scholarly journals Investigation of hemotoxicologic potential of an ayurvedic preparation Kutajarista used in Sprue syndrome after chronic administration to male Sprague-Dawley rats

2020 ◽  
Vol 14 (8) ◽  
pp. 308-315
Author(s):  
Tohidul Amin Mohammad ◽  
Fatema Kaniz ◽  
karmakar Palash ◽  
Abdur Rahman Md. ◽  
Haque Tazmel ◽  
...  
Keyword(s):  
Chronic Administration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Acute cyclosporine-induced renal vasoconstriction: lack of effect of theophylline

1990 ◽  
Vol 258 (1) ◽  
pp. F41-F45
Author(s):  
P. C. Churchill ◽  
N. F. Rossi ◽  
M. C. Churchill ◽  
A. K. Bidani ◽  
F. D. McDonald
Keyword(s):  
Renal Plasma Flow ◽  
Left Kidney ◽  
Chronic Administration ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Adenosine Receptor Antagonist ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Group 1

Both acute and chronic administration of cyclosporine A (CSA) lead to renal vasoconstriction, but the mechanism is not fully understood. The present studies were designed to explore the possible role of adenosine in acute CSA-induced renal vasoconstriction in rats. Six groups of anesthetized Sprague-Dawley rats were studied using standard clearance techniques: group 1 rats were controls; groups 2, 4, and 6 received CSA intravenously at 20, 30, and 40 mg.h-1.kg body wt-1, respectively; groups 3 and 5 were identical to groups 2 and 4 except that a priming injection of theophylline was given (56 mumol/kg body wt) and theophylline was included in the intravenous infusate (0.56 mumol.min-1.kg body wt-1). CSA produced acute and concentration-dependent reductions in renal plasma flow (left kidney) and in the clearances of p-aminohippuric acid and inulin (both kidneys). Except in group 6, these changes were observed in the absence of a decrease in arterial blood pressure, demonstrating that CSA produced an acute and concentration-dependent increase in renovascular resistance. Theophylline not only failed to block CSA-induced renal vasoconstriction, if anything, it potentiated it. Because theophylline is an adenosine receptor antagonist, these findings contradict the hypothesis that adenosine mediates acute CSA-induced renal vasoconstriction.

Orally administered L-arginine does not alter right ventricular hypertrophy in chronically hypoxic rats

1994 ◽  
Vol 266 (2) ◽  
pp. R559-R563 ◽  
Author(s):  
T. C. Resta ◽  
B. R. Walker
Keyword(s):  
Right Ventricular ◽  
Pulmonary Circulation ◽  
Wistar Rats ◽  
Chronic Hypoxia ◽  
Chronic Administration ◽  
Hypoxic Exposure ◽  
Sprague Dawley ◽  
Pulmonary Vasodilation ◽  
Pulmonary Vasodilators ◽  
Sprague Dawley Rats

Evidence suggests that nitric oxide synthesis within the pulmonary circulation may be attenuated during chronic hypoxia in Wistar rats due to reduced L-arginine availability. In contrast, chronically hypoxic Sprague-Dawley rats exhibit normal endothelium-dependent pulmonary vasodilation. The purpose of the present study was to determine whether 1) Wistar rats demonstrate greater right ventricular (RV) hypertrophy in response to chronic hypoxia than Sprague-Dawley rats and 2) chronic administration of L-arginine would diminish this response in Wistar rats. L-Arginine had no effect on the degree of hypoxia-induced RV hypertrophy or polycythemia in either strain of rat. However, Wistar rats demonstrated greater hypoxia-induced RV hypertrophy and polycythemia compared with Sprague-Dawley rats. To determine whether chronically hypoxic Wistar rats indeed exhibit impaired endothelium-dependent pulmonary vasodilation, isolated lungs from control and chronically hypoxic Wistar rats were administered the endothelium-dependent pulmonary vasodilators A23187 or vasopressin. Vasodilatory responses to either agent were unaffected by chronic hypoxic exposure. We conclude that endothelium-dependent pulmonary vasodilation is maintained in the pulmonary circulation of chronically hypoxic Wistar and Sprague-Dawley rats.

