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Results for “Infusions, Intraventricular”

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At least 19 recordsLinked to original sources
PubMed1991

Toxicology and kinetics of long-term intraventricular infusion of phenytoin and valproic acid in pigs: experimental study.

The effect of continuous intraventricular infusion of phenytoin and valproic acid into the brain of pigs was studied through quantitative measurement of animal behavior, pathological study of animal's brain and measurement of the levels of these drugs in the blood and C.S.F. Two groups of five animals each were treated with increasingly doses of the drugs until the apparition of toxic effects and the dead of animals. Normal behavior was observed with doses up to 3 mg/day of phenytoin and 1.5 mg/day of valproic acid. Toxic effects consisted on severe unsteadiness and muscular rigidity. Pathological study of the brains revealed that there were no damage attributable to the intraventricular infusion of the drugs. The present study suggests that intrathecal or intraventricular infusion of phenytoin and valproic acid could be well tolerated by humans and it leads us to consider subsequent clinical studies in epileptic patients.

Animals↗
PubMed1976

Pre- and post-junctional supersensitivity: differentiation by intraventricular infusions of norepinephrine and methoxamine.

Intraventricular infusions of methoxamine, an adrenergic agonist that has a relatively low affinity for the presynaptic uptake mechanism, produces a significant dose-dependent increase in locomotor activity comparable to the increase elicited by infusion of equimolar doses of norepinephrine (NE). The behavioral responsiveness to infusion of both NE and methoxamine was more than doubled 3 weeks after pretreatment with 6-hydroxydopamine (6-OHDA). These results indicate that the increased responsiveness to NE induced by 6-OHDA is due to enhanced postsynaptic receptor sensitivity rather than to a loss of presynaptic uptake inactivation.

Animals↗
PubMed1977

Differential motor effects of intraventricular infusion of morphine and etonitazene.

The motor effects produced by intraventricular infusions of morphine were compared to the effects of etonitazene. Despite the similarity in the peripheral actions of these drugs, motor effects of central infusions differed dramatically. Intraventricular morphine infusions resulted in explosive motor behavior whereas etonitazene produced extreme muscular rigidity. The periaqueductal grey (PAG) has been proposed as the substrate of morphine-induced explosive motor behavior. However, considerations of the dose of morphine and the mobility of this drug in tissue suggests that sites other than the PAG may also be involved in explosive motor behavior.

Analgesics, Opioid↗
PubMed1992

Intraventricular infusion of leupeptin decreases Bmax of the D2 receptor in the striatum of young rats.

Intraventricular infusion of a thiol protease inhibitor, leupeptin, was previously shown to induce several morphological and immunochemical manifestations of normal and pathological aging in rat brain. The present study attempted to elucidate whether this treatment also perturbs another brain function which declines in aging, dopamine D2 receptor binding in striatum. Intraventricular infusion of leupeptin (0.6 mg per day) for two weeks caused a significant (about 20%) reduction in the binding maximum (Bmax) of dopamine D2 receptors (as examined by [3H] spiperone binding) in the striatum of young male Fischer-344 rats in comparison to (saline-infused) control rats. The apparent Kd values did not differ significantly between the control and leupeptin-treated rat groups. The results suggest that decreased protein turnover may be a factor in the decline in Bmax of D2 receptors during aging.

Animals↗
PubMed1991

Treatment of severe intraventricular hemorrhage by intraventricular infusion of urokinase.

Six patients with severe intraventricular hemorrhage were treated with direct intraventricular infusion of urokinase. In each case, hemorrhage extended into all ventricular chambers, and a cast formation and expansion of the third and fourth ventricles were found. Immediately after the therapy was started (within 7 days from onset of symptoms), reduction of intraventricular hematoma volume was observed on computerized tomography. On average, both the third and fourth ventricles became clear on the third day after hemorrhage; there was one exception, a case of ruptured aneurysm. Five of the six patients showed excellent or good outcome, although two developed delayed hydrocephalus. No infection or rebleeding was observed. The outcome in a retrospectively studied group of five patients not treated with urokinase is also reported. The authors conclude that this relatively easy method of treatment will greatly improve the prognosis of severe intraventricular hemorrhage.

