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Results for “Infusions, Intraventricular”

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PubMed1977

Effects of cerebral lateral, ventricular infusions of phloridzin on feeding and body weight in Gallus domesticus (L.).

Contrary to earlier findings in rats, cerebral lateral ventricular infusions of 1 X 10(-3) M or 2 X 10(-3) M solutions of phloridzin at a rate of 2.5 micronl/min for 90 min had no significant stimulating effects on food intake and weight gain in hens and cocks. These different responses to intraventricular phloridzin might reflect a difference of sensitivity to the inhibitory action of phloridzin on glucose transport in cerebral cells or certain peculiarities of mechanisms controlling food intake in chickens.

Animals↗

PubMed1975

Hemodynimic effects of systemic and central administration of clonidine in the monkey.

Systemic and regional hemodynamic changes were measured in restrained, conscious rhesus monkeys with indwelling arterial and venous catheters before and after clonidine (5 and 15 mug/kg) was slowly infused intravenously or smaller doses (2 mug/kg) were injected into a lateral cerebral ventricle. Dye-dilution cardiac outputs and the complete distribution of cardiac output were obtained intermittently with the use of the radioactive microsphere method. After the higher intravenous dose and the intraventricular injection, systemic arterial pressure was significantly lowered for 30-45 min. Both of these groups had similar changes in the redistribution of cardiac output and blood flow that outlasted the hypotensive period. Blood flow was maintained or increased in the hepatic and renal arteries at the expense of skin; flow to skeletal muscle and brain also decreased during the first hour. These data support previous studies that indicate that the primary action of clonidine is in the central nervous system and, in addition, add new information about the regional blood flow changes evoked by clonidine.

Animals↗

PubMed2005

Direct thrombolytic therapy for intraventricular thrombosis in patients with the Jarvik 2000 left ventricular assist device.

One of the complications that can occur with continuous, axial-flow left ventricular assist devices (LVADs) is thrombosis within the left ventricle, adjacent to the device's inflow conduit, which may cause inflow obstruction and recurrent heart failure. We describe 2 cases in which we used a catheter to continuously infuse recombinant tissue plasminogen activator (tPA) into the left ventricle until signs of successful thrombolysis was achieved. By monitoring the result and administering only as much tPA as necessary to achieve thrombolysis, we were able to successfully lyse the obstructing thrombus with a minimal dose of tPA without causing any significant bleeding problems. This technique may be useful for managing this potentially serious complication while minimizing the risk of treatment.

Cardiac Catheterization↗

PubMed2005

Blockade of angiotensin II AT1 receptors inhibits pressor action of centrally administered interleukin-1beta in Sprague Dawley rats.

The aim of the present study was to evaluate the influence of intraventricular administration of recombinant rat interleukin-1beta (IL-1beta) on regulation of resting blood pressure and heart rate and to test the hypothesis that the brain angiotensinergic system is involved in regulation of hemodynamic parameters by centrally applied IL-1beta. The experiments were performed on Sprague Dawley rats, assigned to three series of experiments. In series 1 (control, n = 6), mean arterial pressure (MAP) and heart rate (HR) were recorded for 15 min under baseline conditions. This was followed by infusion of saline (0.9% sterile NaCl 5 microL/h) into the left cerebral ventricle (LCV). Measurements were continued during the next 60 min. In series 2 (n = 6) and 3 (n = 6) the experimental design was similar, except that in series 2 the animals were LCV infused with saline containing IL-1beta (100 ng/h) and in series 3 with saline containing IL-1beta (100 ng/h) and angiotensin type 1 (AT1) receptors antagonist (Losartan, 10 microg/h). LCV infusion of saline alone did not influence MAP and HR while administration of IL-1beta elicited significant increase in MAP, but not in HR. The pressor effect was absent during combined infusion of IL-1beta and Losartan. Results of the study provide evidence that centrally administered IL-1beta exerts pressor effect, and reveal that this effect is mediated by stimulation of the brain angiotensin system and requires activation of AT1 receptors.

Angiotensin II Type 1 Receptor Blockers↗

PubMed2001

Distribution of intraventricularly administered antiamyloid-beta peptide (Abeta) antibody in the mouse brain.

