Intragastric administration of a low dose of potassium ions decreases sensitivity to gastric distention in anesthetized rats

1998 ◽  
Vol 114 ◽  
pp. A828
Author(s):  
M.L. Rouzade ◽  
J. Fioramonti ◽  
L. Bueno
Endocrinology ◽  
2017 ◽  
Vol 158 (7) ◽  
pp. 2200-2211 ◽  
Author(s):  
Catherine Hume ◽  
Nancy Sabatier ◽  
John Menzies

Abstract Oxytocin is a potent anorexigen and is believed to have a role in satiety signaling. We developed rat models to study the activity of oxytocin neurons in response to voluntary consumption or oral gavage of foods using c-Fos immunohistochemistry and in vivo electrophysiology. Using c-Fos expression as an indirect marker of neural activation, we showed that the percentage of magnocellular oxytocin neurons expressing c-Fos increased with voluntary consumption of sweetened condensed milk (SCM). To model the effect of food in the stomach, we gavaged anesthetized rats with SCM. The percentage of supraoptic nucleus and paraventricular nucleus magnocellular oxytocin-immunoreactive neurons expressing c-Fos increased with SCM gavage but not with gastric distention. To further examine the activity of the supraoptic nucleus, we made in vivo electrophysiological recordings from SON neurons, where anesthetized rats were gavaged with SCM or single cream. Pharmacologically identified oxytocin neurons responded to SCM gavage with a linear, proportional, and sustained increase in firing rate, but cream gavage resulted in a transient reduction in firing rate. Blood glucose increased after SCM gavage but not cream gavage. Plasma osmolarity and plasma sodium were unchanged throughout. We show that in response to high-sugar, but not high-fat, food in the stomach, there is an increase in the activity of oxytocin neurons. This does not appear to be a consequence of stomach distention or changes in osmotic pressure. Our data suggest that the presence of specific foods with different macronutrient profiles in the stomach differentially regulates the activity of oxytocin neurons.


2021 ◽  
Vol 17 ◽  
Author(s):  
Yuxian Lin ◽  
Faxin Sun ◽  
Jinlai Liu ◽  
Qinghua Weng ◽  
Lijun Jin ◽  
...  

Background: To mitigate diabetes and its complications in cardiovascular diseases, the antidiabetic agent glimepiride is usually administered with ferulic acid concomitantly in clinics. However, both drugs are prone to be metabolized partly by CYP2C9, thus they have the potential drug-drug interaction affecting the safety and efficacy. Objective: This project aimed to evaluate the pharmacokinetic (PK) effects of ferulic acid (FA) on glimepiride (GLM) and its metabolite hydroxy glimepiride (OH-GLM) in plasma by using the HPLC-MS/MS method. Methods: Healthy male Sprague Dawley (SD) rats were randomly divided into three groups. They received intragastric administration of 0.5% sodium carboxymethyl cellulose (CMC), low-dose FA (20 mg•kg-1), and high-dose FA (40 mg•kg-1) for 8 days, respectively. Rats were given 0.5% sodium CMC or FA on the last day and then uniformly given 1.0 mg•kg-1 glimepiride by gavage. Blood samples were obtained from retro-orbital plexus at the time points of 0.167, 0.5, 1, 2, 3, 4, 6, 8, 10, 12, and 24 h after administration. Plasma samples were analyzed for GLM and its metabolite OH-GLM on an HPLC-MS/MS system. Results: No statistically significant difference was found in the effect of low-dose FA on the pharmacokinetics of GLM. High-dose FA significantly decreased Cmax of GLM by 30.05% and CLz/F of OH-GLM by 47.45%. It also increased Tmax and t1/2z of GLM by 95.87% and 140.00%. Conclusion: Low-dose FA did not alter GLM metabolism, while high-dose treatment of FA caused pharmacokinetics interaction with GLM in rats.


