8 resultados para Injection experiment

em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"


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The microinjection of carbachol into the medial preoptic area (MPO) of the rat induced natriuresis, kaliuresis and anti-diuresis in a dose-related manner. Atropine blocked all responses to carbachol. Hexamethonium impaired the dose-response effect of carbachol on kaliuresis, but had no effect on natriuresis and enhanced the antidiuretic effect of carbachol. Nicotine alone had no effects, but pre-treatment with nicotine enhanced the responses to carbachol. These data show that activity of the muscarinic receptors of the MPO increases renal electrolyte and reduces water excretion. They also suggest that nicotinic receptors have an inhibitory effect on water excretion. Nicotine could act through mechanisms unrelated to nicotinic receptors to enhance the effect of the carbachol. © 1989.

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The development of a fever in response to intravenous (IV, 1.5 μg/kg body mass) and intracerebroventricular (ICV, 1.5 μg/animal) injections of Escherichia coli lipopolysaccharide (LPS) was studied in control, thyroidectomised and protein-calorie malnourished rabbits (New Zealand Whites, n = 55). ICV injection of LPS is control rabbits produced a fever response, the characteristics of which differed from those obtained after IV pyrogen injection. Thyroid deficiency caused an attenuated fever response, irrespective of whether LPS had been administered by IV or ICV injection. Protein-calorie malnourished rabbits showed a smaller fever response after IV or ICV pyrogen injections. Malnourished rabbits, refed over a period of 15 days, showed a typical biphasic fever response, but with lower magnitude than controls. The results of these experiments suggest that ICV injection of LPS is not an appropriate model for the study of fever mechanisms in disease states, and that the attenuated fever response observed in protein-calorie malnourished rabbits may be related, at least in part, to a decreased ability to produce the endogenous pyrogen interleukin-1.

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We investigated the effects of losartan, an AT 1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol (a cholinergic receptor agonist). Male Holtzman rats (250-300 g) with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The injection of losartan (50 nmol/l μl) into the LV blocked the pressor response induced by ANG II (12 ng/l μl) and carbachol (2 nmol/l μl). After injection of ANG II and carbachol into the LV, mean arterial pressure (MAP) increased to 31 ± 1 and 28 ± 2 mmHg, respectively. Previous injection of losartan abolished the increase in MAP induced by ANG II and carbachol into the LV (2 ± 1 and 5 ± 2 mmHg, respectively). The injection of ramipril (12 ng/l μl) prior to carbachol blocked the pressor effect of carbachol to 7 ± 3 mmHg. These results suggest an interaction between central cholinergic pathways and the angiotensinergic system in the regulation of arterial blood pressure.

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The subfornical organ (SFO) and the lateral hypothalamus (LH) have been shown to be important for the central action of angiotensin II (ANG II) on water and salt regulation. Several anatomical findings have demonstrated neural connections between the SFO and the LH. The present experiments were conducted to investigate the role of the α-adrenergic antagonists and agonists injected into the LH on the water and salt intake elicited by injections of ANG II into the SFO. Prazosin (an α1-adrenergic antagonist) injected into the LH increased the salt ingestion, whereas yohimbine (an α2-adrenergic antagonist) and propranolol (a β-adrenergic antagonist) antagonized the salt ingestion induced by administration of ANG II into the SFO. Previous administration of clonidine (an α2-adrenergic agonist) or noradrenaline into the LH increased, whereas pretreatment with phenylephrine decreased the sodium intake induced by injection of ANG II into the SFO. Previous treatment with prazosin and propranolol reduced the water intake induced by ANG II. Phenylephrine increased the dipsogenic responses produced by ANG II, whereas previous treatment with clonidine injected into the LH reduced the water intake induced by ANG II administration into the SFO. The LH involvement with SFO on the excitatory and inhibitory mechanisms related to water and sodium intake is suggested.

