PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Infusions, Intraventricular”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed1987

Proglumide has access to brain and antagonizes the central satiety effect of cholecystokinin octapeptide in the dog.

Intra-third cerebroventricularly administered cholecystokinin octapeptide (CCK-8) decreased food intake through central mechanisms in the dog. Proglumide, administered intravenously, did enter into cerebrospinal (ventricular) fluid, and partially, but significantly, reversed this effect. CR1409, one of the newly synthesized glutaramic derivatives, blocked CCK-8-induced satiety more strongly than proglumide. These results indicate that systemic proglumide and CR1409 result in antagonism of the central CCK receptor for satiety in the dog.

Animals↗
PubMed1993

Evidence for the involvement of excitatory amino acid pathways in the development of precipitated withdrawal from acute and chronic morphine: an in vivo voltammetric study in the rat locus coeruleus.

Previous studies have demonstrated that activation of excitatory amino acid (EAA) pathways projecting to the locus coeruleus may be involved in the increased firing of locus coeruleus (LC) neurons during opioid withdrawal. Using differential normal pulse voltammetry to monitor catechol oxidation current (CA.OC), an index of neuronal activity in the LC, the role of EAA pathways in naloxone precipitated withdrawal after acute and chronic morphine treatment was examined. Acute morphine treatment (10 micrograms i.c.v.) significantly reduced the CA.OC signal in the LC to 54.3 +/- 3.1% of baseline. Naloxone challenge (1 mg/kg i.v.) completely reversed the morphine effect and produced a significant increase in the CA.OC signal above baseline, peak 145.4 +/- 10.1% of baseline. This naloxone-induced rebound response was attenuated by pretreatment with the EAA receptor antagonists gamma-D-glutamylglycine (DGG) (2, 20, 200 micrograms i.c.v.) and (-)-2-amino-7-phosphonoheptanoic acid (D-APH), but not L-APH (25 micrograms i.c.v.). In chronically morphine-treated rats (25 micrograms/h i.c.v., 5 days), naloxone challenge (1 mg/kg i.v.) produced a significant increase in CA.OC signal, peak 466.5 +/- 112.7% of baseline. This naloxone-induced response was attenuated by pretreatment with DGG (200 micrograms i.c.v.) or D-APH (25 micrograms i.c.v.). To the extent that CA.OC reflects locus coeruleus neuronal activity, the present findings further suggest that increases in locus coeruleus activity during naloxone precipitated withdrawal after both acute and chronic morphine treatment are mediated at least in part by activation of EAA pathways.

2-Amino-5-phosphonovalerate↗
PubMed1994

CNS regulation of blood lactate concentration in anesthetized rats.

This study evaluated the effect of stimulating the central nervous system (CNS) with neostigmine, an inhibitor of acetylcholinesterase, on the blood lactate concentration in fed rats and in rats fasted for 48 hours. After the rat was anesthetized with pentobarbital, neostigmine was stereotaxically injected into the third cerebral ventricle. In fed rats, the central injection of neostigmine significantly increased the blood lactate level, while concomitantly increasing plasma glucagon, epinephrine and norepinephrine concentrations. Constant infusion of somatostatin throughout the experiments, to inhibit glucagon secretion from the pancreas, did not affect alterations in blood lactate by central injection of neostigmine. In adreno-medullated rats, CNS-stimulation by neostigmine still increased plasma norepinephrine significantly, however, the alteration in blood lactate was only one-third of that in intact rats. Intraperitoneal propranolol, but not phentolamine, prevented the rise in lactate. Neostigmine increased lactate in fasted rats as well as in fed rats. We conclude that in anesthetized rats, stimulation of the CNS by neostigmine increases blood lactate mainly through circulating epinephrine and partially through circulating norepinephrine or direct sympathetic nervous stimulation; glucagon does not appear to be involved in the increase in blood lactate.

Anesthesia, General↗
PubMed1983

Influence of peripheral and intracerebroventricular glucose and insulin infusions on peripheral and cerebrospinal fluid glucose and insulin levels.

There is much evidence that glucose and insulin are related to the regulation of food intake and the maintenance of peripheral glucose homeostasis through actions of the central nervous system. However, evidence concerning the penetration of peripheral glucose and insulin into the cerebrospinal fluid (CSF) and the relationship between both peripheral and CSF glucose and insulin levels is still missing. In the reported experiments it is shown that insulin is present in the CSF (17 +/- 3.6 microU/ml CSF versus 44 +/- 6.0 microU/ml plasma) but that CSF insulin does not follow rises of peripheral insulin to 136 microU/ml plasma during 4.5 hours. On the other hand CSF glucose (55 +/- 3.1 mg/dl CSF) follows rises of peripheral glucose levels with a delay of about 30 min. Increase of CSF glucose by infusing glucose into the third brain ventricle elicits a prolonged decrease in peripheral glucose levels. Infusion into the third ventricle of insulin only does not change peripheral glucose. However, infusion of a combination of insulin and glucose in the third ventricle leads to a gradual increase in peripheral glucose and elicits a disappearance of the decrease in peripheral glucose after glucose only infusion into the CSF. During third ventricle infusion experiments no change in peripheral insulin could be observed. It will be argued that changes in CSF glucose and insulin contribute to maintenance of peripheral glucose homeostasis.