2007 ◽  
Vol 97 (4) ◽  
pp. 3004-3014 ◽  
Author(s):  
David W. Adelson ◽  
Hovsep P. Kosoyan ◽  
Yuhua Wang ◽  
Justin Z. Steinberg ◽  
Yvette Taché

Corticotropin-releasing factor (CRF) injected peripherally or released in response to stressful challenges to the organism reduces gastric tone and contractility, in part by vagal pathways. However, information on the changes in gastric vagal impulse activity evoked by peripheral CRF administration is entirely lacking. Using a novel “dual recording” method in urethane-anesthetized rats, vagal efferent (VE) and afferent (VA) impulse activities were recorded simultaneously from separate, fine bundles dissected from the ventral gastric vagus nerve branch innervating the glandular stomach. Activity records for 38 VA single units (SUs) and 33 VE SUs were sorted from multiunit records obtained from 13 preparations. Intravenous (iv) administration of saline had no effect on multiunit VE activity, whereas CRF (1 μg/kg, iv) immediately inhibited VE activity, reaching a nadir of 54 ± 8.0% of preinjection levels at 3.0 min postinjection. CRF (1 μg/kg, iv) inhibited 25/33 (75.8%) VE SUs and excited three of 33 (9.1%) VE SUs. In contrast to potent effects on VE activity, iv CRF did not alter multiunit VA activity. Single-unit analysis, however, revealed five of 38 (13.1%) VA SUs excited by iv CRF at widely varying latencies (suggesting an indirect mode of action) and one inhibited VA SU. VA SUs excited after iv CRF did not respond during gastric distention and vice versa. These experiments are the first to use simultaneous recording of gastric VA and VE units. The data demonstrate a predominantly inhibitory influence of iv CRF on VE outflow to the hindstomach, not driven by gastric vagovagal reflex activity.


1979 ◽  
Vol 42 (05) ◽  
pp. 1429-1433 ◽  
Author(s):  
J J F Belch ◽  
G D O Lowe ◽  
J G Pollock ◽  
C R M Prentice

SummaryAn optimal inhibition of tissue fibrinolysis, studied by a histochemical fibrin slide technique in the rat stomach, was obtained by administration of tranexamic acid in a dose of 60 mg/100 g body weight. A significant fibrinolysis inhibition was found within 5 min, when tranexamic acid in this dose was given either intravenously or intragastrically. A prolonged duration of fibrinolysis inhibition was observed after intragastric administration. After 4 hr no inhibitory effect of tranexamic acid could be recorded, irrespective of the route of administration.


1984 ◽  
Vol 246 (4) ◽  
pp. E306-E310 ◽  
Author(s):  
W. E. Grizzle ◽  
N. E. Dunlap

We report that adrenal compensatory hypertrophy occurs in intact and hypophysectomized anesthetized rats as well as in rats in which endogenous ACTH is suppressed by administration of dexamethasone or of dexamethasone plus low-dose ACTH. However, adrenal compensatory hypertrophy is blocked in intact and hypophysectomized animals when aldosterone alone or the combination of aldosterone, dexamethasone, and ACTH is administered using Alzet pumps. These data support previous reports that questioned the validity of the hypothesis that adrenal compensatory hypertrophy is controlled by the glucocorticoid-ACTH negative feedback system. These results require modification of current hypotheses concerning the mechanism of adrenal compensatory hypertrophy to allow for a central nervous system or other effect of aldosterone.


2009 ◽  
Vol 296 (1) ◽  
pp. F170-F176 ◽  
Author(s):  
Luis C. Matavelli ◽  
Philip J. Kadowitz ◽  
L. Gabriel Navar ◽  
Dewan S. A. Majid

Peroxynitrite (ONOO−) is formed endogenously by the reaction of nitric oxide (NO) and superoxide (O2−). To examine the hypothesis that OONO− cause renal vasodilation at low concentrations but cause vasoconstriction at higher concentrations, we examined renal responses to intra-arterial infusion of incremental doses of OONO− (10, 20, and 40 μg·kg−1·min−1; 45 min each) in anesthetized rats. Renal blood flow (RBF) and glomerular filtration rate (GFR) were determined by PAH and inulin clearance. In control rats ( n = 6), low dose (10 μg·kg−1·min−1) of OONO− increased RBF by 10 ± 3% and GFR by 15 ± 5%. The higher doses (20 and 40 μg·kg−1·min−1) mostly reversed these responses which were −7 ± 4 and −27 ± 7% ( P < 0.05) in RBF and −0.1 ± 4.8 and −14 ± 12% in GFR, respectively. There were no appreciable changes in urine flow (V) and sodium excretion (UNaV) during OONO− infusion. However, in rats pretreated with NO synthase (NOS) inhibitor, l-NAME (50 μg·kg−1·min−1; n = 5), these doses of ONOO− significantly reduced RBF (−26 ± 7, −27 ± 6, and −44 ± 3%) and GFR (−21 ± 6, −25 ± 8, and −32 ± 12%) with variable increases in V or UNaV. Long-term infusion of OONO− (10 μg·kg−1·min−1 for 75 min) in another set of control rats ( n = 5) also showed similar vasodilator and hyperfiltration responses. These data indicate that ONOO− acts as an oxidant at high concentration but provides renoprotective function at low concentration that depends on intact NOS activity.


