. PGC-1α siRNA adenovirus transfection was used to knock down PGC-1α gene expression of cardiomyocytes to determine the effect of PGC-1α in the energy regulating pathway. Results: H/R increased [Ca2+]i and cTnI protein expression in cardiomyocytes. CIHH treatment decreased [Ca2+]i (p< 0.01) and cTnI protein expression (p< 0.01) in cardiomyocytes after H/R. Both mRNA and protein expression of PGC-1α increased after CIHH treatment, which was reversed by PGC-1α siRNA adenovirus transfection. Furthermore, CIHH treatment increased the expression of HIF-1α, AMPK and p-AMPK in cardiomyocytes, and pretreatment with AMPK inhibitor dorsomorphin abolished the enhancement of PGC-1α protein expression in cardiomyocytes by CIHH (p< 0.01). In addition, PGC-1α knock down also abolished the increased protein level of GLUT4 (p< 0.01) and decreased the protein level of CPT-1b (p< 0.05) in cardiomyocytes by CIHH treatment. Conclusion: CIHH treatment could reduce the calcium overload and H/R injury in cardiomyocytes by up-regulating the expression of PGC-1α and regulating the energy metabolism of glucose and lipid. The HIF-1α-AMPK signaling pathway might be involved in the process.

The Effect of Intermittent Hypobaric Hypoxia Exposure on Reduced-Glutathione Level in Rat Lung and Renal Tissues

2018 ◽  
Vol 24 (8) ◽  
pp. 6249-6251
Author(s):  
N. S Hardiany ◽  
A. A Asa ◽  
D Safirina ◽  
W Mulyawan
Keyword(s):  
Hypobaric Hypoxia ◽  
Reduced Glutathione ◽  
Renal Tissue ◽  
Rat Lung ◽  
Sprague Dawley ◽  
Hypoxia Exposure ◽  
Intermittent Hypobaric Hypoxia ◽  
Sprague Dawley Rats ◽  
Adaptation Response ◽  
Ellman’S Method

Hypobaric hypoxia is basically a hypoxia condition experienced in high altitude commonly during flight, that increase reactive oxygen species (ROS). When hypoxia hypobaric does not undergo continuation or in other word, intermittent, it will cause adaptation response in a form of protection mode into ROS. Moreover, ROS could be eliminated by reduced-glutathione (GSH) as an endogenous non enzymatic antioxidant. Therefore, the aim of this study was to analyze the effects of intermittent hypobaric hypoxia exposure on GSH level in rat lung and renal tissue. Lung and renal samples were collected from 6–8 weeks old male Sprague-Dawley rats weighing 150–200 g, previously exposed 1–4 times to intermittent hypobaric hypoxia in 35,000 ft (1 minute), 25.000 ft (5 minute) and 18,000 ft altitude (25 minute). Afterwards, GSH level was calculated from lung and renal extracts using the Ellman’s method. In lung tissues, GSH level was decreased in hypoxia 1×, 2×, 3×, 4× treatment, and were significant between the control–hypoxia 3×, control–hypoxia 4×, hypoxia 1×–hypoxia 3× and hypoxia 1×–hypoxia 4×. On the contrary, GSH level was increased in renal tissues on hypoxia 1× and hypoxia 2× treatment compared to control. Nevertheless, GSH level was decreased after 3× treatment and found almost stabilized at 4× treatment of hypoxia in renal tissues. Intermittent hypobaric hypoxia exposure affect GSH in rat lung and renal tissues with varying level as an adaptive response system.

PSD 95 and NMDAR Alteration as Plasticity Responses After Intermittent Hypobaric Hypoxia Induction in Sprague-Dawley Rats

2017 ◽  
Vol 23 (7) ◽  
pp. 6858-6860
Author(s):  
Rinaldo Fanny S Farhan ◽  
Angelina S. R Masengi ◽  
Margaretha Herawati ◽  
Wardaya ◽  
Nurhadi Ibrahim ◽  
...  
Keyword(s):  
Hypobaric Hypoxia ◽  
Sprague Dawley ◽  
Intermittent Hypobaric Hypoxia ◽  
Sprague Dawley Rats

scholarly journals Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

2001 ◽  
Vol 91 (4) ◽  
pp. 1828-1835 ◽  
Author(s):  
Nicole Stupka ◽  
Peter M. Tiidus
Keyword(s):  
Muscle Damage ◽  
Ischemia Reperfusion Injury ◽  
Serum Insulin ◽  
Ischemia Reperfusion ◽  
Neutrophil Infiltration ◽  
Female Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
17Β Estradiol

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

scholarly journals PENGARUH SINBIOTIK KEFIR PISANG BATU TERHADAP KADAR KOLESTEROL-LDL DAN KOLESTEROL-HDL TIKUS MODEL SINDROM METABOLIK

