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Results for “Infusions, Intraventricular”

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PubMed1977

Characterization of a delta-electroencephalogram (-sleep)-inducing peptide.

A peptide that induces slow-wave (delta) and spindles electroencephalogram enhancement after intraventricular (brain) infusion has been isolated from rabbits and given the name delta-sleep-inducing peptide (DSIP). Amino acid seqeunce: Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu. This compound, five possible metabolic products (containing residues 1--8, 2--9, 2--8, 1--4, and 5--9), two nonapeptide analogues with two amino acids exchanged, and a related tripeptide (Trp-Ser-Glu) were synthesized. All nine synthetic peptides were infused intraventricularly in rabbits under double-blind conditions. A total of 58 rabbits including controls were evaluated. The electroencephalogram leads from the neocortex and the archicortex were directly fast-Fourier transformed and analyzed by a Univac 1108 computer system. Only the delta-sleep-inducing peptide (snythetic) showed significant and specific enhancement/induction of delta and spindle electroencephalogram patterns.

Animals↗

PubMed1996

The luteinizing hormone but not the cortisol response to arginine vasopressin is prevented by naloxone and a corticotropin-releasing hormone antagonist in the ovariectomized rhesus monkey.

In the primate, arginine vasopressin (AVP) is known to activate the hypothalamo-pituitary-adrenal axis and to inhibit LH secretion. In the present study, we investigate the role of the endogenous opioid peptides and corticotropin-releasing hormone (CRH) in these processes. Adult ovariectomized rhesus monkeys bearing a chronic cannula in the lateral ventricle for intraventricular (i.c.v.) infusion were used. In experiment 1, the effects of 5-hour i.c.v. infusions of saline (n = 7), AVP (50 micrograms/h, n = 7), naloxone (2 mg bolus + 2 mg/h i.v., n = 4) and AVP plus naloxone (n = 4) on LH and cortisol secretion were investigated. As compared to saline and naloxone alone, LH pulse frequency was significantly decreased by AVP (p < 0.05) and by 5 h, the mean LH expressed as a percentage from the 3-hour baseline was also significantly reduced (saline 100.9 +/- 5.1%; naloxone 112.3 +/- 2.9%; AVP 63.3 +/- 8.2%). Coadministration of naloxone abolished the effects of AVP on LH (107.3 +/- 12.1% of baseline). AVP increased cortisol secretion (p < 0.05 vs. baseline), but naloxone did not prevent the increase. In experiment 2, the LH and cortisol responses to AVP were compared in the absence and presence of a CRH antagonist. The antagonist was infused intraventricularly at two doses: 60 and 180 micrograms/h. At both doses, the inhibitory effect of AVP on LH was significantly attenuated (at 4 h, 86.9 +/- 3.2% of baseline; NS vs. saline). However, the CRH antagonist did not block the AVP-induced increase in cortisol. The results confirm previous evidence in the primate of a role of vasopressin in inhibiting the hypothalamo-pituitary-gonadal axis and demonstrate a role of hypothalamic opioid peptides in this process. They also demonstrate that, although CRH is a prerequisite for AVP's action on the hypothalamo-pituitary-gonadal axis, AVP can stimulate the adrenal axis in the primate in the presence of decreased CRH activity.

Adrenal Glands↗

PubMed2005

Enhanced hippocampal neurogenesis by intraventricular S100B infusion is associated with improved cognitive recovery after traumatic brain injury.

Evidence of injury-induced neurogenesis in the adult hippocampus suggests that an endogenous repair mechanism exists for cognitive dysfunction following traumatic brain injury (TBI). One factor that may be associated with this restoration is S100B, a neurotrophic/mitogenic protein produced by astrocytes, which has been shown to improve memory function. Therefore, we examined whether an intraventricular S100B infusion enhances neurogenesis within the hippocampus following experimental TBI and whether the biological response can be associated with a measurable cognitive improvement. Following lateral fluid percussion or sham injury in male rats (n = 60), we infused S100B (50 ng/h) or vehicle into the lateral ventricle for 7 days using an osmotic micro-pump. Cell proliferation was assessed by injecting the mitotic marker bromodeoxyuridine (BrdU) on day 2 postinjury. Quantification of BrdU-immunoreactive cells in the dentate gyrus revealed an S100B-enhanced proliferation as assessed on day 5 post-injury (p < 0.05), persisting up to 5 weeks (p < 0.05). Using cell-specific markers, we determined the relative numbers of these progenitor cells that became neurons or glia and found that S100B profoundly increased hippocampal neurogenesis 5 weeks after TBI (p < 0.05). Furthermore, spatial learning ability, as assessed by the Morris water maze on day 30-34 post-injury, revealed an improved cognitive performance after S100B infusion (p < 0.05). Collectively, our findings indicate that an intraventricular S100B infusion induces neurogenesis within the hippocampus, which can be associated with an enhanced cognitive function following experimental TBI. These observations provide compelling evidence for the therapeutic potential of S100B in improving functional recovery following TBI.

