scholarly journals Rhodiola crenulataExtract Alleviates Hypoxic Pulmonary Edema in Rats

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Shih-Yu Lee ◽  
Min-Hui Li ◽  
Li-Shian Shi ◽  
Hsin Chu ◽  
Cheng-Wen Ho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Capillary Barrier ◽  
Lung Water ◽  
Stress Markers ◽  
Rhodiola Crenulata ◽  
High Altitude Illness ◽  
Alveolar Capillary

Sudden exposure of nonacclimatized individuals to high altitude can easily lead to high altitude illnesses. High altitude pulmonary edema (HAPE) is the most lethal form of high altitude illness. The present study was designed to investigate the ability ofRhodiola crenulataextract (RCE), an herbal medicine traditionally used as an antiacute mountain sickness remedy, to attenuate hypoxia-induced pulmonary injury. Exposure of animals to hypobaric hypoxia led to a significant increase in pathological indicators for pulmonary edema, including the lung water content, disruption of the alveolar-capillary barrier, and protein-rich fluid in the lungs. In addition, hypobaric hypoxia also increased oxidative stress markers, including (ROS) production, (MDA) level, and (MPO) activity. Furthermore, overexpression of plasma (ET-1), (VEGF) in (BALF), and (HIF-1α) in lung tissue was also found. However, pretreatment with RCE relieved the HAPE findings by curtailing all of the hypoxia-induced lung injury parameters. These findings suggest that RCE confers effective protection for maintaining the integrity of the alveolar-capillary barrier by alleviating the elevated ET-1 and VEGF levels; it does so by reducing hypoxia-induced oxidative stress. Our results offer substantial evidence to support arguments in favor of traditional applications ofRhodiola crenulatafor antihigh altitude illness.

scholarly journals Hypericum perforatum (ethanolic extract) ameliorates simulated hypobaric hypoxia induced oxidative stress and neuronal damage in brains of Balb/c mice

2018 ◽  
Vol 9 (2) ◽  
pp. 1-8
Author(s):  
Amardeep Gautam ◽  
Rizwana Tabassum ◽  
Anju Katyal
Keyword(s):  
Oxidative Stress ◽  
High Altitude ◽  
Passive Avoidance ◽  
Hypobaric Hypoxia ◽  
Hypericum Perforatum ◽  
Elevated Plus Maze ◽  
Ethanolic Extract ◽  
Amnesic Effect ◽  
Plus Maze ◽  
High Altitude Illness

Background: Hypobaric hypoxia refers to lower oxygen availability at high altitudes and is the cause of high altitude illness. Drugs such as acetazolamide and dexamethasone provide symptomatic relief and are associated with undesired side effects. Plant extracts such as Hypericum perforatum, which are documented to have neuromodulatory role can be more beneficial in ameliorating high altitude illness. Aims and Objective: Progressive cognitive decline is the hallmark characteristic of hypobaric hypoxia induced neuropathology attributed to ensuing oxidative stress and subsequent hippocampal damage. We have explored the efficacy of ethanolic extracts of Hypericum perforatum in amelioration of hypobaric hypoxia induced oxidative stress and associated behavioral deficits in mice.Material and Methods: Male Balb/c mice were exposed to simulated altitude of 25,000 ft. for 7 days (6 hr. per day) in a specially designed chamber. Ethanolic extract of Hypericum perforatum (HPE)(25mg/kg of body weight) was given orally prior to hypoxia exposure and effects were compared to hypoxia and control groups.Results: Animals exposed to hypobaric hypoxia showed sign of cognitive deterioration at day 3 and day 7 in the Elevated Plus Maze and Passive Avoidance Step through behavioral paradigms as compare to normoxic animals. Administration of HPE was able to alleviate the amnesic effect in treatment group, indicated by reduction in transfer latencies at day 3(IR-3 = -0.66±0.07) and day 7 IR-7 = -0.81±0.06) in elevated plus maze task and increased passive avoidance step through latency at day 3, (IR-3 = 3.23±0.67),as compared to ±hypoxic mice. Hypoxia group of animals suffered significant oxidative stress compared to normoxic mice as indicated by up-regulated malondialdehyde and total nitrite levels in hippocampal homogenates. The plasma lactate dehydrogenase activity was also increased following hypoxia indicating tissue damage. Co-treatment with HPE in simulated hypobaric hypoxia insult for seven days resulted in significant reduction in malondialdehyde, total nitrites and plasma LDH levels in animals.Conclusion: Hypericum perforatum extract improves cognitive performance in hypobaric hypoxia exposed mice with a concomitant reduction in oxidative stress burden suggesting its plausible use for preventing high altitude illness.Asian Journal of Medical Sciences Vol.9(2) 2018 1-8

scholarly journals Acute Lung Edema as a Presentation of Severe Acute Reentry High-Altitude Illness in a Pediatric Patient

