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.

Solute permeability of the alveolar epithelium in acute hemodynamic pulmonary edema in dogs

1977 ◽  
Vol 233 (1) ◽  
pp. H80-H86 ◽  
Author(s):  
E. A. Egan ◽  
R. M. Nelson ◽  
I. H. Gessner
Keyword(s):  
Pulmonary Edema ◽  
Isotonic Saline ◽  
Alveolar Epithelium ◽  
Lung Epithelium ◽  
Solute Permeability ◽  
Blue Dextran ◽  
Lung Segment ◽  
Anesthetized Dogs ◽  
The One ◽  
Alveolar Edema

Ten anesthetized dogs, 48 h postintravenous 131I-albumin injection, had a segment of lung airspace isolated by a balloon-tipped catheter lodged in a bronchus. An isotonic saline solution containing trace amounts of Blue Dextran, 125I-albumin, and 57Co-cyanocobalamin was instilled into the lung segment. During control periods, lung saline was absorbed at a rate of 0.133% per minute as measured by indicator dilution of Blue Dextran. Only 57Co-cyanocobalamin crossed the epithelium. Acute hemodynamic pulmonary edema was produced by aortic constriction plus saline overload. In pulmonary edema the fluid volume in the airspace increased at the rate of 0.96% per minute, and there was a significant influx of 131I-albumin into the lung saline from the blood in all animals. However, neither 125I-albumin nor Blue Dextran diffused from the airspace into blood during edema; both were merely diluted by fluid influx. The rate of diffusion of 57Co-cyanocobalamin increased fivefold during edema. A small number of discrete breaks in the lung epithelium allowing bulk flow of interstitial fluid is proposed to account for the one-way movement of albumin in hemodynamic alveolar edema.

scholarly journals Experimental Transmission of Neisseria gonorrhoeae from Pregnant Rat to Fetus

1999 ◽  
Vol 67 (9) ◽  
pp. 4974-4976 ◽  
Author(s):  
Stella Nowicki ◽  
Rangaraj Selvarangan ◽  
Garland Anderson
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Fetal Mortality ◽  
Local Infection ◽  
Gonococcal Infection ◽  
Sprague Dawley ◽  
Pregnant Rat ◽  
Experimental Transmission ◽  
Sprague Dawley Rats ◽  
Intraperitoneal Inoculation ◽  
Dependent Mechanism

ABSTRACT Sprague-Dawley rats were infected on day 20 of pregnancy by intraperitoneal inoculation with Neisseria gonorrhoeae. Disseminated gonococcal infection (DGI) and pelvic inflammatory disease (PID) strains in the presence of C1q but not in the presence of bovine serum albumin (BSA) were able to spread from the pregnant rat to the fetus and resulted in fetal mortality. Transmission of DGI and PID strains that are serum resistant (serr) andsac-4 positive but not of a local infection strain that is sers and sac-4 negative was facilitated by the C1q-dependent mechanism. This study provides the first experimental model that may mimic the transmission of gonococcal infection from mother to the fetus during pregnancy.

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.

scholarly journals Maturation of the Na+/H+ antiporter (NHE3) in the proximal tubule of the hypothyroid adrenalectomized rat

2004 ◽  
Vol 287 (3) ◽  
pp. F521-F527 ◽  
Author(s):  
Neena Gupta ◽  
Vangipuram Dwarakanath ◽  
Michel Baum
Keyword(s):  
Proximal Tubule ◽  
Brush Border Membrane ◽  
Mrna Abundance ◽  
Protein Abundance ◽  
Sprague Dawley ◽  
Sham Control ◽  
Sprague Dawley Rats ◽  
Sodium Dependent ◽  
Combined Deficiency