Animals↗

PubMed1990

A rhesus monkey model for continuous infusion of drugs into cerebrospinal fluid.

A new rhesus monkey model with two intraventricular catheter systems was developed to examine the pharmacokinetics and neurotoxicity of chemotherapeutic agents administered by continuous intraventricular infusion. A lateral ventricular catheter system implanted in the lateral ventricle and attached to a subcutaneous access port on the animal's back is used for infusion of drugs into the ventricle. A Pudenz catheter implanted in the fourth ventricle and connected to a subcutaneous Ommaya reservoir permits repetitive CSF sampling in unanesthetized animals. The model was evaluated in five animals for over 12 months for catheter patency, surgical complications, and utility in studying the pharmacokinetics of continuous intraventricular infusion of methotrexate. There were no perioperative complications. Three of the five monkeys maintained both systems successfully. The other two animals developed staphylococcal ventriculitis, one at 7 days as a result of manipulation of the incision by the animal leading to cellulitis around the catheter site and subsequent ventriculitis, the other at 5 months. Both animals were treated successfully with antibiotics and catheter removal. An infusion of 0.05 mg of methotrexate over 24 hours maintained ventricular drug concentrations of 1 mol/L without evidence of neurotoxicity. This new model has applications both for the development of continuous intraventricular infusion as a therapeutic approach for the treatment of meningeal cancers in humans and as a research tool to study the distribution and elimination of drugs from the CSF.

Animals↗

PubMed1985

CSF outflow resistance and pressure-volume index determined by steady-state and bolus infusions.

Intraventricular or lumbar CSF pressure was measured in 58 adult hydrocephalic patients. CSF outflow resistance (Rcsf) and pressure-volume index (PVI) were determined by steady-state and bolus infusion techniques, using mathematical models with and without a constant term. Comparison of the various Rcsf and PVI values indicates that the most reliable Rcsf is obtained by steady-state infusion. The best approximation of the PVI is obtained by bolus infusions, provided the pressure decay curve is excluded. Mathematically a model with a constant term is to be preferred.

Biomechanical Phenomena↗

PubMedDate not supplied

Intracerebroventricular infusions of corticotrophin releasing factor (CRF) and ACTH raise blood pressure in sheep.

Infusion of synthetic ovine CRF (10 or 100 micrograms/h) into the lateral lateral cerebral ventricle for 24 h increased mean arterial blood pressure of conscious sheep. CRF infusion also increased urine output and sodium excretion. Intravenous infusion of CRF (100 micrograms/h) or intraventricular infusion of artificial CSF had no effect on blood pressure. Intraventricular infusion of ACTH (1-24) at 0.5 micrograms/kg per day, a rate of infusion which has no systemic effect on blood pressure, also raised mean arterial pressure. These studies suggest that two peptides involved in the physiological response to 'stress' may influence blood pressure by mechanisms which do not involve stimulation of adrenocortical steroid production.

Adrenocorticotropic Hormone↗

PubMed1987

Pertussis toxin or 8-bromo-cAMP block inhibition of the acoustic startle response by the alpha 2-adrenergic agonist ST-91.

Stimulation of supraspinal alpha 2-adrenergic receptors by intraventricular infusion of the alpha 2-adrenergic agonist ST-91 depresses a simple vertebrate behavior, the acoustic startle response. Intraventricular pretreatment with pertussis toxin, an agent known to inactivate the inhibitory guanine nucleotide binding protein (Gi) which can inhibit adenylate cyclase, completely prevented the depressant behavioral effect of ST-91. In contrast, pertussis toxin did not alter the depressant effect of intraventricular infusion of the 5-HT 1B agonist 1-m-chlorophenylpiperazine (mCPP). Intraventricular infusion of the cyclic adenosine monophosphate (cAMP) analog 8-bromo-cAMP also reversed the depressant effect of ST-91 without altering the effect of mCPP. These data suggest that inhibition of adenylate cyclase may be involved in the effect of activation of central alpha 2-adrenergic receptors.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2006

Intraventricular baclofen infusion for dystonia. Report of two cases.