scholarly journals Glucocorticoids attenuate the central sympathoexcitatory actions of insulin

2014 ◽  
Vol 112 (10) ◽  
pp. 2597-2604 ◽  
Author(s):  
Jennifer L. Steiner ◽  
Megan E. Bardgett ◽  
Lawrence Wolfgang ◽  
Charles H. Lang ◽  
Sean D. Stocker
Keyword(s):  
Food Intake ◽  
Mammalian Target Of Rapamycin ◽  
Chronic Administration ◽  
Sprague Dawley ◽  
Sympathetic Function ◽  
Sprague Dawley Rats ◽  
Access To Water ◽  
The Central Nervous System ◽  
Regulate Food Intake ◽  
Few Data

Insulin acts within the central nervous system to regulate food intake and sympathetic nerve activity (SNA). Strong evidence indicates that glucocorticoids impair insulin-mediated glucose uptake and food intake. However, few data are available regarding whether glucocorticoids also modulate the sympathoexcitatory response to insulin. Therefore, the present study first confirmed that chronic administration of glucocorticoids attenuated insulin-induced increases in SNA and then investigated whether these effects were attributed to deficits in central insulin-mediated responses. Male Sprague-Dawley rats were given access to water or a drinking solution of the glucocorticoid agonist dexamethasone (0.3 μg/ml) for 7 days. A hyperinsulinemic-euglycemic clamp significantly increased lumbar SNA in control rats. This response was significantly attenuated in rats given access to dexamethasone for 7, but not 1, days. Similarly, injection of insulin into the lateral ventricle or locally within the arcuate nucleus (ARC) significantly increased lumbar SNA in control rats but this response was absent in rats given access to dexamethasone. The lack of a sympathetic response to insulin cannot be attributed to a generalized depression of sympathetic function or inactivation of ARC neurons as electrical activation of sciatic afferents or ARC injection of gabazine, respectively, produced similar increases in SNA between control and dexamethasone-treated rats. Western blot analysis indicates insulin produced similar activation of Akt Ser473 and rpS6 Ser240/244 in the ventral hypothalamus of control and dexamethasone-treated rats. Collectively, these findings suggest that dexamethasone attenuates the sympathoexcitatory actions of insulin through a disruption of ARC neuronal function downstream of Akt or mammalian target of rapamycin (mTOR) signaling.

scholarly journals Chronic use of chloroquine disrupts the urine concentration mechanism by lowering cAMP levels in the inner medulla

2012 ◽  
Vol 303 (6) ◽  
pp. F900-F905 ◽  
Author(s):  
Tobias N. von Bergen ◽  
Mitsi A. Blount
Keyword(s):  
Lupus Erythematosus ◽  
Urine Analysis ◽  
Water Channel ◽  
Chronic Administration ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Chloroquine Treatment ◽  
Camp Levels

Chloroquine, a widely used anti-malaria drug, has gained popularity for the treatment of rheumatoid arthritis, systemic lupus erythematosus (SLE), and human immunodeficiency virus (HIV). Unfortunately, chloroquine may also negatively impact renal function for patients whose fluid and electrolyte homeostasis is already compromised by diseases. Chronic administration of chloroquine also results in polyuria, which may be explained by suppression of the antidiuretic response of vasopressin. Several of the transporters responsible for concentrating urine are vasopressin-sensitive including the urea transporters UT-A1 and UT-A3, the water channel aquaporin-2 (AQP2), and the Na+-K+-2Cl−cotransporter (NKCC2). To examine the effect of chloroquine on these transporters, Sprague-Dawley rats received daily subcutaneous injections of 80 mg·kg−1·day−1of chloroquine for 4 days. Twenty-four hour urine output was twofold higher, and urine osmolality was decreased by twofold in chloroquine-treated rats compared with controls. Urine analysis of treated rats detected the presence chloroquine as well as decreased urine urea and cAMP levels compared with control rats. Western blot analysis showed a downregulation of AQP2 and NKCC2 transporters; however, UT-A1 and UT-A3 abundances were unaffected by chloroquine treatment. Immunohistochemistry showed a marked reduction of UT-A1 and AQP2 in the apical membrane in inner medullary collecting ducts of chloroquine-treated rats. In conclusion, chloroquine-induced polyuria likely occurs as a result of lowered cAMP production. These findings suggest that chronic chloroquine treatment would exacerbate the already compromised fluid homeostasis observed in diseases like chronic kidney disease.

