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 775 records · Page 43Linked to original sources
PubMed1997

Effects of probenecid on brain-cerebrospinal fluid-blood distribution kinetics of E-Delta 2-valproic acid in rabbits.

E-Delta 2-valproic acid (E-Delta 2-VPA), a major active metabolite of VPA, has been proposed as an alternative to VPA because it is less hepatotoxic and is nonteratogenic. In rodents, VPA and E-Delta 2-VPA have a brain tissue/free plasma concentration ratio less than unity, which suggests rapid removal of the alkanoate anticonvulsants from the central nervous system. This study in rabbits employed a simultaneous iv infusion-ventriculocisternal (VC) perfusion technique to investigate the steady-state kinetics of E-Delta 2-VPA transport at the blood-brain barrier, the blood-cerebrospinal fluid (CSF) barrier, and the neural cell membrane. Probenecid (PBD) was coadministered to probe the mediation of transport by organic anion transporter(s). Rabbits in the control group (N = 6) received an iv infusion of E-Delta 2-VPA to achieve a steady-state plasma concentration of 50 to 60 microg/ml. Blood and cisternal outflow of mock CSF perfusate were continuously sampled. Midway through the experiment, the VC perfusate was switched to one containing [3H]E-Delta 2-VPA. At 225 min, the rabbits were sacrificed, and each brain was removed and dissected into ten regions. Rabbits in the PBD group (N = 9) received an iv infusion and VC perfusion as in the control group as well as concomitant iv infusion of the inhibitor. The mean steady-state VC extraction ratio for [3H]E-Delta 2-VPA did not differ between the control and PBD groups (63.7 +/- 8.3% vs. 60. 6 +/- 9.6%), indicating the lack of a significant PBD-sensitive transport at the choroidal epithelium. Coadministration of PBD elevated brain concentration of cold E-Delta 2-VPA in the absence of a significant change in total or free steady-state plasma concentration. Mean E-Delta 2-VPA brain tissue/free plasma concentration ratios in the various brain regions were 3.5- to 5.2-fold higher in PBD-treated animals than in the controls. Significant increases (3.0- to 4.5-fold) in the mean brain tissue/cisternal perfusate concentration ratios were also observed. Compartmental modeling of the steady-state distribution data suggested that clearance of E-Delta 2-VPA from the brain parenchyma is governed jointly by efflux transporters at the neural cell membrane and brain capillary endothelium. Moreover, PBD-induced elevation of E-Delta 2-VPA tissue concentrations is attributed primarily to inhibition of E-Delta 2-VPA efflux transport at the neural cell membrane, resulting in both intracellular trapping and greater tissue retention of E-Delta 2-VPA.

Animals↗
PubMed1979

Hemodynamics of central infusion of angiotensin II in normal and sodium-depleted dogs.

The intraventricular (IVT) administration of angiotensin II (AII) (100 ng.kg-1.min-1) produced significant elevations of arterial blood pressure in pentobarbital-anesthetized dogs on either normal or sodium-deficient diets. In both groups of dogs the intraventricular administration of AII caused comparable and significant elevations in blood pressure averaging 15 +/- 2 and 17 +/- 4 mmHg, respectively, within 10 min after onset of the infusion. The rises in blood pressure were due to increased peripheral resistance (2.87 +/- 1.20 vs. 1.67 +/- 0.43 units). At the peak of the pressor response bradycardia was a constant feature in sodium-depleted animals, but was not present in the normal ones. In both groups of dogs regional cerebral blood flow (rCBF), determined by the xenon-133 washout method, remained unchanged during the development of the pressor response, and peripheral plasma renin activity failed to increase in response to the central infusion of AII. In conclusion, sodium deprivation appears not to influence the sensitivity of the central AII receptor because comparable pressor responses and hemodynamic changes were obtained following the intraventricular administration of AII in both normal and sodium-depleted dogs.

Angiotensin II↗
PubMed1991

Effects of bradykinin on inducible sustained ventricular tachycardia two weeks after myocardial infarction in pigs.