2020 ◽  
Vol 7 (2) ◽  
pp. 280-288
Author(s):  
Dina Khoiriyah ◽  
Taufik Maryusman ◽  
Santi Herlina
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Ldl Cholesterol ◽  
Hdl Cholesterol ◽  
Positive Control ◽  
Negative Control ◽  
Sprague Dawley ◽  
Musa Balbisiana ◽  
Cholesterol Levels ◽  
Sprague Dawley Rats

Effect of Banana Kefir Synbiotic on LDL-Cholesterol and HDL-Cholesterol of Metabolic Syndrome Rats Metabolic syndrome (SM) is characterized by several risk factors including dyslipidemia. This study aims to analyze the effect of kefir synbiotic produced from banana stone flour (Musa balbisiana) on LDL-cholesterol and HDL-cholesterol of metabolic syndrome rat model. The 24 Sprague Dawley rats were divided into four groups, namely negative control (healthy rats fed standard feed), positive control (metabolic syndrome rats fed standard feed), treatment I and treatment II (metabolic syndrome rats each given synbiotic kefir banana stone flour 1.8 mL/200 g mouse BW/day and 3.6 mL/200 g mouse BW/day, respectively). The intervention was carried out for three weeks. After the intervention, the levels of LDL-cholesterol in treatment I and II experienced a decrease of 44.66% and 56.94%, respectively, while the-HDL-cholesterol levels in treatment I and II experienced an increase of 104.5% and 172.71%, respectively. The biggest change occurred in treatment II. Synbiotic kefir banana stone flour improved lipid profile in metabolic syndrome rats. Sindrom metabolik (SM) ditandai dengan beberapa faktor risiko termasuk dislipidemia. Penelitian ini bertujuan untuk menganalisis pengaruh sinbiotik kefir tepung pisang batu (Musa balbisiana) terhadap kadar kolesterol-LDL dan kolesterol-HDL tikus model SM. Subjek menggunakan 24 ekor tikus Sprague Dawley yang dibagi menjadi empat kelompok, yaitu kontrol negatif (tikus sehat yang diberi pakan standar), kontrol positif (tikus model SM yang diberi pakan standar), perlakuan I dan perlakuan II (tikus model SM yang masing-masing diberi sinbiotik kefir tepung pisang batu 1,8 mL/200 g BB tikus/hari dan 3,6 mL/200 g BB tikus/hari). Proses intervensi dilakukan selama tiga minggu. Setelah intervensi, kadar kolesterol-LDL perlakuan I dan II mengalami penurunan sebesar 44,66% dan 56,94%, sedangkan kadar kolesterol-HDL perlakuan I dan II mengalami peningkatan sebesar 104,5% dan 172,71%. Perubahan terbesar terjadi pada perlakuan II. Sinbiotik kefir tepung pisang batu memperbaiki profil lipid tikus sindrom metabolik.

Hepatic Stellate Cells Play a Functional Role in Exacerbating Ischemia-Reperfusion Injury in Rat Liver

2019 ◽  
Vol 60 (1-2) ◽  
pp. 74-85 ◽  
Author(s):  
Tomokazu Takahashi ◽  
Masato Yoshioka ◽  
Hiroshi Uchinami ◽  
Yasuhiko Nakagawa ◽  
Naohiko Otsuka ◽  
...  
Keyword(s):  
Rat Liver ◽  
Hepatic Stellate Cells ◽  
Functional Role ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stellate Cells ◽  
Treated Group ◽  
Sprague Dawley ◽  
Perfusion Rate ◽  
Sprague Dawley Rats

Purpose: The involvement of hepatic stellate cells (HSCs) with ischemia-reperfusion (I/R) injury in rat liver was examined using gliotoxin, which is known to induce HSC apoptosis. Methods: Male Sprague-Dawley rats were used. HSC was represented by a glial fibrillary acidic protein (GFAP)-positive cell. Liver ischemia was produced by cross-clamping the hepatoduodenal ligament. The degree of I/R injury was evaluated by a release of aminotransferases. Sinusoidal diameter and sinusoidal perfusion rates were examined using intravital fluorescence microscopy. Results: Gliotoxin significantly decreased the number of GFAP-positive cells 48 h after dosing (2.50 ± 0.19% [mean ± SD] in the nontreated group vs. 1.91 ± 0.46% in the gliotoxin-treated group). Liver damage was significantly suppressed by the pretreatment with gliotoxin. Sinusoidal diameters in zone 3 were wider in the gliotoxin group (10.25 ± 0.35 µm) than in the nontreated group (8.21 ± 0.50 µm). The sinusoidal perfusion rate was maintained as well in the gliotoxin group as in normal livers, even after I/R. Conclusions: Pretreatment with gliotoxin significantly reduced the number of HSCs in the liver and further suppressed liver injury following I/R. It is strongly suggested that HSCs play a functional role in exacerbating the degree of I/R injury of the liver.

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