Two children with generalized dystonia were given continuous intraventricular baclofen (IVB) infusions. The first was a 12-year-old girl with mixed dystonia and spasticity caused by methylmalonic aciduria whose spinal anatomy precluded administration of intrathecal baclofen (ITB). The second was an 11-year-old boy whose dystonia was associated with cerebral palsy and had not improved significantly in response to conventional ITB treatment. The girl improved dramatically with IVB; the boy experienced no greater improvement from IVB than from ITB. No adverse effects were noted in either child during 2 to 6 months of infusion. These are the first reports of the use of IVB in this clinical setting. The results warrant additional investigation.

Baclofen↗

PubMed1993

Acidic fibroblast growth factor infusion reduces ischemic CA1 hippocampal damage in the gerbil.

Occlusion of the carotid arteries for 5 minutes in the Mongolian gerbil results in selective necrosis of CA1 pyramidal neurons. In the present experiments we studied whether intraventricular infusion of acidic fibroblast growth factor (aFGF) could attenuate this damage. Intraventricular infusions of bovine serum albumin (BSA-10 ng/h) or aFGF (1, 10 or 100 ng/h) were started 2 days prior to 5 minutes of bilateral carotid occlusion and continued for 5 days post-ischemia. The brains were perfused and fixed at 5 days post-ischemia and histological assessment of CA1 damage was made. Animals receiving intraventricular infusions of 10 or 100 ng/h aFGF showed a significant reduction of CA1 neuronal damage in comparison to no treatment ischemic controls (no treatment-8 +/- 1; aFGF 10 ng/h-147 +/- 28; aFGF 100 ng/h-168 +/- 35 cells/mm CA1; P < 0.05 for both aFGF groups). The results indicate that aFGF infusion can attenuate the severity of ischemic neuronal necrosis in the gerbil hippocampus.

Animals↗

PubMed1986

Suppression of progesterone-induced gonadotropin surge by adrenergic agonists in estrogen-primed ovariectomized rats.

An involvement of catecholamines in the preovulatory gonadotropin surge has been proposed for many years. Specifically, an alpha-adrenergic mechanism has been implicated in the stimulation of ovulation and LH release. On the other hand, little is known regarding the possible role of adrenergic neurotransmission once a gonadotropin surge has been initiated. In this study, drugs which affect adrenergic receptors were administered centrally to estrogen-primed ovariectomized rats and the effects on serum concentrations of LH and FSH induced by treatment with progesterone at 08:00 h were examined. As expected, the progesterone treatment caused a significant (p less than 0.05) increase in blood LH and FSH levels by 14:00 and 15:00 h, respectively, when compared with those seen at 13:00 h. In control rats that received isotonic saline intraventricularly at 15:00-16:00 h, both LH and FSH levels continued to rise linearly and reached peak levels by 17:00 and 18:00 h. By contrast, intraventricular infusion of norepinephrine at 16:00 h caused a significant decrease (p less than 0.05) in LH levels when compared with the saline-infused control groups. Moreover, rats that received intraventricular infusion of phenylephrine (an alpha 1-adrenergic agonist) at 15:00 h failed to show a significant increase in LH and FSH levels until 19:00 h; this inhibitory effect was mimicked by a relatively more specific alpha 1-adrenergic agonist, methoxamine. Consistent with our previous findings, animals which received intraventricular isoproterenol (a specific beta-adrenergic agonist) at 15:00 h also responded with suppressed serum LH levels at 16:00-19:00 h when compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Rodent models of Alzheimer's disease: rat A beta infusion approaches to amyloid deposits.

The development of rodent models for Alzheimer's disease is a critical step for both understanding the disease and developing therapeutic drugs. Transgenic and knockout mouse models will elucidate some important aspects of the etiology of the disease and the development of pharmaceutical treatments. Here, we will focus on the advantages of nontransgenic models. In nontransgenic rat models, intraventricular infusion of A beta 1-40 (alone) generally results in diffuse deposition of A beta with very few focal plaque-like amyloid deposits after a 30-day intraventricular infusion. However, we have recently found that large numbers of scattered A beta immunoreactive plaque-like deposits can be produced in retired female Sprague-Dawley rat breeders using intraventricular infusion of A beta combined with neuropil injection of transforming growth factor beta 1(TGF beta). A beta that was not associated with the large deposits was often immunolocalized with neurons and cell processes. Immunogold electron microscopy demonstrated the presence of A beta in endosome/lysosomes of neuronal processes and glia and basal lamina. In some cases this labeling was clearly in lysosomes of degenerating neurites. This model allows one to introduce A beta and other plaque-associated factors without overexpression of potentially confounding APP domains. We conclude that A beta infusion models will be a useful complement to transgenic approaches to Alzheimer's pathology.