There is considerable interest in utilizing the intracerebroventricular (icv) route of administration of antibodies in the brain for various studies and for the therapy of malignancies, but very little is known about the anatomic extent of distribution of the antibody in brain after injection into the third ventricle. To explore the potential for icv administration of antiamyloid-beta peptide (Abeta) in reducing Abeta toxicity in brain in Alzheimer's disease, we first mapped the time course and path of transit of horseradish peroxidase (HRP)-labeled antibody. The results show that, after a single injection into the mouse third venticle, the HRP-labeled antibody is localized within the microvasculature, first that of the corticohippocampal region close to the site of injection at 3 hr. By 24 hr, the antibody is distributed throughout the hippocampus and frontoparietal cortex close to the injection site, as well as in the deep and outer cerebral cortex and cerebellar cortex remote from the injection site. The injected antibody is almost entirely removed by 4 days. Therefore, the antibody had diffused throughout all the brain by 24 hr, showing the feasibility of small quantities of anti-Abeta antibody infused into the third ventricle to reach extracellular epitopes throughout the brain parenchyma rapidly.

Alzheimer Disease↗

PubMed2000

Effects of betamethasone administration to the fetal sheep in late gestation on fetal cerebral blood flow.

Glucocorticoid administration to women at risk of preterm delivery to accelerate fetal lung maturation has become standard practice. Antenatal glucocorticoids decrease the incidence of intraventricular haemorrhage as well as accelerating fetal lung maturation. Little is known regarding side effects on fetal cerebral function. Cortisol and synthetic glucocorticoids such as betamethasone increase fetal blood pressure and femoral vascular resistance in sheep. We determined the effects of antenatal glucocorticoid administration on cerebral blood flow (CBF) in fetal sheep. Vehicle (n = 8) or betamethasone (n = 8) was infused over 48 h via the jugular vein of chronically instrumented fetal sheep at 128 days gestation (term 146 days). The betamethasone infusion rate was that previously shown to produce fetal plasma betamethasone concentrations similar to human umbilical vein concentrations during antenatal glucocorticoid therapy. Regional CBF was measured in 10 brain regions, using coloured microspheres, before and 24 and 48 h after onset of treatment, and during hypercapnic challenges performed before and 48 h after onset of betamethasone exposure. Betamethasone exposure decreased CBF in all brain regions measured except the hippocampus after 24 h of infusion (P < 0.05). The CBF decrease was most pronounced in the thalamus and hindbrain (45-50% decrease) and least pronounced in the cortical regions (35-40% decrease). It was mediated by an increase in cerebral vascular resistance (CVR, P < 0.05) and led to a decrease in oxygen delivery to subcortical and hindbrain structures of 30-40%, to 8.6 +/- 1.1 ml x (100 g)(-1) x min(-1), and 40-45 %, to 11.0 +/- 1.6 ml x 100 g(-1) x min(-1), respectively (P < 0.05). After 48 h of betamethasone treatment, the reduction in CBF was diminished to about 25-30 %, but was still significant in comparison to vehicle-treated fetuses in all brain regions except three of the five measured cortical regions (P < 0.05). CVR and oxygen delivery were unchanged in comparison to values at 24 h of treatment. The CBF increase in response to hypercapnia was diminished (P < 0.05). These observations demonstrate for the first time that glucocorticoids exert major vasoconstrictor effects on fetal CBF. This mechanism may protect the fetus against intraventricular haemorrhage both at rest and when the fetus is challenged. Betamethasone exposure decreased the hypercapnia-induced increase in CBF (P < 0.05) due to decreased cerebral vasodilatation (P < 0.05).

Animals↗

PubMed1993

Methotrexate induced brain necrosis and severe leukoencephalopathy due to disconnection of an Ommaya device.

A 63-year old woman with breast carcinoma developed leucoencephalopathy and local brain necrosis after intraparenchymal infusion of methotrexate. This iatrogenic condition was caused by drain disconnection of the Ommaya device (bore hole type). The diagnosis of this rare complication of an Ommaya device was based on multiplanar MR-imaging. The case is discussed with regard to the complications of intraventricular chemotherapy by means of an Ommaya reservoir.

Brain↗

PubMed1988

[Acute toxicity of local anesthetics as a function of the patient's condition].