Upregulation of Na+ transporter abundances in response to chronic thiazide or loop diuretic treatment in rats

2003 ◽  
Vol 284 (1) ◽  
pp. F133-F143 ◽  
Author(s):  
Ki Young Na ◽  
Yoon Kyu Oh ◽  
Jin Suk Han ◽  
Kwon Wook Joo ◽  
Jung Sang Lee ◽  
...  
Keyword(s):  
Tap Water ◽  
Chronic Administration ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
Volume Depletion ◽  
Diuretic Treatment ◽  
Sprague Dawley Rats ◽  
Collecting Ducts ◽  
Site Of Action

Furosemide and hydrochlorothiazide (HCTZ) exert their diuretic actions by binding to apical Na+ transporters, viz., the Na+-K+-2Cl− cotransporter in the thick ascending limb and the Na+-Cl−cotransporter in the distal convoluted tubule, respectively. We carried out semiquantitative immunoblotting and immunohistochemistry of rat kidneys to investigate whether chronic administration of furosemide or HCTZ is associated with compensatory changes in the abundance of Na+ transporters downstream from the primary site of action. Osmotic minipumps were implanted into Sprague-Dawley rats to deliver furosemide (12 mg/day) or HCTZ (3.75 mg/day) for 7 days. To prevent volume depletion, all animals were offered tap water and a solution containing 0.8% NaCl and 0.1% KCl as drinking fluid. The diuretic/natriuretic response was quantified in response to both agents by using quantitative urine collections. Semiquantitative immunoblotting revealed that the abundances of thick ascending limb Na+-K+-2Cl− cotransporter and all three subunits of the epithelial Na+ channel (ENaC) were increased by furosemide infusion. HCTZ infusion increased the abundances of thiazide-sensitive Na+-Cl−cotransporter and β-ENaC in the cortex and β- and γ-ENaC in the outer medulla. Consistent with these results, β-ENaC immunohistochemistry showed a remarkable increase in immunoreactivity in the principal cells of collecting ducts with either diuretic treatment. These increases in the abundance of Na+transporters in response to chronic diuretic treatment may account for the generation of diuretic tolerance associated with long-term diuretic use.

scholarly journals Preclinical HbA1c level studies of Brihat Khadir Batika and Chandraprabha Batika after chronic administration to male Sprague-Dawley rats

2018 ◽  
Vol 7 (11) ◽  
pp. 2151
Author(s):  
Umma Hafsa Asha ◽  
Nilay Saha ◽  
Md. Mamun Sikder ◽  
Khadija Akter ◽  
Tahmina Akter Sony ◽  
...  
Keyword(s):  
Hba1c Level ◽  
Hemoglobin A1c ◽  
Glycated Hemoglobin ◽  
Chronic Administration ◽  
Male Rat ◽  
Sprague Dawley ◽  
Traditional Medicines ◽  
Glycated Hemoglobin A1c ◽  
Sprague Dawley Rats

Background: Brihat Khadir Batika (BKD) and Chandraprabha Batika (CPB) are Ayurvedic preparations used as traditional medicines for different clinical indications in the rural population. BKD is used in diseases of throat and CPB is used in glandular enlargement. In this study we evaluate the influence of these preparations on HbA1c (%) level.Methods: To find out the average plasma glucose concentration over prolonged period of time, Ayurvedic medicinal preparations BKD and CPB were administered chronically to the male Sprague-Dawley rats at a dose of 400 mg/kg. After 28 days of chronic administration of BKD and CPB the following changes were noted. In this experiment Glycated Hemoglobin A1C level was determined.Results: The results of the study of in vitro quantitative determination of rat Glycated hemoglobin A1c concentrations in serum studies are thus: BKD caused a statistically insignificant (p=0.066) increase in the HbA1c level of the male rat (16.87% increase). CPB demonstrated a statistically insignificant (p=0.079) (17.47%) increase in the HbA1C level of the blood of the male rat.Conclusions: Both preparation BKD and CPB found in increasing HbA1c level of the blood of the male rat.

