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PubMed1993

Pulmonary distribution and efficacy of exogenous surfactant in lung-lavaged rabbits are influenced by the instillation technique.

Surfactant bolus instillation has been reported to cause changes in arterial blood pressure (BP) and cerebral blood flow velocities which may increase the risk of intraventricular haemorrhage. To avoid these effects, slow tracheal infusion was evaluated as a possible alternative method of surfactant administration. Saline lung lavages were performed in 13 anesthetized and artificially ventilated adult rabbits to produce respiratory distress syndrome. Curosurf (CS, 200 mg/kg) labeled with 14C-dipalmitoyl-phosphatidylcholine (-DPPC) and/or red microspheres (RMS) was instilled into the trachea either as a single bolus (n = 8) or by infusion during 45 min via a side-channel within the wall of the tracheal tube (n = 5). An arterial cannula was placed for monitoring of blood gases and BP. To determine surfactant distribution, the lungs were cut into 60-70 pieces and radioactivity and/or the number of RMS were measured in each piece. The distribution of RMS was closely related to the distribution of 14C-DPPC (r = 0.96). Bolus instillation of CS led to a prompt and sustained increase in PaO2 (from < 10.5 to > 40 kPa within 2 min), a transient decrease in BP, and a reasonably homogeneous pulmonary surfactant distribution. Tracheal infusion of CS changed neither BP nor PaO2 during the observation period of 60 min. The pulmonary distribution of CS was extremely uneven after infusion. The distribution of exogenous surfactant and its effects on gas exchange are influenced by the instillation method. An inadequate instillation technique may add to the causes of "poor response" after surfactant replacement.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1995

Intracerebroventricular administration of morphine for control of irreducible cancer pain.

Intracerebroventricular morphine analgesic for the treatment of cancer pain was administered, using implanted access ports, in 82 patients from 1984 to January 1994. All of the patients who were selected for treatment were no longer responsive and had developed drug side effects to oral or parenteral opiates in varying doses (60-400 mg/d). The mean follow-up was 66 days (range, 12-443 d) for this series of 82 patients. The effective control of pain was achieved in nearly all of the patients, with only two failures. During the treatment, the daily morphine doses were moderately increased. The initial doses of morphine were a mean of 0.30 mg (range, 0.10-2 mg), and the final doses were a mean of 2.5 mg (range, 0.10-60 mg). The results show that the ratio of the terminal dose to the initial dose increased more rapidly for patients who had a follow-up of over 60 days. However, the increase seems to have been because of the progress of the disease rather than because of drug tolerance.

Adult↗
PubMed1994

Memory impairment and neuronal dysfunction induced by beta-amyloid protein in rats.

Alzheimer's disease (AD) is characterized by the presence of senile plaques. The core of the plaque consists of beta-amyloid protein. In AD patients, learning and memory are impaired with a concomitant loss of the cholinergic marker enzyme, choline acetyltransferase (ChAT). However, direct evidence that beta-amyloid protein is related to the impairment of learning and memory has not been demonstrated. In this study, we investigated whether memory impairment and neuronal dysfunction were produced after 2 weeks continuous infusion of beta-amyloid protein (3, 30 and 300 pmol/day) into the cerebral ventricles in adult rats. To investigate the ability of learning and memory in beta-amyloid protein-treated rats, water maze and passive avoidance tasks were carried out. The performance of both tasks in beta-amyloid protein-treated rats was impaired. ChAT activity in the frontal cortex (3 and 30 pmol/day) and hippocampus (300 pmol/day) significantly decreased. These results suggest that beta-amyloid protein is related to the impairment of learning and memory, and neurodegeneration, and that beta-amyloid protein-treated rats could be used as an animal model for AD.

Acetylcholinesterase↗
PubMed1990

Changes in gastric secretion after intracerebroventricular infusion of bombesin in dogs.

