Hypoxia reduces airway epithelial sodium transport in rats

1999 ◽  
Vol 277 (5) ◽  
pp. L881-L886 ◽  
Author(s):  
L. A. Tomlinson ◽  
T. C. Carpenter ◽  
E. H. Baker ◽  
J. B. Bridges ◽  
J. V. Weil
Keyword(s):  
Sodium Transport ◽  
Hypobaric Hypoxia ◽  
Alveolar Epithelium ◽  
Airway Epithelial ◽  
Sprague Dawley ◽  
Edema Formation ◽  
Significant Fall ◽  
Moderate Hypobaric Hypoxia ◽  
Sprague Dawley Rats ◽  
Lung Liquid

Ascent to high altitude leads to pulmonary edema formation in some individuals. Recent laboratory evidence supports the hypothesis that hypoxia may impair the function of the alveolar epithelium and thus augment edema accumulation via reduced clearance of lung liquid. We investigated the effect of hypobaric hypoxia on epithelial sodium transport in adult Sprague-Dawley rats by measuring the nasal transepithelial potential difference (PD) as an index of airway sodium transport. Baseline PDs were similar to those previously reported in other species. Administration of amiloride resulted in a significant fall in nasal PD, as did ouabain administration for 24 h (−27.8 vs. −18.8 mV; P = 0.001; n = 5 rats). Exposure to hypobaric hypoxia (0.5 atm) for 24 h caused a significant fall in nasal PD (−23.7 vs. −18.8 mV; P = 0.002; n = 15 rats), which was not additive to the changes in nasal PD produced by amiloride or ouabain. We conclude that subacute exposure to moderate hypobaric hypoxia can inhibit sodium transport by the airway epithelium in rats.

Endothelin-A receptor antagonist BQ-610 blocks cigarette smoke-induced mitogenesis in rat airways and vessels

1997 ◽  
Vol 272 (4) ◽  
pp. L614-L618 ◽  
Author(s):  
F. Dadmanesh ◽  
J. L. Wright
Keyword(s):  
Cell Proliferation ◽  
Cigarette Smoke ◽  
Airway Epithelial ◽  
Sprague Dawley ◽  
Cell Nuclei ◽  
Sprague Dawley Rats ◽  
Endothelin A ◽  
Bq 610 ◽  
Air Control ◽  
Wall Components

To ascertain whether endothelin may play a role in cigarette smoke-induced cell proliferation in the airways and arterial vasculature of the lung, we exposed groups of seven Sprague-Dawley rats to either room air (control) plus saline infusion, an intravenous infusion of the selective endothelin A antagonist BQ-610 (control BQ-610), the smoke of 10 cigarettes (smoke only), or the smoke of 10 cigarettes after intravenous BQ-610 infusion (smoke + BQ-610). Cell proliferation was quantified by determining the percentage of cell nuclei labeled by 5-bromo-2'-deoxyuridine. We separately evaluated the cells in the epithelium and wall components of the bronchioles, and endothelium and wall components of the peribronchiolar and perialveolar ductular arteries. We found that cigarette smoke produced significant cell proliferation in the airway epithelium and wall, in the peribronchiolar arterial endothelial compartment, and in both the endothelial and wall compartments of the perialveolar ductular arteries. Pretreatment with BQ-610 reduced the peribronchiolar arterial endothelial and the perialveolar ductular arterial wall proliferation to control lev- els and reduced but did not totally abrogate the smoke-in- duced proliferation of the airway epithelial, airway wall, and perialveolar ductular arterial endothelial compartments. We conclude that cigarette smoke-induced cell proliferation of the airways and pulmonary arterial vessels is at least partially mediated through stimulation of the endothelin-A receptors.

Increased Oxygen Hemoglobin Affinity Mitigates Hypobaric Hypoxia‐dependent Spatial Learning Decrements In Sprague‐Dawley Rats

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Brian T. Williams ◽  
W. Rainey Johnson ◽  
Geoffrey E. Ciarlone ◽  
Chelsea N. Willoughby ◽  
Hanbing Zhou ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Hypobaric Hypoxia ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

scholarly journals Hypobaric Hypoxia Induces Depression-like Behavior in Female Sprague-Dawley Rats, but not in Males

2015 ◽  
Vol 16 (1) ◽  
pp. 52-60 ◽  
Author(s):  
Shami Kanekar ◽  
Olena V. Bogdanova ◽  
Paul R. Olson ◽  
Young-Hoon Sung ◽  
Kristen E. D'Anci ◽  
...  
Keyword(s):  
Hypobaric Hypoxia ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Contribution of polyamine oxidase to brain injury after trauma

1999 ◽  
Vol 90 (6) ◽  
pp. 1078-1082 ◽  
Author(s):  
Aclan Doğan ◽  
a. Muralikrishna Rao ◽  
Muştafa K. Baskaya ◽  
James Hatcher ◽  
Cuneyt Temiz ◽  
...  
Keyword(s):  
Brain Injury ◽  
Traumatic Injury ◽  
Polyamine Oxidase ◽  
Cresyl Violet ◽  
Sprague Dawley ◽  
Edema Formation ◽  
Content Type ◽  
Sprague Dawley Rats ◽  
Mdl 72527 ◽  
Fine Print