Alzheimer Disease↗

PubMed1989

Third ventricular chloride infusions enhance drinking in water deprived rats.

The influence of intraventricularly infused anions on drinking was studied in 54 water deprived male rats, divided in 9 equal groups. Stainless steel cannulae were chronically implanted into the anteroventral part of the third ventricle (AV3V) and the animals were water deprived for 24 hr prior to the infusions. Control group (n = 6) was given 10 microliters of artificial cerebrospinal fluid. The rats of the remaining 8 groups received similar quantity of equiosmolar chloride or bicarbonate solution of either sodium, potassium, calcium or barium. Cumulative quantity of water consumed in 30 min, 1 hr, and 24 hr after the infusion was recorded. All the chloride solutions, irrespective of the associated cation, enhanced drinking. Effects of the bicarbonates were relatively weak and transient. Dipsogenic effects of the solutions depended on their anionic composition. Thus, chlorides of all the cations elicited greater drinking than their bicarbonates. Responses of the similar anionic solutions were comparable. It appears that intraventricularly infused chloride ions stimulate drinking in water deprived rats.

Animals↗

PubMed1991

Loss of AChE- and NGFr-labeling precedes neuronal death of axotomized septal-diagonal band neurons: reversal by intraventricular NGF infusion.

The time course of cellular changes in the medial septum (MS) and vertical limb of the diagonal band area (VDB) after a complete unilateral fimbria-fornix (FF) transection has been studied using prelabeling of the septohippocampal neurons by bilateral hippocampal injections of the fluorescent retrograde tracer Fluoro-Gold (FG), in combination with acetylcholine esterase (AChE) histochemistry and nerve growth factor receptor (NGFr) immunocytochemistry. The results show that the long-term disappearance of AChE-positive and NGFr-positive cells represents a combination of down-regulation of the marker proteins, cell shrinkage, and an actual cell loss. By 4 weeks after lesion the loss of FG-prelabeled cells amounted to 50% in MS and 30% in VDB. A further 25-30% of the MS neurons survived (as indicated by the presence of FG label), but were undetectable by the AChE and NGFr markers. Down-regulation of the marker proteins and cell shrinkage preceded the cell loss by more than a week: while shrinkage and reduced numbers of AChE/NGFr positive cells was evident already by 4-7 days, an actual cell loss (i.e., loss of FG-prelabeled cells) became evident only at 4 weeks after lesion. Continuous intraventricular NGF infusion (0.15 micrograms/day) was capable of counteracting all three types of changes. Infusion over 2 weeks reversed both atrophy and loss of AChE/NGFr staining, whereas infusion over 4 weeks completely prevented the later occurring cell loss. In addition, the NGF infusions induced significant hypertrophy in the undamaged cholinergic neurons in both nucleus basalis and striatum. It is concluded that down-regulation of marker proteins, such as AChE and NGFr, and cellular atrophy precede cell death in the axotomized septohippocampal system and that about 1/3 of the axotomized septal cholinergic neurons may survive for a long time in a down-regulated atrophic state. Exogenous NGF can prevent both the atrophic and the degenerative processes.

Acetylcholinesterase↗

PubMed1997

Continuous intraventricular drug infusion for the in vivo study of transneuronal degeneration in the striatonigral system of the rat.

Injuries to certain parts of the brain may induce neuronal death in distant areas innervated by the sites of the primary lesion. Such characteristic pathological changes, known as anterograde transneuronal degeneration, may occur at the next and more distant synaptic levels and play a part in the slow progression of some types of system degeneration. Delayed transneuronal degeneration of the substantia nigra pars reticulata (SNr) is one example of this form of cell death, and it occurs as a consequence of a neostriatal lesion caused by focal ischemia, Huntington's disease, or experimental axon-sparing injections of neurotoxin. Ever since the demonstration by Saji and Reis that the administration of GABA receptor agonist effectively prevented delayed transneuronal degeneration of the SNr, the degeneration of nigral reticulata cells has been attributed to the loss of striatal inhibition (Fig. 1A). The latter process severely upset the balance of membrane potential of nigral reticulata cells, producing an effect resembling excitotoxicity. In this report, we describe a continuous intraventricular MK-801 infusion technique that is useful in clarifying the role of glutamatergic action via N-methyl-D-aspartate (NMDA) receptor subclasses involved in exo-focal postischemic death of the SNr.

Animals↗

PubMed2002

Continuous intraventricular clonidine infusion in controlled morphine withdrawal--case report.