Synthetic bombesin (BBS) was infused intracerebroventricularly in 14 mongrel dogs, to study the effects of the peptide on gastric secretion and on gastrin and neurotensin levels. The infusion was performed with a specific apparatus, and gastric fluid was collected with a Pavlov pouch. BBS was given in two series of experiments: as a bolus intracerebroventricular injection of 308.6 pmol/kg and as a continuous intracerebroventricular infusion at a rate of 617.3 pmol/kg/h for 30 min. The bolus injection caused a very significant decrease of gastric fluid volume, a significant decrease of HCl output, and a significant increase of its pH, while serum immunoreactive gastrin increased significantly. The continuous infusion of BBS caused similar changes in gastric secretion. The plasma neurotensin levels did not change. In conclusion, the intracerebroventricular administration of BBS increases the serum gastrin levels, decreases the volume and HCl content of gastric fluid, and increases its pH.

Animals↗
PubMed1989

Ultrastructure of the orbital pathway for cerebrospinal fluid drainage in rabbits.

An increasing number of physiological and morphological studies indicate that cerebrospinal fluid (CSF) drains via nonarachnoidal pathways in several mammalian species. Ultrastructural tracer studies were undertaken to examine the orbital route for CSF absorption in the rabbit. At the termination of the optic nerve subarachnoid space, an area of connective tissue containing numerous small tortuous channels is present. Ferritin (molecular weight 400,000) infused into the ventricles at normal and increased intraventricular pressure was present in these channels by 15 minutes postinfusion, and subsequently reached the intraorbital connective tissue. Elevating the intraventricular pressure did not noticeably alter the morphological appearance of this region or change the gross distribution pattern of the ferritin. Ferritin did not penetrate the scleral barrier to reach the choriocapillaris, nor did it breach the arachnoid barrier layer proximal to the transitional zone at the optic subarachnoid space to reach the dura mater. These results are very similar to those described for the hamster orbital region and the rabbit cribriform region. These experiments support the concept that macromolecules exit the subarachnoid space at the termination of the optic nerve via open channels, and that no significant barrier to drainage of macromolecules in CSF is present at this location.

Animals↗
PubMedDate not supplied

[Practice guidelines for cancer pain management. Task Force for Cancer Pain Management].

Cancer pain is a frequent medical problem in our society. This syndrome affects from 80 to 90% of cancer patients and can be solved with relatively simple measures in 90% of the cases. Approximately 40% of cancer patients reported to be unsatisfied with the physician or nurse about their pain management. For these reasons, we gathered a task force in order to generate practice guidelines based on medical evidence and on the opinion of experts in this area. These guidelines were generated by a task force of 31 physicians who were leaders in this field and based on 599 papers selected by a previous literature search. This group evaluated the results of this search in three work sessions, during which a level of evidence was assigned to each recommendation.

Adjuvants, Pharmaceutic↗
PubMed1989

Optimal use of the Ommaya reservoir in clinical oncology.

A major obstacle to the effective systemic therapy of intracranial malignancies and infections, the bloodbrain barrier was overcome by the development of the Ommaya reservoir in 1963. Initially used in treating cryptococcal meningitis, this closed system for continued access to the ventricular spaces has a variety of applications. They include treatment of cancer pain, chronic or recurrent CNS infection, prophylaxis of CNS involvement in acute lymphoblastic leukemia, and treatment of leptomeningeal malignancy. The authors outline the rationale, latest indications, surgical technique, and potential complications arising from the use of the Ommaya reservoir and other such subcutaneous reservoirs.

Brain Neoplasms↗
PubMed1993

Induction of tolerance to and physical dependence on pentobarbital continuous intracerebroventricular administration.