Adolescent↗
PubMed1977

Intraventricular infusion of angiotensin II on the hemodynamics and renal function of alpha-chloralose anesthetized cats.

Intraventricular infusion of angiotensin II (50, 100, and 200 ng/kg per min) produced significant elevations of arterial blood pressure (20-25%) in alpha-chloralose-anesthetized cats. The pressor responses were not accompanied by significant changes in heart rate,cardiac output, or contractility and were chiefly due to significant increases in total peripheral resistance. In contrast, pressor responses to intravenous infusion of angiotensin II (100 ng/kg per min) were accompanied by reflex decrease in cardiac activity. While intravenous angiotensin II caused increases in the resistance of skeletal, mesenteric, and renal vasculature, the intraventricular administration of angiotensin II increased resistance only in the mesenteric and renal vasculature. Further, centrally administered angiotensin II significantly enhanced urinary output and the rate of Na+ excretion both in the intact as well as in the denervated kidneys. However, the diuretic and natriuretic effects were significantly greater in the intact than in the denervated kidneys, indicating a centrally mediated neurogenic mechanism. The significant increase in the urinary concentration of Na+ (mEq/liter) following intraventricular angiotensin appeared to be secondary to the elevation of arterial blood pressure, since this effect was unaltered by acute renal denervation. The results of this investigation are consistent with the hypothesis that an elevation in the concentration of angiotensin II within the cerebrospinal fluid may trigger neurogenic mechanisms resulting in the constriction of glomerular efferent arterioles. Such an effect would be expected to increase glomerular filtration pressure and filtration fraction, and may play a role in the diuretic and natriuretic effects noted.

Anesthesia, General↗
PubMed1990

Intraventricular infusion of HBGF-2 promotes cerebral angiogenesis in Wistar rat.

The angiogenic effects of chronic intraventricular infusion of basic fibroblastic growth factor (HBGF-2) were assessed in the Wistar rat cerebral cortex. HBGF-2 increased both capillary density and area of perfused vasculature without altering capillary diameters in periventricular cortex adjacent to the site of infusion. Although it has been demonstrated that growth factors can cause brain endothelial proliferation in vitro, this is the first report of in vivo cerebral angiogenesis.

Animals↗
PubMed1990

Long-term intraventricular infusion of morphine for intractable pain in cancer of the head and neck.

The authors' experience with seven patients with intractable pain that was treated by continuous intraventricular infusion of morphine through an implanted Infusaid pump is reported. The pain was caused by head and neck cancer in six patients and was associated with postpolio syndrome in one. The average follow-up was 7 months. Pain was effectively managed through intraventricular administration of a combination of morphine and mild oral narcotic analgesics. Complications included one case of transient respiratory depression, one pump pocket infection, and one pump failure. The morphine dose required to maintain analgesia increased over time in all patients treated. This is a safe and effective method of pain management in patients with head and neck cancer. It is useful as well in patients who have intractable pain that cannot be managed through an intrathecal route because of a contraindication to lumbar puncture or an inaccessible subarachnoid space.

Head and Neck Neoplasms↗
PubMed1990

Intraventricular infusions of antibodies to amyloid-beta-protein precursor impair the acquisition of a passive avoidance response in the rat.

Intraventricular infusions of an antiserum raised against a 14 amino acid residue in the extracellular domain of amyloid-beta-protein precursor significantly decreased stepdown latency, at both 24 h and 48 h recall times, in rats trained to avoid an electroshock by remaining on a platform. The antiserum was effective when infused up to 2.5 h following training and no retention deficit was noted when it was administered at 4h or 6h after training. An antiserum generated against a 17 amino acid residue of the A4 amyloid peptide had no effect on learning. Thus the amyloid precursor protein, which is aberrantly processed in Alzheimer's disease, appears to be directly involved in memory formation.

Adult↗
PubMed1992

Intraventricular infusion of N-methyl-D-aspartate. 1. Acute blood-brain barrier consequences.

