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PubMed1999

Brain-derived neurotrophic factor infusion delays amygdala and perforant path kindling without affecting paired-pulse measures of neuronal inhibition in adult rats.

Kindling is an animal model of human temporal lobe epilepsy in which excitability in limbic structures is permanently enhanced by repeated stimulations. Kindling also increases the expression of nerve growth factor, brain-derived neurotrophic factor, and brain-derived neurotrophic factor receptor messenger RNAs in both the hippocampus and cerebral cortex and causes structural changes in the hippocampus including hilar hypertrophy. We have recently shown that intraventricular nerve growth factor infusion enhances the development of kindling, whereas blocking nerve growth factor activity retards amygdaloid kindling. Furthermore, we have shown that nerve growth factor protects against kindling-induced hilar hypertrophy. The physiological role of brain-derived neurotrophic factor in kindling is not as clear. Acute injection of brain-derived neurotrophic factor increases neuronal excitability and causes seizures, whereas chronic brain-derived neurotrophic factor infusion in rats slows hippocampal kindling. In agreement with the latter, we show here that intrahilar brain-derived neurotrophic factor infusion delays amygdala and perforant path kindling. In addition, we show that brain-derived neurotrophic factor, unlike nerve growth factor, does not protect against kindling-induced increases in hilar area. To test the hypothesis that brain-derived neurotrophic factor suppresses kindling by increasing inhibition above normal levels, we performed paired-pulse measures in the perforant path-dentate gyrus pathway. Brain-derived neurotrophic factor infused into the hippocampus had no effect on the stimulus intensity function (input/output curves); there was also no significant effect on paired-pulse inhibition. We then kindled the perforant path 10 days after the end of brain-derived neurotrophic factor treatment. Once again, kindling was retarded, showing that the brain-derived neurotrophic factor effect is long-lasting. These results indicate that prolonged in vivo infusion of brain-derived neurotrophic factor reduces, rather than increases, excitability without increasing inhibitory neuron function, at least as assessed by paired-pulse protocols. This effect may be mediated by long-lasting effects on brain-derived neurotrophic factor receptor regulation.

Amygdala↗

PubMed1989

Development of ethanol tolerance not altered by 6-OHDA lesions of dorsal bundle.

It has been demonstrated via intraventricular (IVT) 6-OHDA infusions that central nervous system norepinephrine is necessary for the development of tolerance to ethanol (ETOH) in the mouse. Because 6-OHDA IVT infusions are not specific, we tested the effects of destruction of a specific NE pathway on development of ETOH tolerance. Rats received 6-OHDA lesions of the dorsal noradrenergic bundle (DB) and the development of ethanol tolerance was measured using the sleeptime test. The time between loss and recovery of the righting reflex was determined after an acute challenge dose of ETOH. Rats were than placed on ETOH diet for 13 days followed by a repeat of the sleeptime test. Sham and 6-OHDA-DB-lesioned rats exhibited the same sleeptime prior to ETOH diet, consumed similar amounts of ETOH diet over the course of 13 days, and exhibited similar significantly (p less than 0.0005) shorter sleeptimes after ETOH diet. Our data suggest that destruction of the DB does not alter development of ETOH tolerance as measured by the sleeptime test.

Animals↗

PubMed1989

Spinal vs. supraspinal sites of action of the alpha 2-adrenergic agonists clonidine and ST-91 on the acoustic startle reflex.

Previous work has shown that stimulation of alpha 2-adrenergic receptors depresses the startle responses in rats. The present study suggests that this depressant effect involves supraspinal rather than spinal alpha 2-adrenergic receptors because intraventricular but not intrathecal infusion of the hydrophilic alpha 2-adrenergic agonist ST-91 depressed the acoustic startle reflex. To determine the point in the acoustic startle pathway where alpha 2-adrenergic receptor activation might ultimately alter neural transmission, startle responses were elicited electrically from different points along the acoustic startle pathway after systemic administration of clonidine. Clonidine depressed acoustically-elicited startle and startle elicited by electrical stimulation of the ventral cochlear nucleus to a comparable magnitude and over a similar time course. It also partially depressed startle elicited by electrical stimulation of the nucleus reticularis pontis caudalis (RPC). Taken together, these data suggest that alpha 2-adrenergic stimulation depresses startle by acting on supraspinal receptors, but that this effect is ultimately expressed, at least in part, by actions at both spinal and brainstem levels of the acoustic startle response pathway. The results are compared to other drugs known to affect the startle reflex.