A new model of barbiturate tolerance and dependence was developed using i.c.v. infusion of pentobarbital. Male Harlan Sprague-Dawley rats weighing 250 to 300 were implanted with i.c.v. cannulae and infused with sodium pentobarbital (500 micrograms/10 microliters/hour) for 6 days. The pentobarbital-infused group had a shorter duration of pentobarbital-induced loss of righting reflex than the saline-infused group. When i.c.v. pentobarbital- and saline-infused rats were injected with sodium pentobarbital (60 mg/kg i.p.), the time course of pentobarbital levels in the serum and in the brain were not significantly different. The infusion of pentobarbital also did not induce hepatic drug-metabolizing enzymes. The depth of thiopental-induced hypothermia was decreased by i.c.v. pentobarbital infusion. During the course of the infusion, the basal body temperature of the pentobarbital-infused rats did not change. Two days after the infusion was discontinued, the basal body temperature was elevated. The increase in body temperature lasted for 8 days. Twenty-four hours after the infusion was discontinued, the pentobarbital-infused rats had a significantly shorter onset of t-butylbicyclophosphorothionate (TBPS)-induced convulsions. These studies show that i.c.v. infusion can be used to induce pentobarbital tolerance and dependence. This model has the advantage that issues related to induction of hepatic drug-metabolizing enzymes are eliminated, and it may be useful in the study of barbiturate addiction.

Animals↗
PubMed1996

In vivo growth factor expansion of endogenous subependymal neural precursor cell populations in the adult mouse brain.

The lateral ventricle subependyma in the adult mammalian forebrain contains both neural stem and progenitor cells. This study describes the in situ modulation of these subependymal neural precursor populations after intraventricular administration of exogenous growth factors. In vivo infusion of epidermal growth factor (EGF) into adult mouse forebrain for 6 consecutive days resulted in a dramatic increase in the proliferation and total number of subependymal cells and induced their migration away from the lateral ventricle walls into adjacent parenchyma. Immediately after EGF infusion, immunohistochemical characterization of the EGF-expanded cell population demonstrated that >95% of these cells were EGF receptor- and nestin-positive, whereas only 0.9% and 0.2% labeled for astrocytic and neuronal markers, respectively. Seven weeks after EGF withdrawal, 25% of the cells induced to proliferate after 6d of EGF were still detectable; 28% of these cells had differentiated into new astrocytes and 3% into new neurons in the cortex, striatum, and septum. Newly generated oligodendrocytes were also observed. These in vivo results (1) confirm the existence of EGF-responsive subependymal neural precursor cells in the adult mouse forebrain and (2) suggest that EGF acts directly as a proliferation, survival, and migration factor for subependymal precursor cells to expand these populations and promote the movement of these cells into normal brain parenchyma. Thus, in situ modulation of endogenous forebrain precursor cells represents a novel model for studying neural development in the adult mammalian brain and may provide insights that will achieve adult replacement of neurons and glia lost to disease or trauma.

Animals↗
PubMed1979

Effect of intraventricular histamine on hormone secretion in dogs.

In pentobarbital-anesthetized dogs, infusion of a low dose of histamine directly into the third ventricle increased plasma ACTH concentration. The increase was unaffected by metiamide, a drug which blocks H2 receptors, but was abolished by mepyramine, a drug which blocks H1 receptors. Mepyramine alone did not produce a decrease in plasma ACTH concentration in stressed dogs. Infusion of the H1 agonist 2-methylhistamine increased plasma ACTH concentration, whereas infusion of the H2 agonist 4-methylhistamine decreased plasma ACTH concentration and blocked the response to surgical stress. Histamine, 2-methylhistamine and 4-methylhistamine had no statistically significant effect on plasma renin activity, blood pressure, or heart rate, and histamine had no effect on plasma prolactin concentration. There were no consistent, specific effects on growth hormone secretion. We conclude that activation of central H1 receptors increases ACTH secretion in dogs, and that activation of central H2 receptors decreases ACTH secretion. Some of the reported effects of cyproheptadine and other drugs on ACTH secretion may be due to their antihistamine activity.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

The changes of propofol concentration in human cerebrospinal fluid after drug infusion.