A patient's condition may alter the pharmacokinetic and pharmacodynamic characteristics of local anaesthetics and so increase the risk of toxicity. In the elderly patient, the elimination half-life is increased for both lidocaine and bupivacaine; the risk of overdose is therefore increased when the local anaesthetic agent is given in repeated doses and as a continuous infusion. Cardiotoxicity due to bupivacaine seems to be worsened by pregnancy. In the foetus and newborn, local anaesthetic toxicity gives the same clinical picture as in the adult and is increased in the presence of acidosis and anoxia. Bupivacaine depressive effects are increased by tachycardias, intraventricular blocks and all the conditions which are known to depolarize the cardiac cell membrane (e.g. hyperkaliemia, acidosis, severe hypoxia, myocardial ischaemia). Drug interactions may also potentiate the toxicity of lidocaine and bupivacaine, such as calcium blockers and diazepam. The effects of other conditions (cirrhosis, renal failure, epilepsy) and other drug interactions, specially those modifying free fraction and elimination of local anaesthetics, are also discussed.

Age Factors↗

PubMed1999

TrkA activation in the rat visual cortex by antirat trkA IgG prevents the effect of monocular deprivation.

It has been recently shown that intraventricular injections of nerve growth factor (NGF) prevent the effects of monocular deprivation in the rat. We have tested the localization and the molecular nature of the NGF receptor(s) responsible for this effect by activating cortical trkA receptors in monocularly deprived rats by cortical infusion of a specific agonist of NGF on trkA, the bivalent antirat trkA IgG (RTA-IgG). TrkA protein was detected by immunoblot in the rat visual cortex during the critical period. Rats were monocularly deprived for 1 week (P21-28) and RTA-IgG or control rabbit IgG were delivered by osmotic minipumps. The effects of monocular deprivation on the ocular dominance of visual cortical neurons were assessed by extracellular single cell recordings. We found that the shift towards the ipsilateral, non-deprived eye was largely prevented by RTA-IgG. Infusion of RTA-IgG combined with antibody that blocks p75NTR (REX), slightly reduced RTA-IgG effectiveness in preventing monocular deprivation effects. These results suggest that NGF action in visual cortical plasticity is mediated by cortical TrkA receptors with p75NTR exerting a facilitatory role.

Action Potentials↗

PubMed2002

In vivo infusions of exogenous growth factors into the fourth ventricle of the adult mouse brain increase the proliferation of neural progenitors around the fourth ventricle and the central canal of the spinal cord.

Stem cells isolated from the fourth ventricle and spinal cord form neurospheres in vitro in response to basic fibroblast growth factor (FGF2)+heparin (H) or epidermal growth factor (EGF)+FGF2 together. To determine whether these growth factor conditions are sufficient to induce stem cells within the fourth ventricle and spinal cord to proliferate and expand their progeny in vivo, we infused EGF and FGF2, alone or together, with or without H, into the fourth ventricle for 6 days via osmotic minipumps. Animals were injected with bromodeoxyuridine (BrdU) on days 4, 5 and 6 of infusion in order to label cells proliferating in response to the growth factors. Infusions of EGF+FGF2+H into the fourth ventricle resulted in the largest proliferative effect, a 10.8-fold increase in the number of BrdU+ cells around the fourth ventricle, and a 33.5-fold increase in the number of BrdU+ cells around the central canal of the spinal cord, as compared to vehicle infused controls. The majority of the cells were nestin+ after 6 days of infusion. Seven weeks post-infusion, 22 and 30% of the number of BrdU+ cells induced to proliferate after 6 days of EGF+FGF2+H infusions were still detected around the fourth ventricle and central canal of the spinal cord, respectively. Analysis of the fates of the remaining cells showed that a small percentage of BrdU+ cells around the fourth ventricle and in the white matter of the spinal cord differentiated into astrocytes and oligodendrocytes. BrdU+ neurons were not found in the brainstem or in the grey matter of the cervical spinal cord 7 weeks post-infusion. These results show that endogenous stem cells and progenitors around the fourth ventricle and central canal of the spinal cord proliferate in response to exogenously applied growth factors, but unlike in the lateral ventricle where they generate some new neurons, they only produce new astrocytes and oligodendrocytes at 7 weeks post-infusion.

Animals↗

PubMed2002

Bupivacaine-induced QRS prolongation is enhanced by lidocaine and by phenytoin in rabbit hearts.

