A flexible technique for long term infusions in unrestrained rats

Nicolaı̈dis, Stylianos; Rowland, Neil E.; Meile, Marie‐José; Marfaing-Jallat, P.; Pesez, Arthur

doi:10.1016/0091-3057(74)90147-6

Cited by 158 publications

(35 citation statements)

References 14 publications

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“…into intact rats and into sodiumreplete adrenalectomized rats prepared at least 1 week before testing with an indwelling atrial catheter. The technique of atrial catheterization was as follows (modified from Nicolaidis, Rowland, Miele, Pesez & Marfang-Jalat, 1974). A 3.5 cm length of silastic tubing (o.d.…”

Section: Methodsmentioning

confidence: 99%

The renin‐angiotensin system and sodium appetite

Fitzsimons

Wirth

1978

The Journal of Physiology

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SUMMARY1. Bilateral nephrectomy or bilateral ureteric ligation greatly reduced the intake and retention of sodium in sodium-depleted adrenalectomized rats which were experienced at drinking aversive concentrations of saline and which otherwise would have drunk and retained substantial quantities of sodium.2. Pharmacological activation of the renin-angiotensin system with isoprenaline or phentolamine caused increased intake of water but did not stimulate sodium appetite in sodium-replete adrenalectomized rats, and decreased sodium appetite in sodium-depleted adrenalectomized animals.3. Neither I.P. injections of renin nor intravenous infusions of angiotensin II stimulated sodium appetite in normal rats or sodium-replete adrenalectomized rats.4. No differences were found in the saline preference-aversion curves of normal rats not maintained on saline given intracranial injections of angiotensin II or carbachol.5. Preoptic injections of renin, renin substrate or angiotensin II into sodiumreplete adrenalectomized rats which were maintained on water and 2-7 % saline induced immediate thirst followed by some saline intake. The saline intake was markedly less than the spontaneous saline intake of the same rats when sodium depleted.6. Similar preoptic injections in sodium-depleted adrenalectomized rats caused increased water intake but did not increase the saline intake any further.7. Intracranial injections of carbachol had little effect on saline intake in either sodium-replete or sodium-depleted adrenalectomized rats but caused increased water intake.8. In conclusion, peripheral activation of the renin-angiotensin system stimulates water intake but has no direct effect on sodium appetite. Secondly, central administration of components of the renin-angiotensin system causes thirst and does not inhibit sodium appetite whereas centrally administered carbachol causes thirst and inhibits sodium appetite. Therefore the renin-angiotensin system has only a minor role in sodium appetite.

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Section: Methodsmentioning

confidence: 99%

The renin‐angiotensin system and sodium appetite

Fitzsimons

Wirth

1978

The Journal of Physiology

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“…Male Sprague-Dawley rats (200 to 250 g; Charles River Laboratories, Saint-Aubin-Les-Elbeuf, France) were housed in individual metabolic cages, which enabled the collection of urine without contamination by feces. Three days before treatment, a bijugular catheter was inserted under ketamine anesthesia (100 mg/kg intraperitoneally), as described previously (29), and left in place throughout the experiment, allowing blood sampling and infusion by a different catheter on conscious animals. The animals had free access to food and water.…”

mentioning

confidence: 99%

Limited protection by small unilamellar liposomes against the renal tubular toxicity induced by repeated amphotericin B infusions in rats

Longuet

Joly

Amirault

et al. 1991

Antimicrob Agents Chemother

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Amphotericin B (AMB), either alone or incorporated into small unilamellar vesicles of pure dipalmitoylphosphatidyl choline (DPPC SUV-AMB), was administered intravenously to male Sprague-Dawley rats once daily for 5 days. Either 1.5 or 3.5 mg of AMB or DPPC SUV-AMB per kg was given, since these concentrations corresponded, respectively, to the lowest nephrotoxic dose and the sublethal dose of AMB in our model. Tubular functions were evaluated daily, and AMB concentrations in plasma, urine, and tissues were measured by high-performance liquid chromatography. AMB at both doses induced tubular toxicity, hyposthenuria being the earliest symptom. DPPC SUV-AMB at 1.5 mg/kg/day was atoxic, but the tubular alterations induced by 3.5 mg of DPPC SUV-AMB per kg were similar to those observed with 3.5 mg of AMB per kg, except that the ability to concentrate urine was partly restored 72 h after the last infusion. Incorporating AMB into DPPC SUV did not influence the pharmacokinetics of the drug. Using this lipidic AMB formulation, we thus observed a beneficial effect toward limiting the renal tubular toxicity of repeated low doses of AMB but, unexpectedly, not that of high doses. These results indicate that tubular renal functions and electrolyte serum values should be closely monitored in patients treated with AMB liposomal formulations, especially high-dose regimens.Systemic mycoses are a major cause of morbidity and mortality among immunocompromised patients (8,42,43). Although several new antifungal agents, particularly triazoles, have recently become available, amphotericin B (AMB) remains the most active drug for the treatment of opportunistic fungal infections (12,28). Its clinical use is limited by side effects, the most serious being nephrotoxicity. Harmful renal effects include inability to concentrate urine (1, 3, 4, 10), defective urinary acidification due to distal tubule dysfunction (10, 27, 31), renal potassium wasting (5), and depressed glomerular filtration rate (GFR) and renal plasma flow (6, 7).AMB toxicity was shown to be reduced when the drug was incorporated into liposomes or complexed with lipids (L-AMB), allowing higher doses to be infused and thereby increasing the efficiency of treatment in experimental fungal infections (23,36,37). However, the in vivo protective effect of liposomes (13, 38) or lipidic emulsions (18) against the experimental renal toxicity of AMB has been evaluated only after a single administration of the drug. Therefore, the experimental nephrotoxicity of L-AMB under conditions of repeated administration remains largely unknown. L-AMB has been used for the treatment of systemic mycoses in cancer patients with encouraging preliminary results (21, 22, 34), but again, the side effects on renal function have not been investigated in detail. Severe underlying disease, poor clinical conditions, previous treatment with free AMB, and multiple drug regimens might account for the difficulties encountered in evaluating renal function alterations in these * Corresponding author. patients. In ...