In previous studies examining the role of glucocorticoids and thyroid hormone on the maturation of the Na+/H+ antiporter (NHE3), we found attenuation in the maturational increase in proximal tubule apical Na+/H+ antiporter activity but no change in NHE3 mRNA abundance in either glucocorticoid-deficient or hypothyroid rats. In addition, prevention of the maturational increase in either hormone failed to totally prevent the maturational increase in Na+/H+ antiporter activity. We hypothesized that one hormone played a compensatory role when the other was deficient. The present study examined whether combined deficiency of thyroid and glucocorticoid hormones would completely prevent the maturation of the Na+/H+ antiporter. Adrenalectomy was performed in 9-day-old hypothyroid Sprague-Dawley rats, a time before the normal postnatal maturational increase in these hormones occurs. Nine- and 30-day-old adrenalectomized (ADX), hypothyroid rats had comparable NHE3 mRNA abundance, which was 5- to 10-fold less than 30-day-old ADX, hypothyroid rats that received corticosterone-thyroxine replacement and 30-day-old sham control rats ( P < 0.05). Brush-border membrane NHE3 protein abundance was comparable in 9- and 30-day-old ADX, hypothyroid groups and ∼20-fold lower than both the 30-day replacement and 30-day sham groups ( P < 0.05). Similarly, the replacement and sham groups had higher sodium-dependent proton secretion than 9- and 30-day-old ADX, hypothyroid groups ( P < 0.05). We conclude that combined deficiency of both hormones totally prevents the maturational increase in NHE3 mRNA and protein abundance and Na+/H+ antiporter activity.

scholarly journals NAFLD Aggravates Septic Shock Due to Inadequate Adrenal Response and 11β-HSDs Dysregulation in Rats

Pharmaceutics ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 403
Author(s):  
Hui-Chun Huang ◽  
Ming-Hung Tsai ◽  
Fa-Yauh Lee ◽  
Te-Yueh Lin ◽  
Ching-Chih Chang ◽  
...  
Keyword(s):  
Septic Shock ◽  
Plasma Corticosterone ◽  
Adrenal Function ◽  
Chow Diet ◽  
Sprague Dawley ◽  
Alcoholic Fatty Liver ◽  
Sprague Dawley Rats ◽  
Diet Control ◽  
Corticosterone Response ◽  
Adrenal Response

Background: Non-alcoholic fatty liver disease (NAFLD) is linked with metabolic syndrome. Previous studies showed that obesity may disrupt adrenal function and adversely affect its counter-regulations against shock. This study hence evaluated adrenal function abnormalities in NAFLD with shock. Methods: Sprague-Dawley rats were fed with regular chow-diet (control) or high fat diet (HFD, 60% energy derived from fat). Blood tests were performed at the end of the 4th, 6th and 8th week, respectively. Experiments were performed at the end of the 8th week. Results: HFD rats developed NAFLD. HFD rats had 27% and 51% increase in plasma corticosterone at the 6th and 8th week in usual status. However, HFD rats had 5 times more reduction of mean arterial pressure in response to lipopolysaccharide-induced sepsis as compared to control rats. The corticosterone increment ratio was also lower in HFD rats, even after ACTH administration. 11β-HSD system tended to generate more corticosterone in HFD rats under hemodynamic stable status without shock and the trend was lost in HFD rats with septic shock. Conclusion: Rats with NAFLD had profound septic shock due to inadequate corticosterone response. This is, at least partly, due to 11β-HSDs dysregulation in sepsis.

scholarly journals Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury

2006 ◽  
Vol 291 (3) ◽  
pp. L354-L361 ◽  
Author(s):  
Michael T. Ganter ◽  
Lorraine B. Ware ◽  
Marybeth Howard ◽  
Jérémie Roux ◽  
Brandi Gartland ◽  
...  
Keyword(s):  
Heat Shock ◽  
Pulmonary Edema ◽  
Stress Protein ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial ◽  
Edema Fluid ◽  
Protein Response ◽  
Alveolar Edema