OBJECTIVE: Investigation of the propofol concentration changes in cerebrospinal fluid (CSF) after the termination of the drug infusion. METHODS: Nine patients (American Society of Anesthesiologists classes I-III) scheduled for elective intracranial procedures were studied. Propofol was applied in the form of target control infusion. During anesthesia, fractional doses of fentanyl and cisatracurium were administered as necessary. After tracheal intubation, the lungs were ventilated to achieve normocapnia with an oxygen-air mixture (fraction of inspired oxygen = 0.33). Arterial blood and CSF samples (from an intraventricular drain) were taken simultaneously at the end of propofol infusion and then at 15, 30, 45, 60, 90, and 120 minutes after the end of infusion. RESULTS: A pronounced decrease of the anesthetic concentration in plasma (P < 0.001) was observed during the first 15 minutes after infusion termination, followed by further yet slower decrease of the drug concentration. At the end of propofol infusion, the concentration of propofol in CSF was 65.59 ng/mL (SD, 26.91 ng/mL) and remained almost stable for approximately 30 minutes; afterward, a slow decrease of CSF propofol concentration was observed. CONCLUSION: The statement that CSF can be regarded as a significant route for drugs delivery to the brain is disputable for propofol. The obtained results show that, in contrast to the situation from induction of anesthesia, back transport of the drug from CSF to blood is markedly slower, supporting the thesis about propofol transport from blood to CSF by passive diffusion.

Adolescent↗
PubMed1986

Pantothenic acid transport and metabolism in the central nervous system.

The mechanisms by which pantothenic acid (PA) enters and leaves brain, choroid plexus, and cerebrospinal fluid (CSF) were investigated by injecting [3H]PA either intravenously or intraventricularly into adult rabbits. [3H]PA, either alone or together with unlabeled PA, was infused at a constant rate into conscious rabbits. At 180 min, [3H]PA readily entered CSF, choroid plexus, and brain. In brain, CSF, and plasma, greater than 90% of the 3H was associated with [3H]PA. The addition of 200 mumol/kg PA to the infusion syringe decreased the penetration of [3H]PA into brain and CSF by approximately 70%. Two hours after the intraventricular injection of [3H]PA, [3H]PA was rapidly cleared from the CSF by a probenecid-sensitive mechanism. No metabolism of the [3H]PA occurred in brain. However, 18 h after the intraventricular injection of 37 microCi (34 nmol) of [3H]PA, approximately 40% of the 3H remaining in forebrain was converted to [3H]CoA. These results show that PA enters and leaves CSF and brain by saturable transport systems. However, [3H]PA is very slowly converted to [3H]CoA in brain in vivo.

Animals↗
PubMed2002

Chronic, controlled GDNF infusion promotes structural and functional recovery in advanced parkinsonian monkeys.

The powerful trophic effects that glial cell line-derived neurotrophic factor (GDNF) exerts on midbrain dopamine neurones suggest its use in treating Parkinson's disease. However, some important questions remain about the possible therapeutic applications of GDNF. Here we demonstrate that the chronic infusion of 5 or 15 micro g/day GDNF into the lateral ventricle or the striatum, using programmable pumps, promotes restoration of the nigrostriatal dopaminergic system and significantly improves motor functions in rhesus monkeys with neural deficits modelling the terminal stages of Parkinson's disease. The functional improvements were associated with pronounced upregulation and regeneration of nigral dopamine neurones and their processes innervating the striatum. When compared with vehicle recipients, these functional improvements were associated with (i) >30% bilateral increase in nigral dopamine neurone cell size; (ii) >20% bilateral increase in the number of nigral cells expressing the dopamine marker tyrosine hydroxylase; (iii) >70 and >50% bilateral increase in dopamine metabolite levels in the striatum and the pallidum, respectively; (iv) 233 and 155% increase in dopamine levels in the periventricular striatal region and the globus pallidus, respectively, on the lesioned side; and (v) a five-fold increase in tyrosine hydroxylase-positive fibre density in the periventricular striatal region on the lesioned side. In addition, chronic GDNF treatment did not induce the side-effects generally associated with chronic administration of levodopa, the most widely used treatment for Parkinson's disease. Thus, the results suggest that the prolonged and controlled delivery of GDNF into the brain could be used to intervene in long-term neurodegenerative disease processes like Parkinson's disease. Additional studies are required to determine the potential differences between chronic, intraventricular and intraputamenal (or intranigral) delivery of GDNF to maximize the efficacy of infusion treatments.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2004

Lower dose intraventricular T-PA fibrinolysis: case report.