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Alfredo Merino-Luna ◽  
Julio Vizcarra-Anaya
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Pediatric Patient ◽  
Lung Edema ◽  
High Altitude Pulmonary Edema ◽  
High Altitude Illness ◽  
The City ◽  
Determining Factor

Acute high-altitude pulmonary edema (HAPE) is a pathology involving multifactorial triggers that are associated with ascents to altitudes over 2,500 meters above sea level (m). Here, we report two pediatric cases of reentry HAPE, from the city of Huaraz, Peru, located at 3,052 m. The characteristics of both cases were similar, wherein acclimatization to sea level and a subsequent return to the city of origin occurred, and we speculate that it was caused by activation of predisposing factors to HAPE. The diagnosis and management associated with pulmonary hypertension became a determining factor for therapy.

scholarly journals Effects of Ischemic Acute Kidney Injury on Lung Water Balance: Nephrogenic Pulmonary Edema?

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Rajit K. Basu ◽  
Derek Wheeler
Keyword(s):  
Acute Kidney Injury ◽  
Pulmonary Edema ◽  
Disease Process ◽  
Kidney Injury ◽  
Fluid Accumulation ◽  
Lung Water ◽  
Edema Formation ◽  
Bulk Fluid ◽  
Capillary Membrane ◽  
Alveolar Capillary

Pulmonary edema worsens the morbidity and increases the mortality of critically ill patients. Mechanistically, edema formation in the lung is a result of net flow across the alveolar capillary membrane, dependent on the relationship of hydrostatic and oncotic pressures. Traditionally, the contribution of acute kidney injury (AKI) to the formation of pulmonary edema has been attributed to bulk fluid accumulation, increasing capillary hydrostatic pressure and the gradient favoring net flow into the alveolar spaces. Recent research has revealed more subtle, and distant, effects of AKI. In this review we discuss the concept of nephrogenic pulmonary edema. Pro-inflammatory gene upregulation, chemokine over-expression, altered biochemical channel function, and apoptotic dysregulation manifest in the lung are now understood as “extra-renal” and pulmonary effects of AKI. AKI should be counted as a disease process that alters the endothelial integrity of the alveolar capillary barrier and has the potential to overpower the ability of the lung to regulate fluid balance. Nephrogenic pulmonary edema, therefore, is the net effect of fluid accumulation in the lung as a result of both the macroscopic and microscopic effects of AKI.

CYBA and GSTP1 variants associate with oxidative stress under hypobaric hypoxia as observed in high-altitude pulmonary oedema

2011 ◽  
Vol 122 (6) ◽  
pp. 299-311 ◽  
Author(s):  
Aastha Mishra ◽  
Zahara Ali ◽  
Arpana Vibhuti ◽  
Rahul Kumar ◽  
Perwez Alam ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Altitude ◽  
Pulmonary Oedema ◽  
Hypobaric Hypoxia ◽  
Glutathione Transferase ◽  
Prostaglandin F2α ◽  
Gene Interactions ◽  
Potential Candidate ◽  
Genotype Distribution ◽  
Risk Alleles

HAPE (high-altitude pulmonary oedema) is characterized by pulmonary hypertension, vasoconstriction and an imbalance in oxygen-sensing redox switches. Excess ROS (reactive oxygen species) contribute to endothelial damage under hypobaric hypoxia, hence the oxidative-stress-related genes CYBA (cytochrome b−245 α polypeptide) and GSTP1 (glutathione transferase Pi 1) are potential candidate genes for HAPE. In the present study, we investigated the polymorphisms −930A/G and H72Y (C/T) of CYBA and I105V (A/G) and A114V (C/T) of GSTP1, individually and in combination, in 150 HAPE-p (HAPE patients), 180 HAPE-r (HAPE-resistant lowland natives) and 180 HLs (healthy highland natives). 8-Iso-PGF2α (8-iso-prostaglandin F2α) levels were determined in plasma and were correlated with individual alleles, genotype, haplotype and gene–gene interactions. The relative expression of CYBA and GSTP1 were determined in peripheral blood leucocytes. The genotype distribution of −930A/G, H72Y (C/T) and I105V (A/G) differed significantly in HAPE-p compared with HAPE-r and HLs (P≤0.01). The haplotypes G-C of −930A/G and H72Y (C/T) in CYBA and G-C and G-T of I105V (A/G) and A114V (C/T) in GSTP1 were over-represented in HAPE-p; in contrast, haplotypes A-T of −930A/G and H72Y (C/T) in CYBA and A-C of I105V (A/G) and A114V (C/T) in GSTP1 were over-represented in HAPE-r and HLs. 8-Iso-PGF2α levels were significantly higher in HAPE-p and in HLs than in HAPE-r (P=2.2×10−16 and 1.2×10−14 respectively) and the expression of CYBA and GSTP1 varied differentially (P<0.05). Regression analysis showed that the risk alleles G, C, G and T of −930A/G, H72Y (C/T), I105V (A/G) and A114V (C/T) were associated with increased 8-iso-PGF2α levels (P<0.05). Interaction between the two genes revealed over-representation of most of the risk-allele-associated genotype combinations in HAPE-p and protective-allele-associated genotype combinations in HLs. In conclusion, the risk alleles of CYBA and GSTP1, their haplotypes and gene–gene interactions are associated with imbalanced oxidative stress and, thereby, with high-altitude adaptation and mal-adaptation.