We studied the in vivo effect of bradykinin infusion on inducible sustained ventricular tachycardia (VT) 2 weeks after myocardial infarction in pigs, based on the assumption that the antiarrhythmic effect of angiotensin-converting enzyme (ACE) inhibitors may, apart from their angiotensin-II lowering effect, also be due to elevation of endogenous bradykinin levels. Of the six pigs with inducible VT in the control state, four were noninducible during subsequent bradykinin infusion (p less than 0.05). The ventricular effective refractory period (VERP) did not change during bradykinin infusion (from 237 +/- 37 to 239 +/- 42 ms), nor did intraventricular conduction change (filtered QRS duration was 45 +/- 17 ms before and 43 +/- 19 ms during infusion). Bradykinin caused both a significant systolic blood pressure (SBP) decrease (from 79 +/- 14 to 49 +/- 4 mm Hg, p less than 0.001) and diastolic BP (DBP) decrease (from 41 +/- 10 to 27 +/- 4 mm Hg, p less than 0.01). In conclusion, exogenous bradykinin reduced the inducibility of sustained VT 2 weeks after myocardial infarction. Because refractory periods or conduction velocity were not affected, the mechanism of action might be associated with the BP decrease, which can decrease wall stress. The previously reported antiarrhythmic effect of ACE inhibitors may be due in part to elevation of endogenous bradykinin levels.

Animals↗
PubMed2005

Periventricular rigidity in long-term shunt-treated hydrocephalus.

OBJECT: The failure of ventricles to enlarge after acute shunt malfunction in long-term shunt-dependent patients is generally attributed to the presence of periventricular rigidity resulting from gliosis. The aim of this study was to test the hypothesis that periventricular rigidity is present in these patients. METHODS: Fifteen pediatric patients who presented with acute shunt malfunction were studied; slit ventricles were detected in all of these patients. Pressure measurements were recorded simultaneously in both the ventricle and the brain parenchyma during shunt revision and then repeated after bolus infusion of fluid into the ventricle. The mean intraventricular pressure (IVP) at presentation was 24.1 mm Hg (standard deviation 10 mm Hg). The mean baseline IVP after drainage of cerebrospinal fluid but prior to the infusion was 7.5 +/- 4.3 mm Hg. There was no significant difference in the increase in the IVP and the intraparenchymal pressure (IPP) after bolus infusion into the ventricle (3.6 +/- 2.4 mm Hg and 3.3 +/- 2.1 mm Hg, respectively; p = 0.39). The mean pressure volume index was 24.1 ml (standard error of the mean 4.6 ml). CONCLUSIONS: The profile of the changes in IVP and IPP indicates that the periventricular wall does not restrict ventricular enlargement following shunt malfunction in long-term shunt-dependent patients.

Adolescent↗
PubMed1980

Thymidine transport in the central nervous system.

The mechanisms by which thymidine enters and leaves brain, choroid plexus, and CSF were investigated by injecting [3H]thymidine intravenously and intraventricularly. [3H]thymidine, with and without unlabeled thymidine, was infused at a constant rate into conscious adult rabbits. At 150 min, [3H]thymidine readily entered CSF, choroid plexus, and brain. In brain, approximately 45% of the nonvolatile radioactivity was [3H]thymidine phosphates. The addition of 0.21 mmol/kg unlabeled thymidine to the infusion syringe decreased the phosphorylation of [3H]thymidine in brain by approximately 85%; the addition of 2.1 mmol/kg of unlabeled thymidine to the infusion syringe decreased the relative entry of [3H]thymidine into CSF and brain by 40 and 78%, respectively. Two h after intraventricular injection of [3H]thymidine, [3H]thymidine was rapidly cleared from CSF, in part, to brain, where approximately 40% of the [3H]thymidine was converted to [3H]thymidine phosphates. The intraventricular injection of unlabeled thymidine (21 mumol) with the [3H]thymidine abolished the phosphorylation of [3H]thymidine in brain and significantly decreased the clearance of [3H]thymidine from the CSF. Rabbit brain slices accumulated [3H]thymidine by an energy-dependent, saturable high-affinity system that depended, in part, on intracellular phosphorylation of the [3H]thymidine. These results were interpreted as showing that the entry of thymidine from blood into CSF and presumably the extracellular space of brain and then into brain cells involves one or more saturable transport and/or metabolic steps.