The purpose of this study was to document the early cerebrovascular consequences of excessive N-methyl-D-aspartate (NMDA) receptor activation. Five microliters of NMDA (100 nmol/microliters) or vehicle was infused over a 15-min period into the lateral ventricle of adult rats. The protein tracer horseradish peroxidase (HRP) was injected intravenously for blood-brain barrier (BBB) studies. The intraventricular infusion of vehicle (n = 5) caused no alterations in arterial blood pressure or microvascular damage away from the intraventricular probe tract. In contrast, NMDA infusion (n = 8) led to a gradual increase in arterial blood pressure (mean 36 mm Hg). Multifocal regions of HRP extravasation were observed bilaterally throughout the neuraxis following NMDA infusion. Sites of BBB disruption and hemorrhage included brain regions bordering ventricular spaces. In addition, isolated foci of protein extravasation were commonly detected in the cerebral cortex, thalamus, basal forebrain, septum and cerebellum. Pretreatment with the noncompetitive NMDA antagonist MK-801 (2 mg/kg) substantially reduced the BBB responses to NMDA. However, microvascular abnormalities were seen in NMDA-infused rats where blood pressure elevations were inhibited by blood removal. In addition to neurons, cerebral blood vessels are also acutely affected by NMDA receptor activation. Blockage of NMDA receptor channels following brain injury may potentially provide protection by attenuating BBB breakdown and subsequent brain edema.

Animals↗
PubMed1992

Intraventricular infusions of anti-neural cell adhesion molecules in a discrete posttraining period impair consolidation of a passive avoidance response in the rat.

Intraventricular infusions of anti-neural cell adhesion molecule (anti-NCAM) are demonstrated to inhibit consolidation of a passive avoidance response when administered in the 6-8 h posttraining period. Anti-NCAM was ineffective when administered during training or at any other time up to 10 h thereafter, and no amnesic effects were observed with absorbed anti-NCAM or anti-neurofilament protein. Amnesia was observed only at the 48-h recall time, and this could not be attributed to poor antibody penetration or a prolonged residence time, as studies with 125I-labelled anti-NCAM in trained animals demonstrated a rapid accumulation into all brain regions, and this was marked in the olfactory bulb and hippocampus, areas showing an inherent and paradigm-specific increase in NCAM sialylation state, respectively. The lack of an amnesic action at the 24-h recall time is attributed to anti-NCAM-impaired synapse structuring becoming apparent following the paradigm-specific increases in NCAM sialylation state.

Amnesia↗
PubMed1975

Fine structure of labelled axons in the cerebellar cortex and nuclei of rodents and primates after intraventricular infusions with tritiated serotonin.

The cerebellar cortex and deep cerebellar nuclei in rats and rhesus monkey were studied after treatment with monoamine oxidase inhibitor and continuous intraventricular infusion with 10(-5) M serotonin-3H. Autoradiographs were prepared for light and electron microscopy. The cerebellum contained no labelled cells. Labelled unmyelinated axons arrive from the brain stem via the periventricular zones of the aqueduct and fourth ventricle. In the parafloccular cortex about 1 per cent of the mossy fibers are labelled, together with a small number of fine varicose axons in the molecular layer that run parallel to the folial axes (less than 0.1%). In the paravermal and vermal cortex there are few labelled fibers in the granular layer and a five-fold greater number of labelled axons in the molecular layer (about 0.5%). Apparently three systems of serotonin-containing axons are present in the cortex: mossy fibers, parallel fiber-like, and a diffuse system in granular and molecular layers. The fastigial (medial), interpositus, and dentate (lateral) nuclei, lateral vestibular and other vestibular nuclei all have numerous labelled axons. The dentate and interpositus nuclei receive labelled fibers which arrive through the superior cerebellar peduncle as well as from the periventricular area. Six morphologically different classes of labelled axon terminals have been differentiated. Class 1a, the mossy fiber rosettes, and class 1b, the CAT2 axons, have small, round, clear synaptic vesicles and large granular vesicles (lgv); class 2 axons have a distinctive collection of round granular vesicles; class 3 boutons have numerous tubular profiles, a few containing dense dots, packed in a dark axoplasmic matrix; class 4 axons have tiny 250 A granular vesicles, clear tubular profiles and occasional LGV; class 5 terminals have numerous LGV, both round and elongated, with clear round and tubular profiles; class 6 terminals have LGV, clear and granular synaptic vesicles and clear tubular profiles. All these axons have LGV 900 A in diameter with 500-600 A variably dense centers that do not fill the vesicle, and Gray's type 1 axodendritic or axasomatic synapses on postsynaptic locations in the cortex and nuclei. Labelled axons in the cortex end as mossy fibers upon granule cell dendrites in glomeruli (Class 1a) or upon dendrites of cortical interneurons, e.g. Golgi cells, basket and stellate cells, and not on Purkinje cells. ...