scholarly journals EFFECT OF OXYGEN SUPPLEMENTATION ON LOW LANDERS ON ASCENDING TO HIGH ALTITUDE WITH PRECORDIAL ECG CHANGES WITHOUT HIGH ALTITUDE ILLNESS

2020 ◽  
pp. 1-4
Author(s):  
Surabhi Venkata Satya Krishna ◽  
MG Vishnoi ◽  
S. Nagamanju
Keyword(s):  
High Altitude ◽  
Hypobaric Hypoxia ◽  
Pulmonary Vasculature ◽  
Ecg Changes ◽  
Oxygen Supplementation ◽  
Coronary Syndrome ◽  
T Wave ◽  
Wave Inversion ◽  
High Altitude Illness ◽  
Pressure Changes

High altitude syndromes are illnesses attributed directly to hypobaric hypoxia. Hypobaric Hypoxic pressure changes in the right side of the heart with ECG changes in right precordial leads are seen in cases like High Altitude Pulmonary Edema (HAPE), Pulmonary Thormboembolism (PTE) and thrombotic cause in acute coronary syndrome (ACS). Cases of these mimics with T wave inversion in precordial chest leads are seen in low landers on induction into high altitude without any high altitude illness, ACS or PTE. These findings may reflect asymptomatic pressure changes in the heart and pulmonary vasculature due to hypobaric hypoxia of high altitude to the point where they are not manifested. High altitude environment is itself being a procoagulant state compounded with hypobaric hypoxia, if these changes are not addressed in time and not treated with oxygen supplementation, these individuals may present at a later stage with HAPE or SAMS. We hypothesized that oxygen supplementation can reverse these changes. Intervention study with oxygen supplementation @ 6/min intermittently over 12 hr/day was given in all those individuals who have T wave inversion in precordial ECG meeting inclusion criteria over a week. The study was conducted at peripheral hospital 11000ft in Himalayan ranges over a period of 06 months. 100 % of cases had shown normalization of T waves in response to oxygen supplementation. However 02 individuals had recurrence of ECG changes and they were deinducted to plains. None of them developed high altitude illness over next 06 months of followup.

Susceptibility to high-altitude pulmonary edema is associated with circulating miRNA levels under hypobaric hypoxia conditions

2020 ◽  
Vol 319 (2) ◽  
pp. L360-L368
Author(s):  
Perwez Alam ◽  
Garima Agarwal ◽  
Rahul Kumar ◽  
Aastha Mishra ◽  
Neeru Saini ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
In Silico ◽  
Hypobaric Hypoxia ◽  
Umbilical Vein ◽  
Direct Interaction ◽  
Vascular Homeostasis ◽  
High Altitude Pulmonary Edema ◽  
In Silico Analyses

Hypobaric hypoxia poses stress to sojourners traveling to high-altitude. A cascade of physiological changes occurs to cope with or adapt to hypobaric hypoxia. However, an insufficient physiological response to the hypoxic condition resulting from imbalanced vascular homeostasis pathways results in high-altitude pulmonary edema (HAPE). The present study aims to identify the implication of miRNAs associating with HAPE and adaptation. We analyzed the expression of 1,113 miRNAs in HAPE-patients (HAPE-p), HAPE-free controls (HAPE-f), and highland natives (HLs). Based on miRNA profiling and in silico analyses, miR-124-3p emerged relevantly. We observed a significant overexpression of miR-124-3p in HAPE-p. In silico analyses revealed a direct interaction of miR-124-3p with vascular homeostasis and hypoxia-associated genes NOS3 (endothelial nitric oxide synthase), Apelin, and ETS1 (V-Ets avian erythroblastosis virus E2 oncogene homolog 1). Moreover, the transcript and biolevel expression of these genes were significantly decreased in HAPE-p when compared with HAPE-f or HLs. Our in vitro analysis in human umbilical vein endothelial cells demonstrated a significant knockdown of these genes both at transcript and protein levels following miR-124-3p overexpression. Conclusively, our results showed that miR-124-3p might play a plausible role in HAPE pathophysiology by inhibiting the expression of NOS3, Apelin, and ETS1.