Animals↗
PubMed1978

Vasopressin release from incubated in situ posterior pituitary lobe after intraventricular injection of carbachol or atropine.

The vasopressin release rate from incubated in situ rats posterior pituitary lobe as observed following intracarotid infusions of hypertonic solutions (3 x 0.1 ml/100 g b.w. contained 1.0 mmol NaCl and 0.1 mmol CaCl2 per 1 ml) was studied when influenced by intraventricular injections of 0.6 microgram carbachol or 240 microgram atropine sulphate, respectively. The increase in the release of vasopressin following intracarotid infusions of hypertonic solution augmented by intraventricular injection of carbachol was found. Atropine was shown to be effective in preventing the vasopressin release caused by hypertonic solution. The effects of carbachol and atropine indicate that mediation at synapses in the nucleus supraopticus involved in the release of vasopressin induced by osmotic stimulation is cholinergic.

Animals↗
PubMedDate not supplied

CNS 3-methoxy-4-hydroxyphenylglycol: its peripheral assessment by isotopic dilution and theoretical significance.

An isotope dilution model for the peripheral measurement of CNS catecholamine metabolism was examined in rabbits. 3H-norepinephrine (3H-norepinephrine (3H-NE) infusions were performed on rabbits before and after central sympathectomy via intraventricular 6-hydroxydopamine (6-OHDA) treatment. Urine samples were obtained 72 hr after 3H-NE infusion and analysed for specific activities (SAs) of 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3-methoxy-4-hydroxymandelic acid (VMA). The SA of MHPG was lower than that of VMA in all animals suggesting a source of unlabelled MHPG. The difference between the SAs of VMA and MHPG was abolished when the brain MHPG was markedly lowered by 6-OHDA injections. In animals which received 6-OHDA but retained moderate levels of brain MHPG, the difference between SAs of VMA and MHPG was maintained. The proposed model is able to predict and differentiate between rabbits that have severe depletion of CNS catecholamines and normal controls. The results suggest important relationships between CNS and peripheral NE metabolism and the compensatory capacity of the CNS to insult.

Animals↗
PubMed1980

Active transport of methotrexate from cerebrospinal fluid in humans.

The cerebrospinal fluid (CSF) efflux kinetics of methotrexate (MTX) were studied in three patients with indwelling Ommaya reservoirs. A small dose of MTX was injected intraventricularly several hr after the start of a high-dose continuous i.v. infusion of MTX. In all patients, the CSF antifolate concentration returned to the preinjection level before the end of the i.v. infusion. This result indicated that the efflux of MTX from CSF in humans is independent of plasma drug concentrations. Efflux kinetics were further characterized in one patient. Serially obtained CSF samples after intraventricular injections demonstrated a biphasic disappearance curve with alpha- and beta-phase half-disappearance times of 1.7 and 6.6 hr, respectively. Prolongation of the beta-phase half-time was associated with oral acetazolamide medication and with increased intracranial pressure, indicating that inhibition of CSF production slows MTX clearance. CSF MTX concentration, however, declined more rapidly than that of simultaneously administered diethylenetriaminepentaacetic acid, an extracellular marker substance excreted by bulk flow, indicating that bulk flow excretion alone is insufficient to account for MTX efflux from human CSF. Evidence that there is an active transport component was provided by probenecid pretreatment which also prolonged the CSF MTX half-life. These findings suggest that both passive and active mechanisms govern MTX efflux from the CSF in humans and that they can be inhibited by acetazolamide and probenecid, respectively.