Animals↗
PubMed1975

Ovulation induced by the intraventricular infusion of norepinephrine in rats made anovulatory by neonatal administration of various doses of testosterone.

Gradually increasing doses of neonatal TP decrease the rate of ovulation induced by intraventricular infusion of 100 mug of NE. This finding suggests that the reduced functional capacity of the LH-RH-producing neurons in androgen-sterilized rats may account for the difference between the ovulatory action of NE in anterior hypothalamus-lesioned and androgen-sterilized rat.

Animals↗
PubMed1991

Treatment of leptomeningeal carcinomatosis with continuous intraventricular infusion of recombinant interleukin-2.

A 42-year-old man developed leptomeningeal carcinomatosis 6 years after treatment of a malignant melanoma. He was treated with two courses of recombinant interleukin-2, administered as a continuous intraventricular infusion (6 X 10E5 U/24 h) during 5 days. During the first day of the first course he also received 5 X 10E9 lymphokine-activated killer cells intraventricularly. This gave rise to a severe elevation of intracranial pressure, with headaches and meningismus. During the second course no LAK cells were administered. This course was tolerated much better. The neurological status did not change during the treatment. Recombinant interleukin-2 levels were maintained at about 300 U/mL during both courses.

Adult↗
PubMed1979

Enhanced responsiveness to intraventricular infusion of amphetamine following its repeated systemic administration.

Previous studies have demonstrated that long-term administration of d-amphetamine produces a progressive augmentation of behavior. In the present experiment, rats receiving repeated systemic injections responded to an intraventricular infusion of d-amphetamine with an augmented increase in locomotor activity. These results indicate that central mechanisms, rather than peripheral dispositional factors, subserve the enhanced behavioral response to repeated amphetamine administration.

Animals↗
PubMed1992

Effects of intraventricular infusion of the N-methyl-D-aspartate (NMDA) receptor antagonist AP5 on spatial memory of rats in a radial arm maze.

Rats were trained to asymptotic performance in an 8-arm radial maze. They then received chronic intraventricular infusion of either artificial CSF or the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5- phosphonopentanoic acid (AP5), at a concentration (30 mM) that has been shown previously to prevent the induction of long-term potentiation in the dentate gyrus of the hippocampus in vivo. Subsequently the rats received another 9 trials in the maze in a quasi-random order, 3 uninterrupted trials, and another 6 trials each with mid-trial delays of 5, 20 or 60 min during which the animals were placed in their home cage. The mean number of errors for the AP5 rats did not differ significantly from that of the controls in the uninterrupted trials throughout the experiment, nor did it differ from that of the controls in any of the 3 delayed trials when these were first introduced. However, the control animals performed better at the longer delays when these were introduced for the second time, whilst there was no such improvement (but rather a deterioration) for the AP5 animals. The impairment of performance in the AP5 rats during the second block of delayed trials was significant, and independent of the length of the delay. These results show that NMDA receptor blockade does not impair working memory in the radial maze per se, but that it does prevent an improvement of working memory persistence with further training.

2-Amino-5-phosphonovalerate↗
PubMed1975

Strain differences during intraventricular infusion of norepinephrine: possible role of receptor sensitivity.

Two rat strains previously shown to differ with respect to behavioral activity, regional brain tyrosine hydroxylase activity, and norepinephrine-elicited accumulation of adenosine 3', 5'-monophosphate exhibited differential behavioral responsiveness during the intraventricular infusion of norepinephrine. The results are interpreted in terms of differential catecholamine receptor sensitivity.

Amphetamine↗