Shorter telomere length, higher telomerase activity in association with tankyrase gene polymorphism contribute to high-altitude pulmonary edema

2020 ◽  
Vol 29 (18) ◽  
pp. 3094-3106
Author(s):  
Manjula Miglani ◽  
Manjari Rain ◽  
Qadar Pasha ◽  
V Samuel Raj ◽  
Tashi Thinlas ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Telomere Length ◽  
Hypobaric Hypoxia ◽  
Telomerase Activity ◽  
Chain Reaction ◽  
Telomere Repeat ◽  
High Altitude Pulmonary Edema ◽  
Polymerase Chain

Abstract High-altitude pulmonary edema (HAPE) is a noncardiogenic form of pulmonary edema, which is induced upon exposure to hypobaric hypoxia at high altitude (HA). Hypobaric hypoxia generates reactive oxygen species that may damage telomeres and disturb normal physiological processes. Telomere complex comprises of multiple proteins, of which, tankyrase (TNKS) is actively involved in DNA damage repairs. We hence investigated the association of TNKS and telomeres with HAPE to delineate their potential role at HA. The study was performed in three groups, High-altitude pulmonary edema patients (HAPE-p, n = 200), HAPE-resistant sojourners (HAPE-r, n = 200) and highland permanent healthy residents (HLs, n = 200). Variants of TNKS were genotyped using polymerase chain reaction–restriction fragment length polymorphism. Plasma TNKS level was estimated using enzyme-linked immunosorbent assay, expression of TNKS and relative telomere length were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and telomerase activity was assessed by the telomere repeat amplification protocol assay. TNKS poly-ADP ribosylates the telomere-repeat factor (TRF), which is a negative regulator of telomere length. Consequently, TRF expression was also measured by RT-qPCR. The TNKS heterozygotes rs7015700GA were prevalent in HLs compared to the HAPE-p and HAPE-r. The plasma TNKS was significantly decreased in HAPE-p than HAPE-r (P = 0.006). TNKS was upregulated 9.27 folds in HAPE-p (P = 1.01E-06) and downregulated in HLs by 3.3 folds (P = 0.02). The telomere length was shorter in HAPE-p compared to HAPE-r (P = 0.03) and HLs (P = 4.25E-4). The telomerase activity was significantly higher in HAPE-p compared to both HAPE-r (P = 0.01) and HLs (P = 0.001). HAPE-p had the lowest TNKS levels (0.186 ± 0.031 ng/μl) and the highest telomerase activity (0.0268 amoles/μl). The findings of the study indicate the association of TNKS and telomeres with HA adaptation/maladaptation.

Susceptibility to high-altitude pulmonary edema in Madison and Hilltop rats. I. Ventilation and fluid balance

1995 ◽  
Vol 78 (6) ◽  
pp. 2279-2285
Author(s):  
G. L. Colice ◽  
Y. J. Lee ◽  
J. Chen ◽  
H. K. Du ◽  
G. Ramirez ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Minute Ventilation ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Simulated Altitude ◽  
Sprague Dawley ◽  
Lung Water ◽  
Fluid Handling ◽  
High Altitude Pulmonary Edema

The pathogenesis of high-altitude pulmonary edema (HAPE) is not well understood. Ventilation and fluid-handling abnormalities at high altitude (HA) may play a role in HAPE. Because ventilatory and cardiopulmonary responses to chronic HA exposure in the Hilltop (H) strain of Sprague-Dawley rat are different from those in the Madison (M) strain, it was hypothesized that these strains would have different susceptibilities to developing HAPE. M and H rats were studied at sea level (SL) and in a hypobaric chamber after 9 and 12 h at a simulated altitude of 24,000 ft (barometric pressure = 295 mmHg) and 1, 12, and 24 h at a simulated altitude of 18,000 ft (barometric pressure = 380 mmHg). Both strains developed HAPE, but the M rat was more susceptible to HAPE, as demonstrated by a higher mortality rate from hemorrhagic pulmonary edema after 9 h at 24,000 ft and an earlier increase in lung water after exposure to 18,000 ft. Minute ventilation was similar in both strains at HA, but arterial PO2 was significantly higher in the M rat. Both strains had a significant decrease in fluid intake and negative sensible water balance at HA. No changes in plasma renin activity, aldosterone concentrations, antidiuretic hormone levels, and atrial natriuretic peptide levels were found at HA. The increased susceptibility of the M rat to HAPE is therefore not explained by ventilation or fluid-handling abnormalities.

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