UNLABELLED: Lidocaine, phenytoin, and bupivacaine are sodium channel blockers. Lidocaine displaces bupivacaine from its receptor on the sodium channel. However, lidocaine does not seem to decrease bupivacaine toxicity. Phenytoin also has been used to treat bupivacaine cardiotoxicity. To test the hypothesis that lidocaine or phenytoin might be used for the treatment of bupivacaine overdose, we compared the effects of bupivacaine on intraventricular conduction in the isolated heart of rabbits with bupivacaine and with either phenytoin or lidocaine added to bupivacaine. Twenty-four rabbit hearts were retrogradely perfused in a nonrecirculating Langendorff apparatus. The duration of QRS was measured without any drug and 10 min after infusion of 3 microM bupivacaine. Saline (control group) or increasing concentrations of either lidocaine or phenytoin was then added by 10-min-step increments. QRS duration was measured for each concentration at the end of a 10-min step. It was also determined 10 min after discontinuation of bupivacaine and after a period of washout for all drugs. QRS duration was significantly increased by adding phenytoin or lidocaine to bupivacaine. These drugs should not be used to treat the manifestations of bupivacaine toxicity. IMPLICATIONS: The effects of lidocaine and phenytoin on bupivacaine-related increases in cardiac conduction time have been studied in an isolated heart preparation. Both drugs increased the QRS widening induced by bupivacaine. We conclude that none of these drugs should be used for treating bupivacaine intoxication.

Anesthetics, Local↗

PubMed2005

Hypothalamic phosphatidylinositol 3-kinase-phosphodiesterase 3B-cyclic AMP pathway of leptin signalling is impaired following chronic central leptin infusion.

Leptin signalling in the hypothalamus is critical for the maintenance of normal body weight. Although hyperleptinaemia in obese people suggests a state of leptin resistance, and diet-induced obesity in rodents is associated with central leptin resistance, the underlying mechanisms remain unclear. Recent evidence suggests that, in addition to the signal transducer and activator of the transcription-3 (STAT3) pathway, leptin action is critical for energy homeostasis through an insulin-like signalling pathway involving an increase in phosphatidylinositol 3-kinase (PI3K) and phosphodiesterase 3B (PDE3B) activities and reduction in cyclic AMP (cAMP) levels in the hypothalamus. Here, we show that chronic central leptin (160 ng/h) infusion, which resulted in the development of resistance to the satiety action of leptin, impaired the PI3K-PDE3B-cAMP pathway of leptin signalling in the hypothalamus in that PI3K and PDE3B activities were increased and cAMP levels were decreased in the hypothalamus on day 2 of leptin infusion but remained unchanged on day 16. Additionally, induction of tyrosyl phosphorylation of insulin receptor substrate-1 observed on day 2 was not evident on day 16 of leptin infusion. By contrast, signalling through the STAT3-pathway remained activated in the hypothalamus throughout 16 days of leptin infusion. These findings show a differential response in PI3K-PDE3B-cAMP (impaired) and STAT3 (up-regulated) pathways to chronic central leptin infusion, and suggest a selective resistance in the PI3K-PDE3B-cAMP pathway of leptin signalling following a chronic increase in hypothalamic leptin tone attained by central infusion of this peptide hormone.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1992

Partner preference development in female prairie voles is facilitated by mating or the central infusion of oxytocin.

Results of these experiments indicate that females given at least 24 hours of cohabitation with a male develop a social preference for the familiar partner versus a stranger. Mating is not essential for the development of partner preferences, but clearly facilitates the onset of preferences. Females given six hours of cohabitation showed partner preferences only if they mated with the partner during cohabitation (Experiment 2) or if they received oxytocin (Experiment 3). Females that continued to mate during preference tests (Experiment 2, n = 4) mated exclusively with the partner. Oxytocin infusions, even in the absence of mating or estrogen priming, facilitated the development of partner preferences.

Animals↗

PubMed1997

Leukocytes and decreased left-ventricular contractility during endotoxemia in rabbits.

We hypothesized that leukocytes contribute to decreased myocardial contractility following endotoxin infusion. To test this hypothesis, we administered endotoxin (1 mg/kg intravenously) to intact, anesthetized rabbits whose arterial blood perfused two isolated hearts at a constant pressure (75 mm Hg). One heart was perfused with blood passed through a leukocyte filter, whereas the other received unfiltered blood. Contractility of both hearts was measured every 30 min for 6 h, using the slope of the end-systolic pressure-volume relationship (Emax) and the maximum rate of change of intraventricular pressure (dP/dt(max)). In the unfiltered hearts at 6 h, Emax decreased to 81 +/- 6% (mean +/- SEM) of baseline (p < 0.05). In the hearts perfused with leukocyte-filtered blood there was no change in Emax. Similarly, dP/dt(max) decreased 74 +/- 9% of baseline in the hearts receiving unfiltered blood (p < 0.05) but did not decrease in the hearts receiving leukocyte-filtered blood. The leukocyte filter significantly reduced the number of neutrophils in perfusing blood (p < 0.01), decreased the number of neutrophils in the heart by 77% (p < 0.01), and decreased myocardial morphometric changes (p < 0.05). A 55 +/- 18% reduction in neutrophil L-selectin expression after endotoxin infusion (p < 0.01) suggests that the neutrophils were significantly activated. We conclude that leukocytes, notably activated neutrophils, may contribute to decreased myocardial contractility during septic shock.