A patient with atypical bilateral facial pain reported the loss of analgesic effect of intracerebroventricular morphine delivered continuously via an implanted pump, accompanied by intolerable adverse side effects associated with the administered high dose of morphine. Clonidine was substituted for morphine over a period of 3 weeks to achieve a drug holiday. The patient did not have significant withdrawal symptoms or major discomfort from pain, leading to a reduced quality of life during this period. Six months after the treatment, the patient continues to require a significantly lower daily dose of morphine. Morphine withdrawal with clonidine substitution produced a significant improvement in the analgesic efficacy of morphine and in the quality of life in the absence of undesirable side effects.

Analgesics↗

PubMed1984

Further studies on norepinephrine-induced suppression of pulsatile luteinizing hormone release in ovariectomized rats.

The present study examined three aspects of the inhibitory effects of continuous intraventricular infusion of norepinephrine (NE) on pulsatile luteinizing hormone (LH) release in ovariectomized, nonsteroid-primed rats: whether the inhibitory effects of NE infusion were exerted on LH pulse frequency and/or amplitude; whether central nervous system desensitization occurred in response to the inhibitory effects of continuous NE infusion on pulsatile LH secretion, and whether dopamine of serotonin were involved as possible interneuronal transmitter mediators of NE-induced suppression of pulsatile LH release. Unanesthetized rats with external jugular cannulae were bled continuously at a rate of 50 microliters whole blood/7 min for 2 h prior to infusion and for 2-3 h during continuous intraventricular infusion of artificial cerebrospinal fluid or NE. Infusion of cerebrospinal fluid had no effect on pulsatile LH release, while continuous infusion of 0.3 or 1.8 micrograms NE/h for 2-3 h produced suppression of pulsatile LH secretion. Although desensitization to the stimulatory effects of NE on LH release in ovariectomized, steroid-primed rats had been observed to occur rapidly within 90 min after the onset of infusion, desensitization to the inhibitory effect of NE on pulsatile LH release did not occur even after continuous infusion of NE for periods up to 20 h. Mean blood LH levels were as low in rats bled 17-20 h after the onset of NE infusion as in those bled at 0-3 h. The suppressive effect of NE on pulsatile LH release was not prevented by prior blockade of dopamine or serotonin receptors with pimozide or metergoline, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Role of catecholamines in release of gonadotrophic hormones in the rabbit.

Role of catecholamines (CA) in transmission of neurohormone releasing gonadotrophin (GnHR) from the hypothalamus to hypophysis was estimated on the basis of the hypothalamic catecholaminergic system blockade with 6-hydroxydopamine (6-OHDA) and intraventricular infusions of CA in the rabbit. 6-OHDA administered intraventricularly in doses 200-500 mug caused temporary blockade of ovulation. Intraventricular infusion of noradrenaline (NA) induced ovulation in 50% of animals tested, whereas dopamine (DA) and adrenaline (A), induced ovulation only in very few cases. It seems, that catecholaminergic system participates in transmission of neurohormones to the hypophysis, and NA plays the most important role in this process.

Animals↗

PubMed1981

Reversal of noradrenaline denervation-induced increase of beta-adrenoreceptor binding in rat neocortex by noradrenaline infusion.

The effect of intraventricular infusion of (-)-noradrenaline (NA) on beta-receptor binding in vitro to homogenates from 6-hydroxydopamine (6-OH-DA)-denervated and from normal rat cerebral cortex was studied. NA was infused with osmotic minipumps connected to cannulas placed in the right lateral ventricle, delivering 1 or 5 microgram (-)-NA/h continuously for 9 days. One day later the rats were sacrificed and cortical tissue taken for beta-receptor (using [3H]dihydroalprenolol ([3H]DHA) as radioligand) and NA assay. The NA level in the cerebral cortex of 6-OH-DA treated rats was decreased to 70-80% of that of controls. No substantial change in the NA level was observed after infusion of 1 microgram (-)-NA/h, whereas infusion of 5 microgram/h led to a 40-60% increase compared to that of control rats infused with vehicle alone. Infusion of vehicle alone into control rats did not cause any change in [3H]DHA binding, whereas in denervated rats there was a 30-50% increase in [3H]DHA binding compared to that of controls. This increase was completely counteracted by infusion of 1 or 5 microgram (-)-NA/h. Infusion of 1 microgram (-)-NA/h to control rats did not cause any change, while infusion of 5 microgram (-)NA/h led to a significant decrease (-24%) in [3]DHA binding. The present results further support the view that the availability of NA at the receptors controls the number of beta-adrenergic receptors, thereby probably regulating the NA sensitivity of cells with beta-receptors.

Animals↗