Acetazolamide↗
PubMed1989

alpha-Melanotropin induced excessive grooming involves brain acetylcholine possible interaction in the ventral tegmental area.

Alpha-melanotropin (alpha-MSH) injected into the ventral tegmental area (VTA) or intraventricularly (icv) elicits excessive grooming. The icv infusion of the peptide also induces the stretching-yawning syndrome (SYS). The present study demonstrates that intra-peritoneal, icv or VTA administration of atropine, suppresses alpha-MSH-induced behavior elicited by i cv or VTA injections of the peptide. Experimental evidence is presented suggesting that alpha-MSH may act specifically on a cholinergic afferent to the VTA. The results appear to indicate that a neural target distinct from the dopamine system may be formerly activated by the peptide to elicit behavioral changes such as excessive grooming.

Animals↗
PubMed2004

Hemodynamic effects of carvedilol infusion and the contribution of the sympathetic nervous system in rats with heart failure.

We investigated the contribution of the sympathetic nervous system (SNS) in maintaining the blood pressure and in regulating the cardiac function during and after carvedilol administration in rats with heart failure (group F). Left ventricular end-diastolic pressure, percent functional shortening, and rates of intraventricular pressure rise were significantly changed by carvedilol infusion as compared with the basal values in group N (normal rats), but not in group F. The left ventricular end-diastolic pressure was elevated, corresponding to the enhancement of the plasma norepinephrine (NE) concentration caused by carvedilol infusion, in group N. The enhancement of the plasma NE concentration induced by carvedilol administration in group F was higher than that in group N. The value for the maximal hypertensive effect of NE intravenous infusion (Emax) was decreased, and the plasma NE concentration at half-maximal effect (EC50) was increased in group F as compared with the values in group N. These results indicate that the SNS (presynaptic) activity is increased and that the SNS receptor sensitivity in the cardiovascular regulation system is decreased in heart failure.

Adrenergic alpha-Antagonists↗
PubMed2002

Intraventricular and intravenous treatment of a patient with refractory primary CNS lymphoma using rituximab.

The treatment of primary central nervous system lymphoma (PCNSL) with chemo- and radiotherapy is efficient in terms of tumor response. However, time to tumor progression often is of short duration and leptomeningeal relapse is common. We present a 66-year-old man in third relapse of a CD20-positive PCNSL. After treatment with intravenous and intraventricular administration of the chimeric anti-CD20 monoclonal antibody rituximab, a total clearing of lymphoma cells in the cerebrospinal fluid (CSF) was achieved. There was no change in the size of the parenchymal tumor mass but there was slight improvement of clinical symptoms after therapy. Rituximab infusions (375 mg/m2) were first given systemically on days 1 and 8. Intraventricular injections of rituximab via Ommaya reservoir were given on days 16 (10 mg), 17 (40 mg), 24 (25 mg) and 25 (25 mg). Reversible side effects such as nausea, chills and hypotension were observed only immediately after intraventricular administration of 40 mg rituximab. Antibody levels in CSF were measured at 7 timepoints during and after the treatment period. These data suggest that intraventicular treatment with rituximab is safe and feasible with a potential activity on leptomeningeal tumor manifestation. Efficacy and pharmacokinetics of rituximab in PCNSL should be investigated in future trials.

Aged↗
PubMed1992

Octreotide: a potent new non-opiate analgesic for intrathecal infusion.

Somatostatin-14 has been reported to relieve severe cancer pain when given intraspinally. We have studied a stable analog, octreotide, which is suitable for long-term infusion by a drug pump. In preclinical trials in dogs, chronic intrathecal and intraventricular perfusion at 40 micrograms/h did not produce neurotoxicity. On the basis of these findings cancer patients with pain unrelieved by oral opiates were treated for periods of 13 to 91 days with intrathecal octreotide 5-20 micrograms/h. During octreotide infusion, pain scores were lower while oral opiate usage was reduced. No central or systemic side effects of intrathecal administration were seen. The pain relief occurred in patients who had previously not obtained satisfactory pain control with systemic or intrathecal opiates, which is consistent with a non-opiate spinal pathway. These preliminary findings, if confirmed, suggest that octreotide is a potent non-opiate analgesic appropriate for long-term intrathecal infusion.