Acoustic Stimulation↗

PubMed1994

Evaluation of copper(II)-pyruvaldehyde bis (N-4-methylthiosemicarbazone) for tissue blood flow measurement using a trapped tracer model.

Copper(II)-pyruvaldehyde bis (N-4-methylthiosemicarbazone) (Cu-PTSM) labelled with 62,64Cu is a promising radiotracer for the study of blood flow using positron emission tomography (PET). We have investigated the application of a simple trapped tracer model to measurements of tissue 64Cu-PTSM uptake combined with continuous arterial sampling. A dual-tracer method was used to compare blood flow estimated by 64Cu-PTSM with values derived from measurements using cobalt-57 microspheres in the rat. Prolonged retention of 64Cu-PTSM following intravenous administration was initially confirmed in both normal tissues and tumours. After intraventricular 64Cu-PTSM infusion, cumulative arterial 64Cu activity increased progressively, and after extraction in n-octanol was found to plateau to levels corresponding with those reached following administration of 57Co microspheres. Rapid and species-dependent rates of 64Cu-PTSM decomposition to non-extractable 64Cu complexes were found in rat and human blood in vitro (70% +/- 6% and 43 +/- 5% respectively at 16 min), demonstrating the need for immediate processing of arterial samples. Close agreement was found between blood flow estimated by 64Cu-PTSM and 57Co microsphere methods in tissues of low to moderate flow: muscle (0.01, 0.08, 0.07 ml/min per gram; mean difference, mean 64Cu, mean 57Co), brain (0.09, 0.52, 0.43 ml/min per gram) and kidney (-0.16, 2.29, 2.45 ml/min per gram). Estimates of cardiac output also compared favourably between the two methods (5.7, 59.8, 54.1 ml/min). We conclude that a simple tissue trapping model may be suitable for the derivation of blood flow estimates using 62,64Cu-PTSM, PET imaging and continuous arterial blood sampling.

Animals↗

PubMed2006

Evaluation of the lumbar and ventricular infusion test in the diagnostic strategy of pediatric hydrocephalus and the therapeutic implications.

AIM: To evaluate the infusion test as a diagnostic tool behind the choice of intervention in pediatric hydrocephalus. MATERIALS AND METHODS: Intracranial pressure (ICP) measurement and infusion test were performed intraventricularly, by lumbar route, or combined in 40 consecutive children as a part of the standard diagnostic program in 1996-1999. RESULTS: The median age was 18.5 months, ranging from 2 weeks to 13 years. In the subgroup of patients with radiological aqueductal stenosis (N=14), mean lumbar/intraventricular ICP was 13 (3-35)/10 (2-27). Mean lumbar/ventricular R(out) were 18 (4-49)/17 (6-37). For patients with radiological communication between the third and fourth ventricles (N=14), the mean lumbar/intraventricular ICP was 11 (7-17)/9 (1-16). Mean lumbar/ventricular R(out) were 8 (3-11)/8 (4-12). A total of 13 patients had a shunt insertion, 10 had an endoscopic third ventriculostomy (ETV), 5 had endoscopic fenestration of a cyst, and 12 had no surgery. Of the patients initially treated with EVT, 50% had a shunt insertion shortly after. For communicating hydrocephalus, 75% of the patients initially not operated based on normal R(out) values ended up having a shunt insertion. DISCUSSION: R(out) has doubtful value as an indicator for conducting an operation or not and in the choice between EVT and shunt in children. This should be interpreted in the light of a growing understanding of hydrocephalus on a molecular level.

Adolescent↗

PubMed1987

5,6-Dihydroxytryptamine, a serotonergic neurotoxin, is formed endogenously in the rat brain.