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Objective - We determined the effects of losartan and PD 123319 (antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar1, Ala8] ANG II (a relatively peptide antagonist of angiotensin receptors) injected into the paraventricular nucleus (PVN) on water and 3% NaCl intake, and the diuretic, natriuretic, and pressor effects induced by administration of angiotensin II (ANG II) into the medial septal area (MSA) of conscious rats. Methods - Holtzman rats were used. Animals were anesthetized with tribromoethanol (20 mg) per 100 grams of body weight, ip. A stainless steel guide cannula was implanted into the MSA and PVN. All drugs were injected in 0.5-μl volumes for 10-15 seconds. Seven days after brain surgery, water and 3% NaCl intake, urine and sodium excretion, and arterial blood pressure were measured. Results - Losartan (40 nmol) and [Sar1, Ala8] ANG II (40 nmol) completely eliminated whereas PD 123319 (40 nmol) partially blocked the increase in water and sodium intake and the increase in arterial blood pressure induced by ANG II (10 nmol) injected into the MSA. The PVN administration of PD 123319 and [Sar1, Ala8] ANG II blocked whereas losartan attenuated the diuresis and natriuresis induced by MSA administration of ANG II. Conclusion - MSA involvement with PVN on water and sodium homeostasis and arterial pressure modulation utilizing ANGII receptors is suggested.

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In this work it was developed a procedure for the determination of vanadium in urine samples by electrothermal atomic absorption spectrometry using successive injections for preconcentration into a preheated graphite tube. Three 60 μL volumes were sequentially injected into the atomizer preheated to a temperature of 110°C. Drying and pyrolysis steps were carried out after each injection. A chemical modifier, barium difluoride (100 mg L-1), and a surfactant, Triton X-100 (0.3% v v-1), were added to the urine sample. When injecting into a hot graphite tube, the sample flow-rate was 0.5 μL s-1. The limits of detection and quantification were 0.54 and 1.82 without preconcentration, and 0.11 and 0.37 μg L-1 with preconcentration, respectively. The accuracy of the procedure was evaluated by an addition-recovery experiment employing urine samples. Recoveries varied from 96.0 to 103% for additions ranging from 0.8 to 3.5 μg L-1 V. The developed procedure allows the determination of vanadium in urine without any sample pretreatment and with minimal dilution of the sample.

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The objective of this experiment was to evaluate the effects of bovine somatotropin administration on serum concentrations of glucose, insulin, NEFA, IGF-I, and progesterone (P4) in ovariectomized non-lactating dairy cows receiving exogenous P4, as a model to estimate treatment effects on hepatic P4 degradation. Ten non-lactating, non-pregnant, and ovariectomized Gir×Holstein cows were assigned to the experiment (d -14 to 27). On d 0, cows were ranked by BW and BCS, and randomly assigned to one of two treatments: (1) bovine somatotropin (BST; n=5) or (2) saline control (control; n=5). Cows assigned to the BST treatment were administered s.c. injections containing 500. mg of sometribove zinc on d 0, 9, and 18 of the experiment, whereas control cows concurrently received a 10-mL s.c. injection of 0.9% saline. On d -2, cows were inserted with an intravaginal releasing device containing 1.9. g of P4, which remained in the cows until the end the experiment (d 27). Cow BW and BCS were assessed on d -14, 0, and 27. Blood samples were collected daily from d 0 to d 27, at 0 (immediately before), 1, and 2. h relative to concentrate feeding for determination of serum glucose, insulin, NEFA, P4, and IGF-I concentrations. Concentrations of glucose, NEFA, and insulin obtained prior to feeding (0. h) were used to determine pre-prandial revised quantitative insulin sensitivity check index (RQUICKI). No treatment effects were detected for BW (P=0.72) and BCS change (P=0.79) during the experiment. Beginning on d 2 of the experiment, BST cows had greater (P≤0.01) serum IGF-I concentrations compared with control cohorts (treatment×day interaction; P<0.01). Cows receiving BST had greater (P≤0.05) insulin concentrations compared with control cohorts from d 8 to d 11, d 16 and 17, as well as from d 19 to d 21 of the experiment (treatment×day interaction; P<0.01). Cows receiving BST had greater (P≤0.01) mean glucose and NEFA concentrations, as well as reduced (P<0.01) mean RQUICKI during the experiment compared with control cohorts. No treatment effects, however, were detected (P=0.73) for serum P4 concentrations. In conclusion, results from this experiment indicate that hepatic P4 catabolism is not directly regulated by circulating IGF-I, whereas BST administration decreases insulin sensitivity in non-lactating dairy cows in adequate nutritional status. © 2013 Elsevier B.V.