Animals↗
PubMed1987

Water drinking caused by intracerebroventricular infusions of hypertonic solutions in cattle.

Infusions into the lateral cerebral ventricle of hypertonic solutions of NaCl, mannitol or sucrose all induced water drinking in cattle. However, infusion of hypertonic NaCl caused a significantly greater water drinking response than did the infusions of mannitol or sucrose, despite the fact that CSF osmolality increase was similar. In contrast, hypertonic solutions of NaCl or mannitol had similar dipsogenic effects when infused intravenously. The intracerebroventricular infusions of hypertonic NaCl or mannitol did not affect the intakes of food or Na solution. The results are consistent with the hypothesis that both cerebral osmoreceptors and Na sensors are involved in regulating thirst in cows.

Animals↗
PubMed1995

Effect of continuous infusion of lysine via different routes and hepatic vagotomy on dietary choice in rats.

The effect of continuous L-lysine (Lys) infusion on dietary choice between Lys deficient and protein-free diets in Sprague-Dawley rats was studied to determine the sensing site of Lys deficiency. After daily intake of each diet became constant, Lys was continuously infused for 11 days via intraperitoneal (IP), intragastric (IG) or intracerebroventricular (ICV) route, with an osmotic pump. Daily intake of each diet was measured. Intake of the Lys deficient diet compared with protein-free diet in either IP or IG Lys-infused group increased significantly (p < 0.001) vs. the intake in the baseline period. The selection of the Lys deficient diet was quite comparable between IP and IG groups. But the intake of the ICV group was unchanged. Hepatic vagotomy during IP infusion transiently delayed selection of the Lys deficient diet. These results imply the roles of postabsorptive mechanisms in sensing an amino acid deficiency, and possible involvement of the hepatic branch of the vagus in the sensing. However, sensing in the brain or indeed in the intestine was not excluded.

Aging↗
PubMed1991

Intracerebroventricular naltrexone treatment attenuates acquisition of intravenous cocaine self-administration in rats.

The influence of centrally administered naltrexone, an opiate antagonist, on acquisition of intravenous cocaine self-administration behaviour in rats was examined. On five consecutive days, three hours per day, they could self-administer a cocaine solution (30 micrograms per infusion) through an indwelling cannula. Treatment consisted of daily injections of naltrexone (2 or 5 micrograms) or placebo into the lateral ventricle 30 minutes before testing. Naltrexone treatment dose dependently attenuated the rate of cocaine self-infusion. Both self-infusion rate and rate of responding on the reinforcement lever in the group treated with 5 micrograms naltrexone differed from placebo, whereas rate of responding on a dummy lever did not. These findings a) support the notion that opioid systems play a role in cocaine reinforcement, and b) suggest that naltrexone exerts its effect on cocaine reinforcement through action in the central nervous system.

Animals↗
PubMed1991

Effects of receptor-selective opioids on operant behavior in morphine-treated and untreated rats.

Selective cross-tolerance is often used as evidence to differentiate opioid receptor subtypes. We used this strategy to study operant behavioral effects of the opioid peptides, [D-Ala2, NMePhe4, Gly-ol5]enkephalin (DAGO), [D-Pen2.5]-enkephalin (DPDPE) and dynorphin, agonists highly selective for mu, delta, and kappa receptors, respectively. Food-deprived rats were trained to lever-press on a fixed-interval 3-min schedule of food-reinforcement. Time-effect and dose-effect curves were generated for each of the peptides, as well as for morphine, administered ICV, 5 min prior to the 1-h operant session. Experiments were performed on untreated subjects and on subjects receiving chronic infusion of morphine (10 mg/kg/day) from osmotic pumps. In untreated animals, morphine and the mu-selective peptide, DAGO, induced relatively long-lasting dose-related decreases in responding, whereas the non-mu agonists, DPDPE and dynorphin, induced only transient effects: response rates increased at low doses and decreased at high doses. Animals receiving chronic morphine infusion were tolerant to the rate-decreasing effects of morphine and DAGO; ED50s increased by factors of 8 and 6, respectively. There was some evidence of cross-tolerance to DPDPE and of sensitization to dynorphin in the morphine-maintained animals.

Animals↗
PubMed1991

A slow intravenous infusion of N-methyl-DL-aspartate as a seizure model in the mouse.