Animals↗

PubMed1996

Lesions of the cholinergic nuclei in the rat basal forebrain: excitotoxins vs. an immunotoxin.

Infusion of the excitotoxins, ibotenic acid, quisqualic acid, or AMPA, into the medial septal nucleus, diagonal band, and the nucleus basalis magnocellularis of rats produced less cholinergic cell loss as assessed by choline acetyltransferase activity in the projection fields, cortex and hippocampus, than that obtainable by intraventricular administration of the immunotoxin, 192 IgG-saporin. All excitotoxins produced reductions in tissue levels of some monoamines, while no decreases were found for the immunotoxin. All toxins produced acquisitional impairment in the hidden platform water maze. This behavioral deficit was slightly greater for the excitotoxic-lesioned rats than for those given 192 IgG-saporin at a dose which produced ChAT depletions similar to the most potent excitotoxin (AMPA). This supports the idea that some of the behavioral effects produced by excitotoxic lesions are due to the cholinergic basal forebrain lesion and some are due to noncholinergic damage.

Animals↗

PubMed1989

Effect of leukotriene D4 on blood flow to cerebrum and choroid plexus.

The purpose of this study was to examine effects of leukotriene D4 on blood flow to the cerebrum and choroid plexus. Blood flow was measured with microspheres in anesthetized rabbits. Under control conditions, blood flow to the cerebrum was 37 +/- 4 ml. min-1.100 g-1 (mean +/- SE) and blood flow to the choroid plexus was 428 +/- 52 ml.min-1.100 g-1. Intra-atrial infusion of leukotriene D4 at 0.1 and 1.0 microgram.kg-1.min-1 did not alter blood flow to the brain or choroid plexus, but produced a 49 +/- 3% and 69 +/- 5% decrease in blood flow to the bowel. We also examined effects of intracerebroventricular administration of leukotriene D4. Intraventricular injection of 1.0 microgram of leukotriene D4 did not affect blood flow to the cerebrum or choroid plexus. In contrast, intraventricular injection of 1.0 microgram of angiotensin II produced a 42 +/- 4% decrease in blood flow to the choroid plexus. In summary, neither intravascular nor intraventricular administration of leukotriene D4 affects blood flow to the brain or choroid plexus.

Angiotensin II↗

PubMed1983

Facilitation of sexual receptivity in the female rat by a fragment of the LHRH decapeptide, Ac-LHRH.

The following fragments of LHRH were administered intraventricularly and tested for their ability to enhance sexual receptivity in ovariectomized, estrogen-primed female rats: LHRH1-6 NH2, Ac-LHRH5-10, des-Tyr5-LHRH and des-Gly10-LHRH. LHRH1-6 NH2 had no effect on sexual behavior compared to saline-infused controls. Ac-LHRH5-10, des-Tyr5 LHRH and des-Gly10-LHRH significantly elevated lordotic responding compared to saline-infused controls. The results suggest that the elements contained in the LHRH structure may be functionally differentiated and indicate that the active sequence for facilitation of mating behavior is contained in the last half of the LHRH molecule.

Animals↗

PubMedDate not supplied

Wallenberg syndrome caused by CSF metastasis from malignant intraventricular meningioma.

A 34-year-old male developed a malignant transitional meningioma of the left lateral ventricle at the trigone. Over a 12-month period, he underwent three apparently complete excisions and one course of radiation therapy, but each time developed rapid local recurrence. The tumor recurred a fourth time seven months following the third operation, was excised, and the patient referred for intracarotid chemotherapy infusion. A left Wallenberg syndrome was noted on exam and CT scan demonstrated a posterior fossa mass. He died two weeks post-infusion from bronchopneumonia, 21 months after initial presentation. At autopsy, the tumor appeared more sarcomatous and had metastasized via the cerebrospinal fluid to the left dorsal medulla as well as to the surface of the pineal gland, the left cerebellar surface, and to several levels of the spinal cord. No extraneural metastases were found.

Adult↗