BACKGROUND: Recombinant tissue plasminogen activator (rtPA) intraventricular fibrinolysis has been demonstrated to be efficacious in clearing blood from the ventricular system. Preliminary studies indicate it may improve survival. There have also been reports of adverse affects from intraventricular fibrinolysis. Optimal dosing of rtPA has not been established. METHODS: A 40-year-old patient with intraventricular hemorrhage extension secondary to a ruptured aneurysm was treated with a one-time infusion of 1 mg of rtPA through a right ventriculostomy. RESULTS: Computed tomography scans demonstrated excellent resolution of intraventricular blood and improvement in cerebral spinal fluid flow after fibrinolysis. Fibrinolysis was most marked in the third and fourth ventricles. There were no adverse effects noted. CONCLUSIONS: Intraventricular fibrinolysis is effective at a lower dose than previously used. Lower doses may have fewer adverse affects.

Adult↗
PubMed1980

Riboflavin homeostasis in the central nervous system.

The mechanisms by which riboflavin, which is not synthesized in mammals, enters and leaves brain, CSF, and choroid plexus were investigated by injecting [14C]riboflavin intravenously or intraventricularly. Tracer amounts of [14C]riboflavin with or without FMN were infused intravenously at a constant rate into normal, starved, or probenecid-pretreated rabbits. AT 3 h, [14C]riboflavin readily entered choroid plexus and brain, and, to a much lesser extent, CSF. Over 85% of the [14C]riboflavin in brain and choroid plexus was present as [14C]FMN and [14C]FAD. The addition of 0.2 mmol/kg FMN to the infusate markedly depressed the relative entry of [14C]riboflavin into brain, choroid plexus, and, less so, CSF, whereas starvation increased the relative entry of [14C]riboflavin into brain and choroid plexus. After intraventricular injection (2 h), most of the [14C]riboflavin was extremely rapidly cleared from CSF into blood. Some of the [14C]riboflavin entered brain, where over 85% of the 14C was present as [14C]FMN plus [14C]FAD. The addition of 1.23 mumol FAD (which was rapidly hydrolyzed to riboflavin) to the injectate decreased the clearance of [14C]riboflavin from CSF and the phosphorylation of [14C]riboflavin in brain. Probenecid in the injectate also decreased the clearance of [14C]riboflavin from CSF. These results show that the control of entry and exit of riboflavin is the mechanism, at least in part, by which total riboflavin levels in brain cells and CSF are regulated. Penetration of riboflavin through the blood-brain barrier, saturable efflux of riboflavin from CSF, and saturable entry of riboflavin into brain cells are three distinct parts of the homeostatic system for total riboflavin in the central nervous system.

Animals↗
PubMed1988

Biotin transport and metabolism in the central nervous system.

The mechanisms by which biotin enters and leaves brain, choroid plexus and cerebrospinal fluid (CSF) were investigated by injecting [3H]biotin either intravenously or intraventricularly into adult rabbits. [3H] biotin, either alone or together with unlabeled biotin was infused at a constant rate into conscious rabbits. At 180 minutes, [3H]biotin had entered CSF, choroid plexus, and brain. In brain, CSF, and plasma, greater than 90% of the nonvolatile 3H was associated with [3H]biotin. The addition of 400 mumol/kg unlabeled biotin to the infusion syringe decreased the penetration of [3H]biotin into brain and CSF by approximately 70 percent. Two hours after an intraventricular injection, [3H]biotin was cleared from the CSF more rapidly than mannitol and minimal metabolism of the [3H]biotin had occurred in brain. However, 18 hours after an intraventricular injection, approximately 35% of the [3H]biotin remaining in brain had been covalently incorporated into proteins, presumably into carboxylase apoenzymes. These results show that biotin enters CSF and brain by saturable transport systems that do not depend on metabolism of the biotin. However, [3H]biotin is very slowly incorporated covalently into proteins in brain in vivo.

Animals↗