A seizure model involving slow i.v. infusion of the excitatory amino acid N-methyl-DL-aspartate (NMDLA) in the mouse is described. It allows determination of the threshold doses of NMDLA required to elicit clonic and tonic seizures in individual mice. The NMDA receptor antagonists MK-801, CPP, ifenprodil and 7-chlorokynurenic acid (7-CLK), and diazepam dose-dependently increased the dose of NMDLA required to elicit a tonic seizure. CPP, 7-CLK and diazepam also increased the dose of NMDLA inducing clonic seizures. In contrast, ifenprodil at doses which antagonised tonic seizures had no effect on clonic seizures. The glycine and polyamine modulatory site agonists, D-serine and spermidine respectively, dose-dependently reduced the dose of NMDLA required to induce clonic and tonic seizures. The NMDLA infusion model appears to be more sensitive than the classical bolus injection test and can detect both anticonvulsant and proconvulsant actions mediated by the NMDA receptor complex.

Animals↗
PubMed1991

Centrally administered NPY stimulated gastric acid and pepsin secretion by a vagally mediated mechanism.

We investigated the possible roles of centrally administered neuropeptide Y (NPY) on gastric secretion, serum gastrin levels and gastric mucosal blood flow in anesthetized rats. Centrally administered NPY dose-dependently stimulated gastric acid and pepsin secretion. The stimulatory effect of intracerebroventricular administration of NPY was more potent than that of intracisternal administration. Centrally administered NPY also increased gastric secretion in the central noradrenaline depleted rats. In contrast, intravenously administered NPY had no influence on gastric secretion. These stimulatory effects were abolished by vagotomy or atropine pretreatment. The serum gastrin levels did not change after central NPY injection. Although intravenously administered NPY slightly increased gastric mucosal blood flow, centrally administered NPY slightly diminished gastric mucosal blood flow. These results indicate that centrally administered NPY markedly influences gastric functions in the rat.

Animals↗
PubMed1995

The galanin-induced feeding stimulation is mediated via alpha 2-adrenergic receptors in goldfish.

In the present study we examined the effects of intracerebroventricular (ICV) or intraperitoneal (IP) galanin administration on food intake in satiated goldfish, at different time intervals after injections, 0-2, 2-8 and 0-8 h. We found that food intake was increased by ICV administered galanin (1 and 3.33 micrograms) at 2 and 8 h postinjection, while no modifications on feeding were observed after intraperitoneal injection in any of the studied time intervals. The galanin receptor antagonist, galantide, blocked the galanin-induced feeding increase. Pretreatment with yohimbine (alpha 2-adrenergic receptor antagonist), but not with prazosin (alpha 1-adrenergic receptor antagonist) antagonized the stimulatory effect of galanin on ingestive behavior. These results suggest that galanin is involved in the central regulation of feeding in goldfish, being the food intake stimulatory effect mediated by the alpha 2-adrenergic system.

Animals↗
PubMed1990

Peripheral angiotensin II is not the cause of sodium appetite in the rat.

Activation of the renin-angiotensin system has been shown to arouse both water and sodium intake in the rat. The following experiments examine the contributions of the peripheral and central renin-angiotensin systems to the expression of sodium appetite in the adrenal-intact rat. Firstly, we find that, unlike intracerebroventricular angiotensin II, intravenous administration of the hormone at dipsogenic doses does not arouse sodium intake in the sodium replete rat when given alone or in combination with systemic mineralocorticoid pretreatment. Secondly, in the sodium depleted rat, we find that interference with central, but not peripheral, angiotensin II action suppresses sodium appetite. Together, these data confirm recent evidence which demonstrates that it is angiotensin II of cerebral origin, not angiotensin II of renal origin, that is necessary for the expression of sodium appetite.

Angiotensin II↗
PubMed1990

Combination of radiation therapy and intracranial bleomycin in the 9L rat brain tumor model.

The rat 9L brain tumor model was used to investigate the therapeutic potential of a combined modality approach using intracranial Bleomycin and radiation therapy. Bolus Bleomycin was delivered intracranially into the tumor volume via cannula guides; for continuous infusions, osmotic mini-pumps were implanted subcutaneously between the scapulae with flexible tubing to deliver the drug directly into the tumor and brain. Two to six bolus injections of Bleomycin (1 unit/kg each) over 5-11 days produced modest (usually statistically significant, p less than 0.05) increases in the median survival time compared to controls. Continuous infusion of Bleomycin by osmotic pump (10 units/kg over 7 days or 15 units/kg over 14 days) was also effective at significantly increasing median survival times compared to that of controls. Radiation therapy schedules of 10 daily fractions in 12 days (2 weeks) or 10 twice-daily fractions in 5 days produced dose-dependent increases in median survival time. Multiple bolus injections of Bleomycin when combined with fractionated radiation therapy significantly increased the median survival time due to fractionated radiation therapy alone for low doses (40 or 50 Gy). However, at higher radiation doses, the addition of Bleomycin either had no effect on median survival time or actually shortened it. Continuous infusion of Bleomycin by osmotic pump was effective when added to low dose radiation therapy in several experiments, twice for a total radiation dose of 50 Gy and once for radiation therapy of 60 Gy. However, it was also observed (once for 60 Gy and twice for 70 Gy) that the addition of continuous infusion Bleomycin either had no effect or served to decrease the improvement of median survival time obtained by radiation therapy alone. Thus, we conclude that increases in normal tissue toxicity can prevent full attainment of improved therapeutic advantage from the addition of Bleomycin to fractionated radiation therapy in the rat 9L model. These results should be considered when attempts are made to combine radiation therapy and intracranial Bleomycin for the treatment of patients with primary malignant brain tumors.