2011 ◽  
Vol 55 (4) ◽  
pp. 1358-1365 ◽  
Author(s):  
Chih-Hsin Hung ◽  
Chih-Feng Kuo ◽  
Chiou-Huey Wang ◽  
Ching-Ming Wu ◽  
Nina Tsao

ABSTRACTIntragastric inoculation of mice withKlebsiella pneumoniaecan cause liver abscesses, necrosis of liver tissues, and bacteremia. A newly isolated phage (φNK5) with lytic activity forK. pneumoniaewas used to treatK. pneumoniaeinfection in an intragastric model. Both intraperitoneal and intragastric administration of a single dose of φNK5 lower than 2 × 108PFU at 30 min afterK. pneumoniaeinfection was able to protect mice from death in a dose-dependent manner, but the efficacy achieved with a low dose of φNK5 by intragastric treatment provided the more significant protection. Phage φNK5 administered as late as 24 h afterK. pneumoniaeinoculation was still protective, while intraperitoneal treatment with phage was more efficient than intragastric treatment as a result of the dissemination of bacteria into the circulation at 24 h postinfection. Surveys of bacterial counts for mice treated with φNK5 by the intraperitoneal route revealed that the bacteria were eliminated effectively from both blood and liver tissue.K. pneumoniae-induced liver injury, such as liver necrosis, as well as blood levels of aspartate aminotransferase and alanine aminotransferase and inflammatory cytokine production, was significantly inhibited by φNK5 treatment. These data suggest that a low dose of φNK5 is a potential therapeutic agent forK. pneumoniae-induced liver infection.


2018 ◽  
Vol 16 (1) ◽  
pp. 155-162 ◽  
Author(s):  
Xin Xin ◽  
Kangwei Zheng ◽  
Yingying Niu ◽  
Miaomiao Song ◽  
Wenyi Kang

AbstractFlammulina velutipes, (Curt. ex Fr.) Sing, a popularly edible fungus, has been widely used both as a restorative drug and a tonic food in China. In the current study, the effect ofF.velutipespolysaccharides was evaluated with a constipated rat model induced by loperamide hydrochloride. The rats were divided into six groups: normal group, model group, positive control group,F.velutipespolysaccharides high, moderate and low dose groups. Rats were given 2 mL of Loperamide hydrochloride (3 mg·kg·d), by intragastric administration 2 times per day for 10 days.F.velutipespolysaccharides at the doses of 600, 400 and 200 mg/kg (1 mL/100g weight) were administered to treat rats with constipation for 7 days. The gastrointestinal hormones, including motilin (MTL), gastrin (GAS), substance P (SP), somatostatin (SS), and intestinal propulsive rate and feces weight at 24 hours after treatment were used as the indexes to evaluate the effects ofF.velutipespolysaccharides on constipation. The levels of MTL, GAS and SP in serum significantly increased and the levels of SS in serum of rats significantly decreased after the treatment of rats withF.velutipespolysaccharides as compared with those of rats in the model group.


2010 ◽  
pp. 177-185 ◽  
Author(s):  
M Tanida ◽  
J Shen ◽  
D Kubomura ◽  
K Nagai

Previous studies have demonstrated that central injection of L-carnosine (β-alynyl-L-histidine), dipeptide synthesized in mammalian muscles, affects renal sympathetic nerve activity (RSNA) and blood pressure (BP) in anesthetized rats. In the present study, using urethane-anesthetized rats, we examined the dose-dependent effects of intravenous (IV) injection of various doses of anserine, dipeptide of similar structure to L-carnosine, on RSNA, BP and heart rate (HR). We found that injection of a low dose of anserine (1 μg) significantly suppressed RSNA, BP and HR. Conversely, a high dose (1000 μg) of anserine significantly elevated RSNA, BP and HR. Pretreatment with lateral cerebral ventricular (LCV) injection of thioperamide, a histaminergic H3-receptor antagonist, eliminated the effects of a low dose of anserine on RSNA, BP and HR. LCV injection of diphenhydramine, a histaminergic H1-receptor antagonist, abolished the effects of a high dose of anserine on RSNA, BP and HR. These findings suggest that anserine affects RSNA, BP and HR in a dose-dependent manner, and that the histaminergic nerve may be involved in the dose-different effects of anserine in rats.


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