Previous studies have shown that heat shock protein 72 (Hsp72) is found in the extracellular space (eHsp72) and that eHsp72 has potent immunomodulatory effects. However, whether eHsp72 is present in the distal air spaces and whether eHsp72 could modulate removal of alveolar edema is unknown. The first objective was to determine whether Hsp72 is released within air spaces and whether Hsp72 levels in pulmonary edema fluid would correlate with the capacity of the alveolar epithelium to remove alveolar edema fluid in patients with ALI/ARDS. Patients with hydrostatic edema served as controls. The second objective was to determine whether activation of the stress protein response (SPR) caused the release of Hsp72 into the extracellular space in vivo and in vitro and to determine whether SPR activation and/or eHsp72 itself would prevent the IL-1β-mediated inhibition of the vectorial fluid transport across alveolar type II cells. We found that eHsp72 was present in plasma and pulmonary edema fluid of ALI patients and that eHsp72 was significantly higher in pulmonary edema fluid from patients with preserved alveolar epithelial fluid clearance. Furthermore, SPR activation in vivo in mice and in vitro in lung endothelial, epithelial, and macrophage cells caused intracellular expression and extracellular release of Hsp72. Finally, SPR activation, but not eHsp72 itself, prevented the decrease in alveolar epithelial ion transport induced by exposure to IL-1β. Thus SPR may protect the alveolar epithelium against oxidative stress associated with experimental ALI, and eHsp72 may serve as a marker of SPR activation in the distal air spaces of patients with ALI.

Simulated microgravity enhances vasoconstrictor responsiveness of rat basilar artery

2001 ◽  
Vol 90 (6) ◽  
pp. 2296-2305 ◽  
Author(s):  
Le-Ning Zhang ◽  
Li-Fan Zhang ◽  
Jin Ma
Keyword(s):  
Arginine Vasopressin ◽  
Simulated Microgravity ◽  
Hindlimb Unloading ◽  
Sprague Dawley ◽  
Brain Vessels ◽  
Simultaneous Control ◽  
Sprague Dawley Rats ◽  
Significant Difference ◽  
Basilar Arteries ◽  
Dependent Mechanism

Recently, hypertrophy and increased myogenic tone of brain vessels have been observed in rats after simulated microgravity. It is expected that simulated microgravity may also induce hyperreactivity of brain vessels. To test this hypothesis, Sprague-Dawley rats were subjected to a 4-wk tail-suspended hindlimb unloading (TS) to simulate the cardiovascular deconditioning effect of microgravity. After 4 wk, the vasoreactivity of isolated basilar arterial rings from TS rats to both receptor- and non-receptor-mediated vasoconstrictors, such as KCl, arginine vasopressin, or 5-hydroxytryptamine (5-HT), and vasodilators such as ACh, thrombin, adenosine, or sodium nitroprusside were examined and compared with those from simultaneous control (Cn) rats. In the first part of this study, it was found that the maximal isometric contractile responsiveness evoked by vasoconstrictors such as KCl, arginine vasopressin, or 5-HT was enhanced in basilar arterial rings from TS rats, whereas vasodilatory responsiveness to vasodilators showed no significant difference between TS and Cn rats. In the second part of this study, it was found that removal of the endothelium had no effects on the contractile responsiveness to 5-HT in basilar arterial rings from TS rats but enhanced markedly the responsiveness in basilar arterial rings from Cn rats to an extent comparable with that of TS rats. Application of tetraethylammonium also had no effects on the contractile response to 5-HT in basilar arterial rings from TS but significantly increased the responsiveness of basilar arterial rings from Cn rats with endothelium intact. These results showed that 4-wk simulated microgravity enhanced the vascular contractile responsiveness of basilar arterial rings to both receptor- and non-receptor-mediated vasoconstrictors, and the enhancement of 5-HT-induced contraction in TS rat basilar arteries was due to an impairment of endothelium-dependent mechanism. These results suggest that endothelium-derived hyperpolarizing factors are responsible for this endothelium-dependent attenuating modulatory mechanism in contractile responsiveness of rat basilar arteries to 5-HT.

Circulating cytokines and endotoxin are not necessary for the activation of the sickness or corticosterone response produced by peripheral E. coli challenge

2003 ◽  
Vol 95 (5) ◽  
pp. 1873-1882 ◽  
Author(s):  
J. Campisi, ◽  
M. K. Hansen, ◽  
K. A. O'Connor, ◽  
J. C. Biedenkapp, ◽  
L. R. Watkins, ◽  
...  
Keyword(s):  
Core Body Temperature ◽  
Sprague Dawley ◽  
E Coli ◽  
Sprague Dawley Rats ◽  
Inflammatory Stimuli ◽  
Corticosterone Response ◽  
Few Data ◽  
Factor Α ◽  
The Brain ◽  
Circulating Cytokines