Adult↗
PubMed1996

Abnormal systolic intraventricular flow velocities after valve replacement for aortic stenosis. Mechanisms, predictive factors, and prognostic significance.

BACKGROUND: Dynamic intraventricular flow velocities after valve replacement for aortic stenosis have been associated with high in-hospital morbidity and mortality. The aims of the present study were to determine the mechanisms and preoperative predictors of abnormal flow velocity (AFV) after valve replacement for aortic stenosis and to assess the clinical course of patients with AFV after surgery. METHODS AND RESULTS: One hundred consecutive patients with pure aortic stenosis were studied prospectively before operation by cardiac catheterization and Doppler echocardiography. After surgery, intraventricular flow was studied by Doppler echocardiography at rest, during nipride infusion, and during dobutamine infusion. AFV (defined as a systolic dagger-shaped Doppler spectrum > 2 m/s) occurred in 14 patients at rest and in 27 patients during nipride and/or dobutamine infusion. In most patients, AFV was associated with left ventricular cavity squeezing. Left ventricular end-diastolic diameter, preoperative intraventricular flow velocity and septal-to-posterior wall thickness ratio by Doppler echocardiography, and mean transvalvular pressure gradient and ejection fraction by catheterization emerged as predictors of resting postoperative AFV. Patients with resting AFV had a higher incidence of dyspnea or hypotension (64% versus 21%, P < .01) and a longer hospital stay (13.1 +/- 5.8 versus 11.1 +/- 2.5, P < .05) than patients without AFV. In contrast, at a 1-year follow-up, no patient with resting AFV died. CONCLUSIONS: First, AFV occurs in 14% of patients at rest after valve replacement for aortic stenosis and can be provoked or worsened by ventricular unloading or inotropic stimulation. Second, AFV is related more frequently to cavity squeezing than to systolic anterior motion of the mitral valve apparatus. Third, a typical pattern (small, hyperdynamic, and asymmetrically hypertrophied ventricle) is predictive for postoperative AFV and should be taken into account for the postoperative management. Finally, the presence of AFV at rest is associated with high in-hospital morbidity but good long-term prognosis.

Adult↗
PubMed1974

Effects of nicotine given into the brain of fowls.

1 The effects of nicotine, given into the IIIrd ventricle of adult conscious fowls (Gallus domesticus) or infused into various brain regions of conscious young chicks, were tested on behaviour, electrocortical activity, respiratory rate and body temperature. Its effects given intraventricularly or applied externally to the brain-stem of anaesthetized fowls were also examined.2 After intraventricular nicotine, fowls squatted for 3 to 5 min with eyes closed, electrocortical activity resembling that during sleep but with superimposed spike activity. Following this, fowls reawakened and tachypnoea developed, together with partial abduction of the wings from the trunk, the back becoming horizontal and the tail flexed. These effects were prevented by pempidine.3 Intraventricular nicotine suppressed or, less commonly, reduced operant key-pecking, an effect unrelated linearly to dose.4 Intraventricular nicotine given to fowls anaesthetized with chloralose produced brief apnoea, followed by increased amplitude of respiratory excursion for about 5 minutes. Respiratory rate accelerated slightly but tachypnoea did not develop. Nicotine applied directly to the ventral brain-stem increased respiratory amplitude in three out of seven fowls.5 In anaesthetized fowls, intraventricular nicotine raised blood pressure for 2 to 3 min, an effect prolonged up to 70 min by acute bilateral vagotomy, whereas pressor effects of intravenous nicotine were extended merely two to three fold. Dividing the spinal cord at C2 prevented pressor effects of intraventricular nicotine; those of intravenous nicotine were unaltered.6 In young chicks, nicotine infused into the diencephalon, telencephalon and myelencephalon induced effects similar to those observed immediately after intraventricular nicotine, i.e. chicks squatted with closed eyes but recovered within 3 to 5 minutes. Simultaneously, electrocortical activity changed from an alert to the sleep pattern, usually with superimposed ;spike' activity. Tachypnoea and associated postural changes did not develop. Pempidine prevented the behavioural and electrocortical effects of nicotine.