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“…Dams were rendered hyperglycemic during the last third of pregnancy by continuous glucose infusion under unrestrained conditions as described previously (9), according to the technique of Nicola'idis et al ( 10). On d 13 of pregnancy, they were operated RESULTS on.…”

Section: Methodsmentioning

confidence: 99%

Impaired Hepatic Glycogenolysis Related to Hyperinsulinemia in Newborns from Hyperglycemic Pregnant Rats

et al. 1990

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ABSTRACT. We have investigated the respective roles of insulin and glucagon in the initiation of hepatic glycogen degradation during the early postnatal period in rats, with special regard on the inhibitory effect of insulin on this process. Pregnant rats were rendered either slightly (8.5 mM) or highly hyperglycemic (22 mM) by infusing glucose during the last week of pregnancy. Fasted, newborn rats were studied from delivery to 16 h postpartum. At birth, newborns from slightly hyperglycemic rats showed higher glvcemia and insulinemia and lower plasma glucagonemia --compared with controls. Newborns from highly hyperglycemic rats were still more hyperglycemic and exhibited low plasma glucagon concentrations, but they were not hyperinsulinemic. In control newborns, hepatic glycogen breakdown was triggered by 2 h after delivery. By contrast, hyperglycemic-hyperinsulinemic newborns (newborns from slightly hyperglycemic rats) were unable to mobilize liver glycogen before 8-10 h after delivery. In hyperglycemicnormoinsulinemic newborns (newborns from highly hyperglycemic rats), hepatic glycogen concentration significantly started to decline 2 h after delivery and was no longer different from controls at 8 h. Anti-insulin serum injection at delivery promoted a prompt decrease in liver glycogen stores in controls as well as in newborns from slightly hyperglycemic rats. Phosphorylase alsynthase a ratio rose rapidly after delivery in controls and in newborns from highly hyperglycemic rats (maximum 4 h), whereas in newborns from slightly hyperglycemic rats, it rose much more slowly than in the two other groups (maximum 16 h). These data suggest that, in newborns from hyperglycemic mothers, hyperinsulinemia during late fetal and early neonatal life is the main factor preventing postnatal hepatic glycogenolysis. glucose homeostasis in newborn mammals. The breakdown of the large glycogen stores that have been accumulated in the fetal liver during late pregnancy represents the more rapidly available endogenous source of glucose (1, 2).Hepatic glycogen metabolism is primarily controlled by the respective concentrations of insulin and glucagon in the plasma (3), and it could be assumed that even a slight change in the secretion of one or both hormones during the fetal life may hamper the metabolic adaptation of the newborn to extrauterine life. This is suggested by the situation of infants of poorly controlled diabetic women in whom the severe postnatal hypoglycemia is mainly due to defective glucose production (4).We have previously shown that newborn rats of dams rendered slightly hyperglycemic by continuous glucose infusion during the last third of pregnancy were hyperglycemic at birth, but were profoundly hypoglycemic in the early postnatal period. This hypoglycemia seemed to be due, in a major part, to a defective postnatal hepatic glycogen breakdown, in contrast to control newborns, which exhibited sustained postnatal hepatic glycogenolysis (5). Concurrently, in newborns from hyperglycemic rats, the insulin/glucagon molar ...

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A flexible technique for long term infusions in unrestrained rats

Cited by 158 publications

References 14 publications

The renin‐angiotensin system and sodium appetite

The renin‐angiotensin system and sodium appetite

Limited protection by small unilamellar liposomes against the renal tubular toxicity induced by repeated amphotericin B infusions in rats

Impaired Hepatic Glycogenolysis Related to Hyperinsulinemia in Newborns from Hyperglycemic Pregnant Rats

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