Peripheral administration of a variety of inflammatory stimuli, such as endotoxin or cytokines, induces an orchestrated set of brain-mediated events referred to as the sickness response. The mechanism for how immune products signal the brain is not clear, but accumulating evidence supports the existence of neural as well as blood-borne pathways. Although endotoxin or cytokine administration results in sickness responses, few data exist regarding the role of circulating endotoxin or cytokines in the induction of sickness during a real bacterial infection. Thus the present studies examined whether subcutaneously administered Escherichia coli can activate sickness responses and whether circulating endotoxin and/or proinflammatory cytokines are a prerequisite for these responses. Male Sprague-Dawley rats were injected subcutaneously with one of three doses (2.5 × 107, 2.5 × 108, 2.5 × 109 colony-forming units) of replicating E. coli, a ubiquitous bacterial strain, or vehicle. Core body temperature (Tc) and activity were measured for 3 days after the injection. A second set of groups of animals were killed 3, 6, 12, 18, 24, and 48 h after the injection, and blood samples and brains were collected. Injections dose dependently and consistently increased Tc and decreased activity, with increases in Tc beginning 4 h after the injection. In addition, E. coli significantly increased serum interleukin (IL)-1β, IL-6, and tumor necrosis factor-α and brain IL-1β levels beginning at the 6-h time point. Corticosterone and endotoxin were first elevated in the circulation at 3 and 18 h after the injection, respectively. Because fever onset preceded brain cytokine induction, we also examined cytokine levels in the serum, brain, and inflammation site 2 and 4 h after injection. Cytokines were elevated at the inflammation site but were not detectable in the serum or brain at 2 and 4 h. We conclude that subcutaneous injection of replicating E. coli induces a consistent and naturalistic infection that includes features of the sickness response as well as increases in circulating, brain, and inflammation site tissue cytokines. In addition, injection of replicating E. coli produces a robust fever and corticosterone response at a time when there are no detectable increases in circulating cytokines or endotoxin. These results suggest that elevated levels of circulating cytokines and endotoxin are not necessary for the activation of the sickness or corticosterone response. Therefore, fever, activity reduction, and corticosterone elevation induced by E. coli infection may have been evoked by a neural, rather than a humoral, pathway from the periphery to the brain.

scholarly journals Evidence for an Alanine, Serine, and Cysteine System of Transport in Isolated Brain Capillaries

1987 ◽  
Vol 7 (5) ◽  
pp. 585-591 ◽  
Author(s):  
Ivan Tayarani ◽  
Jeanne-Marie Lefauconnier ◽  
Françoise Roux ◽  
Jean-Marie Bourre
Keyword(s):  
Amino Acids ◽  
Water Volume ◽  
Sprague Dawley ◽  
Brain Capillaries ◽  
Independent System ◽  
System A ◽  
Sprague Dawley Rats ◽  
System L ◽  
Sodium Dependent ◽  
Energy Dependent

Brain capillaries isolated from 2-month-old male and female Sprague-Dawley rats were used to study the transport of neutral amino acids. The uptake of alanine, leucine, and alpha-methylaminoisobutyric acid (MeAIB) was a linear function of time for the first minute of incubation. Based on these observations, an incubation time of 1 min was used to measure transport activities. The intracellular water volume of the isolated capillaries was 2.2 μl/mg protein. This value was significantly lower (1.8 μl/mg protein) when measured in the absence of sodium. L-Alanine, L-serine, and L-cysteine were taken up from the abluminal surface of brain capillaries by a sodium- and energy-dependent, carrier-mediated system. This uptake, for the most part, was not inhibited by MeAIB. System ASC (alanine-serine-cysteine) appeared to be of primary importance for the transport of these amino acids in isolated brain capillaries. The apparent Km and Vmax values for L-alanine uptake by ASC transport, based on the Hofstee plot presentation, were 1.3 m M and 0.975 nmol/μl water content/min, respectively. The results also indicate that the transport of MeAIB and 2-aminobicyclo(2,2,1)heptane-2-carboxylic acid (BCH) was limited to the sodium-dependent system A (alanine) and the sodium-independent system L (leucine), respectively.

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