Aging↗
PubMed1997

Nerve growth factor attenuates cholinergic deficits following traumatic brain injury in rats.

Traumatic brain injury (TBI) results in chronic derangements in central cholinergic neurotransmission that may contribute to posttraumatic memory deficits. Intraventricular cannula (IVC) nerve growth factor (NGF) infusion can reduce axotomy-induced spatial memory deficits and morphologic changes observed in medial septal cholinergic neurons immunostained for choline acetyltransferase (ChAT). We examined the efficacy of NGF to (1) ameliorate reduced posttraumatic spatial memory performance, (2) release of hippocampal acetylcholine (ACh), and (3) ChAT immunoreactivity in the rat medial septum. Rats (n = 36) were trained prior to TBI on the functional tasks and retested on Days 1-5 (motor) and on Day 7 (memory retention). Immediately following injury, an IVC and osmotic pump were implanted, and NGF or vehicle was infused for 7 days. While there were no differences in motor performance, the NGF-treated group had significantly better spatial memory retention (P < 0.05) than the vehicle-treated group. The IVC cannula was then removed on Day 7, and a microdialysis probe was placed into the dorsal hippocampus. After a 22-h equilibration period, samples were collected prior to and after administration of scopolamine (1 mg/kg), which evoked ACh release by blocking autoreceptors. The posttraumatic reduction in scopolamine-evoked ACh release was completely reversed with NGF. Injury produced a bilateral reduction in the number and cross-sectional area of ChAT immunopositive medial septal neurons that was reversed by NGF treatment. These data suggest that cognitive but not motor deficits following TBI are, in part, mediated by chronic deficits in cholinergic systems that can be modulated by neurotrophic factors such as NGF.

Acetylcholine↗
PubMed1976

Reversal of advanced digoxin intoxication with Fab fragments of digoxin-specific antibodies.

Purified Fab fragments of ovine digoxin-specific antibodies reversed severe digoxin intoxication in a patient who had taken 22.5 mg of the drug with suicidal intent. Atrioventricular block with extreme bradycardia was temporarily managed by pacing, but progressive, intractable hyperkalemia (serum potassium of 8.7 meq per liter) with increasing pacing threshold and progressive intraventricular conduction delay was controlled only after infusion of 1100 mg of Fab. Sinus rhythm returned 10 minutes after completion of Fab infusion. Within five hours, the serum potassium concentration fell to 4.0 meq per liter. Free digoxin concentrations in serum fell sharply to undetectable levels, whereas total serum digoxin concentration concomitantly increased 12-fold. Renal excretion of digoxin bound to Fab was documented. Reversal of toxicity was not accompanied by hemodynamic instability, and antibodies to sheep Fab fragments were not detected in the patient's serum after treatment. Thus, purified digoxin-specific Fab fragments are capable of rapid reversal of advanced digoxin toxicity.

Adult↗
PubMed2001

Auditory event-related potentials differentiate patients with normal pressure hydrocephalus and patients with concomitant Alzheimer's disease verified by brain biopsy.

We studied 51 patients with clinical symptoms and CT findings suggesting normal pressure hydrocephalus (NPH). Tests included head MRI, auditory event-related potentials (ERPs), thorough neuropsychological testing and intraventricular intracranial 24 h pressure recording and infusion testing. A brain biopsy was also obtained to verify a concomitant dementing process (Alzheimer's disease; AD). Patients were divided into subgroups according to the need of shunt and the biopsy findings, and their ERPs were analysed blindly. The present results suggest that non-invasive ERPs aid in the differentiation of pure NPH from NPH with concomitant AD.

Aged↗