Preclinical Anemia Panel Studies of “Makardhvaja” after Chronic Administration to Male Sprague-Dawley Rats

2017 ◽  
Vol 09 (02) ◽  
Author(s):  
Sagor Chandra Roy ◽  
Md Mamun Sikder ◽  
Arjyabrata Sarker ◽  
Md Afaz Uddin ◽  
Neshat Masud ◽  
...  
Keyword(s):  
Chronic Administration ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Panel Studies

Target Organ Specificity: Diethylnitrosamine-and Dibenzylnitrosamine-induced Single-strand Breaks Plus Alkali-labile Bonds

1984 ◽  
Vol 3 (2) ◽  
pp. 207-216
Author(s):  
Douglas E. Brash ◽  
Cheng M. Su ◽  
Hani A. Nabi ◽  
Kathleen S. Reuter ◽  
Judith Ortman ◽  
...  
Keyword(s):  
Dna Damage ◽  
Chronic Administration ◽  
Target Organ ◽  
Single Strand ◽  
Organ Specificity ◽  
Tumor Promoters ◽  
Sprague Dawley ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Sprague Dawley Rats

Quantitative dose response measurements of diethylnitrosamine-and dibenzylnitrosamine-induced DNA single-strand breaks plus alkali-labile bonds (SSB + ALB) (single-strand breaks, apurinic/apyrimidinic sites, and phosphotriesters) were performed on samples of 100,000 nuclei from Sprague-Dawley rats. Twenty-four hours after diethylnitrosamine injection, there were no SSB + ALB in brain (nontarget), SSB + ALB in kidney (target), and SSB + ALB in liver (target only after partial hepatectomy, tumor promoters, or chronic administration). Seven days after diethylnitrosamine injection, liver SSB + ALB had declined. The noncarcinogenic diethylnitrosamine analog, dibenzylnitrosamine, induced no SSB + ALB at 6 hours or 7 days postinjection. Induction of DNA damage, therefore, correlates well with target organ specificity of tumorigenesis when specificity is broadened to include those organs that exhibit tumors only when DNA damage is followed by additional treatments.

scholarly journals Preclinical HbA1c level studies of makaradhwaja and siddha makaradhwaja after chronic administration to male Sprague-Dawley rats

2017 ◽  
Vol 6 (6) ◽  
pp. 1249
Author(s):  
Arjyabrata Sarker ◽  
Kushal Biswas ◽  
Manjurul I. Chowdhury ◽  
Farzana Khan ◽  
Taposhi Sultana ◽  
...  
Keyword(s):  
Hba1c Level ◽  
Glycated Hemoglobin ◽  
Chronic Administration ◽  
Male Rat ◽  
Sprague Dawley ◽  
Traditional Medicines ◽  
Failure Treatment ◽  
Sprague Dawley Rats

Background: Makaradhwaja (MD) and Siddha Makaradhwaja (SMD) are Ayurvedic preparations used as traditional medicines for different clinical indications in the rural population. Principle purpose of using MD is controlling hypotension and while SMD is useful in peripheral circulatory failure treatment. In this study we evaluate the influence of these preparations on HbA1c (%) level.Methods: To find out the average plasma glucose concentration over prolonged period of time, MD and SMD were administered chronically to the male Sprague-Dawley rats at a dose of 40 mg/kg. After 28 days of chronic administration of MD and SMD the following changes were noted and Glycated Hemoglobin (HbA1c) level was determined.Results: The results of the study of in vitro quantitative determination of rat HbA1c concentrations in serum studies, MD demonstrated a negligible (0.61%) decrease in the HbA1c level of the blood of the male rat (p=0.902). Whereas SMD demonstrated a negligible (1.83%) increase in the HbA1c level of the blood of the male rat (p=0.782).Conclusions: Between these preparation MD slightly decreases HbA1c level of the blood of the male rat, whereas SMD found in increasing HbA1c level of the blood of the male rat.

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