Object. The possible role of the polyamine interconversion pathway on edema formation, traumatic injury volume, and tissue polyamine levels after traumatic brain injury (TBI) was studied using an inhibitor of the interconversion pathway enzyme, polyamine oxidase.Methods. Experimental TBI was induced in Sprague—Dawley rats by using a controlled cortical impact device at a velocity of 3 m/second, resulting in a 2-mm deformation. Immediately after TBI was induced, 100 mg/kg of N1,N4-bis(2,3-butadienyl)-1,4-butanediamine 2HCl (MDL 72527) or saline was injected intraperitoneally. Brain water content and tissue polyamine levels were measured at 24 hours after TBI. Traumatic injury volume was evaluated using 2% cresyl violet solution 7 days after TBI occurred. The MDL 72527 treatment significantly reduced brain edema (80.4 ± 0.8% compared with 81.2 ± 1.2%, p < 0.05) and injury volume (30.1 ± 6.6 mm3 compared with 42.7 ± 13.3 mm3, p < 0.05) compared with the saline treatment. The TBI caused a significant increase in tissue putrescine levels at the traumatized site (65.5 ± 26.5 pmol/g in the cortex and 70.9 ± 22.4 pmol/g in the hippocampus) compared with the nontraumatized site (7 ± 2.4 pmol/g in the cortex and 11.4 ± 6.4 pmol/g in the hippocampus). The increase in putrescine levels in both the traumatized and nontraumatized cortex and hippocampus was reduced by a mean of 60% with MDL 72527 treatment.Conclusions. These results demonstrate, for the first time, that the polyamine interconversion pathway has an important role in the increase of putrescine levels after TBI and that the polyamine oxidase inhibitors, blockers of the interconversion pathway, can be neuroprotective against edema formation and necrotic cavitation after TBI.

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 Effect of adrenalectomy on pulmonary edema resolution

2019 ◽  
Vol 42 (2) ◽  
pp. E33-37
Author(s):  
Chantal Massé ◽  
Yves Berthiaume
Keyword(s):  
Pulmonary Edema ◽  
Alveolar Epithelium ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Endogenous Catecholamines ◽  
Sodium Dependent ◽  
Corticosterone Response ◽  
Permeability Pulmonary Edema ◽  
Dependent Mechanism ◽  
Alveolar Edema

Purpose: The capacity of the lung to clear edema fluid has been shown to be one of the factors that can influence the prognosis of cardiogenic and noncardiogenic pulmonary edema. Active Na+ transport across the alveolar epithelium is the main driving force involved in this physiological process. Since endogenous catecholamines are known to activate the sodium-dependent mechanism of alveolar edema clearance, the objective of the present study was to explore if adrenalectomy, which prevents the release of endogenous catecholamines and other hormones, such as corticosterone, into circulation, would affect edema resolution in a model of lung injury induced by thiourea. Methods: A high-permeability pulmonary edema was induced in adult male Sprague-Dawley rats using a thiourea-induced pulmonary edema model. To determine if the release of adrenalin and corticosterone is essential for resolution of the thiourea-induced edema, we measured 1) the release of adrenalin and corticosterone in urine and 2) edema resolution in control animals and adrenalectomized animals. Results: The administration of thiourea significantly increased the wet-to-dry ratio after four and eight hours. After 12 and 24 hours, the wet-to-dry ratio gradually returned to baseline. Although thiourea-induced pulmonary edema was associated with a significant increase in urine adrenalin and corticosterone, the absence of adrenalin and corticosterone response in adrenalectomized animals did not prevent the resolution of the edema. Conclusions: These experiments demonstrated that resolution of thioureainduced pulmonary edema can occur in the absence of hormonal secretion by the adrenal glands.

Characterization of Bronchiolar Metaplasia of the Alveolar Epithelium in Female Sprague—Dawley Rats Exposed to 3,3',4,4',5-Pentachlorobiphenyl (PCB126)

2004 ◽  
Vol 32 (3) ◽  
pp. 333-337 ◽  
Author(s):  
Amy E. Brix ◽  
Michael P. Jokinen ◽  
Nigel J. Walker ◽  
Donald M. Sells ◽  
Abraham Nyska
Keyword(s):  
Alveolar Epithelium ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

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.

Alteration of Rat Brain Catecholamine Metabolism During Exposure to Hypobaric Hypoxia

1972 ◽  
Vol 50 (4) ◽  
pp. 321-327 ◽  
Author(s):  
A. Cymerman ◽  
S. M. Robinson ◽  
D. McCullough
Keyword(s):  
Hypobaric Hypoxia ◽  
Specific Activity ◽  
Fluid Composition ◽  
Catecholamine Metabolism ◽  
Turnover Rates ◽  
Brain Catecholamines ◽  
Sprague Dawley ◽  
Brain Norepinephrine ◽  
Sprague Dawley Rats ◽  
Hypoxic Environment

The effect of hypobaric hypoxia on the metabolism of brain catecholamines in the rat was studied using intracisternal injections of 3H-tyrosine (3H-TYR) and 3H-dihydroxyphenylalanine (3H-DOPA) and intraperitoneal injections of α-methyltyrosine. Adult male Sprague–Dawley rats were housed singly or in pairs in barometric chambers and either maintained as controls or exposed to a hypoxic environment (380 mm Hg) for periods ranging up to 30 h. Whole brain norepinephrine (NE) and dopamine (DA) concentrations were significantly less than controls after exposures of 6, 12, and 18 h and normal after 24 h. Significant increases in specific activity of 3H-NE and 3H-DA derived from 3H-DOPA were obtained from brains of animals exposed for 6–18 h. The increase in 3H-NE specific activity was also evident with exposures lasting up to 30 h. Levels of 3H-NE derived from 3H-TYR were also increased with 12 h exposure when compared to controls. Turnover rates of NE, determined after pool size returned to normal (24 h), were not altered. Changes in cerebrospinal fluid composition, flow, and pressure may be responsible for the observed increases in 3H-NE derived from 3H-TYR or 3H-DOPA.

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