Animals↗
PubMed1985

Noradrenergic innervation of the paraventricular nucleus: specific role in control of carbohydrate ingestion.

Acute injections of norepinephrine (NE) into the hypothalamic paraventricular nucleus (PVN) have been shown to elicit eating in satiated rats. The present report examines the effects of acute and chronic PVN infusion of NE on intake of various liquid and mixed solid diets and on selection of the pure macronutrients, carbohydrate, protein, and fat. The results demonstrate that noradrenergic stimulation of the PVN (40 nmoles of NE) reliably enhances ingestion of pure sucrose diets (liquid and solid) and also of sweet and non-sweet milk solutions. Saccharin intake, in contrast, is unaffected. In preference tests, rats injected with NE show a greater increase in consumption of sucrose cubes compared with lab chow pellets, but exhibit an equivalent preference for sweet and non-sweet carbohydrate-rich diets. Tests with the three pure macronutrients simultaneously available reveal, after NE injection, a strong and selective increase in consumption of carbohydrate, with little or no change in intake of fat and, in some cases, a suppression of protein intake. This clear preference for carbohydrate can be seen with chronic NE infusion (5 nmoles every 30 min over a 14-day period), as well as after acute NE injection (40 nmoles), and also with long-term (24-hr) as well as short-term (1-hr) food intake measurements. This and other evidence suggests that the PVN noradrenergic system may play a specific and unique role in the control of carbohydrate ingestion.

Animals↗
PubMed1992

Chronic intracerebral infusions of vasopressin and vasopressin antagonist modulate behavioral effects of interleukin-1 in rat.

To assess the role of sex dependent brain vasopressinergic transmission in the modulation of the neural effects of interleukin-1, castrated male rats that are deficient in vasopressin were implanted intracerebroventricularly with an Accurel collodion mini device containing 10 micrograms AVP whereas intact male rats were implanted with a similar device containing 50 micrograms of dPTyr(Me)AVP, a specific antagonist of the vasopressor-like receptors of vasopressin. Control rats in each sex group were implanted with an Accurel device containing distilled water. Acute intracerebroventricular injection of 1.25-2.50 ng recombinant human interleukin-1 beta decreased in a dose and time-dependent manner social investigation of a juvenile conspecific. This effect was more intense in intact rats chronically infused with dPTyr(Me)AVP and less intense in castrates infused with AVP. These results confirm the modulatory role of sex-dependent vasopressinergic neurotransmission on the neural effects of interleukin-1.

Analysis of Variance↗
PubMed1994

Central interleukin-1 beta enhances splenic sympathetic nerve activity in rats.

The central administration of immune cytokines such as interleukin-1 (IL-1) and interferon-alpha (IFN-alpha) results in the suppression of peripheral cellular immunity, which depends, at least partly, on the sympathetic nervous activity. An intrathird cerebroventricular (I3V) infusion of recombinant human IL-1 beta (rhIL-1 beta) (1-5 ng/rat) elicited a dose-dependent increase in the electrical activity of the splenic sympathetic nerve in urethane and alpha-chloralose anesthetized rats. The effect of rhIL-1 beta (1 ng/rat) was completely blocked by pretreatment with an IL-1 receptor antagonist (1 microgram/rat, I3V 10 min before rhIL-1 beta), sodium salicylate (1 microgram/rat), or alpha-melanocyte stimulating hormone (alpha-MSH) (400 ng/rat). Furthermore, an antagonist of corticotropin-releasing factor (CRF), alpha-helical CRF9-41 (2 micrograms/rat), completely abolished the rhIL-1 beta-induced increase in the splenic nerve activity, although an I3V infusion of CRF (1 microgram/rat) excited it. These results suggest that IL-1 beta in the brain activates splenic sympathetic activity by its receptor-mediated and prostaglandin-dependent action that is sensitive to alpha-MSH, depending on CRF system. Our findings, together with the previous results, suggest that the splenic sympathetic nerve represents one of the communication channels from the brain to the immune system.

Analysis of Variance↗