Methamphetamine (MA) in high doses produces long-term toxic effects on the serotonergic system in the rat brain, including depletions of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid and reductions in 5-HT reuptake and tryptophan hydroxylase activity. In this study, the formation of 5,6-dihydroxytryptamine (5,6-DHT), a serotonergic neurotoxin, was observed in the rat hippocampus after a single 100 mg/kg injection of MA. The 5,6-DHT was detected by reverse-phase high-performance liquid chromatography with electrochemical detection in tissue samples taken 0.5-4 h after MA administration; the highest levels of 5,6-DHT (0.032 ng/mg wet tissue) were detected at 1 h. Following administration of MA, 5-HT was also depleted in the neocortex, but 5,6-DHT was not detected as frequently in this brain region as in the hippocampus. Comparisons were made between the long-term hippocampal 5-HT depletions seen either after an injection of MA or after intraventricular 5,6-DHT infusions and the levels of 5,6-DHT measured in the hippocampus shortly after each treatment. The amount of 5,6-DHT produced after MA administration appears to be adequate to cause the observed long-term 5-HT depletions. We suggest that 5,6-DHT formed from 5-HT may mediate the neurotoxic effects of MA on serotonergic nerve terminals.

5,6-Dihydroxytryptamine↗

PubMed1989

Nerve growth factor effects on cholinergic neurons of neostriatum and nucleus accumbens in the adult rat.

Following intraventricular nerve growth factor infusion in adult rats, the choline acetyltransferase immunostaining of the neuropil and neuronal cell bodies of the neostriatum (caudate-putamen) and nucleus accumbens was more intense on the side of the infusion. Furthermore, the average cross-sectional size (micron2) of the cholinergic somata was increased by about 40 and 20% in the striatum and accumbens, respectively. This unilateral response could be elicited in intact rats as well as in rats receiving a prior aspirative transection of the fimbria-fornix. The reported lack of (low-affinity) nerve growth factor receptor immunostaining in these neurons suggests that the nerve growth factor effects are most likely transduced by high-affinity receptors. The ability of these apparently undamaged cholinergic interneurons to respond to exogenous nerve growth factor with an increase in choline acetyltransferase content and cell body size suggests that they are benefiting from a less-than-maximal support by endogenous nerve growth factor in the normal young adult rat.

Animals↗

PubMed2000

Antigen-specific T cell trafficking into the central nervous system.

The initiation step of cell-mediated immune responses in the central nervous system (CNS) involves the trafficking of the antigen-specific T cells into the brain. To study this trafficking, we developed an in vivo system for studying antigen-specific responses in the CNS. In this assay, T cell receptor (TCR) transgenic mice having 95% of T cells specific for a defined antigen-pigeon cytochrome c (PCC) were cannulated intraventricularly for PCC antigen infusion and cerebrospinal fluid (CSF) sampling. Upon PCC infusion into the CNS, the number of alpha/beta TCR(+) Vbeta3(+) Mac1(-) cells in the CSF was characterized. We found that infusion of antigen into the CSF induced an increased number of antigen-specific T cells in the CNS and activation of antigen-specific T cells in the peripheral blood. Hence, the drainage of CNS antigen into the periphery might play an important role in sustaining autoimmune reactivity in CNS inflammatory diseases.

Animals↗

PubMed1982

Effect of glycerol and hyperosmolality on intracranial pressure.

Glycerol has been used in cerebral edema for hyperosmolar dehydration of brain tissue, but only empirical relationships govern this use. Since the efficacy of treatment with glycerol would likely increase with data on the relationship between drug blood levels and intracranial pressure (ICP), we examined the clinical pharmacology of the drug. Plasma samples were assayed for glycerol by a new method using gas chromatography with a flame ionization detector. Data were collected from 12 children who were in Children's Hospital of Pittsburgh (CHP) and who had cerebral edema of differing etiology that was treated with glycerol; they were monitored by intraventricular catheter. Glycerol was infused according to CHP guidelines. ICP reduction correlated with glycerol concentration and plasma concentrations of 1 to 3 mg/ml (10 to 30 mOsm/ml) were necessary to maintain an ICP below 20 torr. The relationship between osmolality and plasma glycerol level was also examined; there was good correlation between the idiogenic osmolality and drug concentration. Our studies support the clinical observations that relatively high doses of glycerol (0.2 to 1.0 gm/kg/hr), leading to plasma concentrations of 10 to 30 mOsm/l, are necessary to control ICP in patients with cerebral edema. Glycerol blood levels may be estimated from serum osmolality.

Brain Edema↗

PubMed2001

Idiopathic normal-pressure hydrocephalus: evaluation and findings in a multidisciplinary memory clinic.

The diagnostic evaluation of patients with possible idiopathic normal-pressure hydrocephalus (INPH) is traditionally performed in the settings of either neurological, neurosurgical or psychiatric departments. The diagnostic procedure and findings in 71 consecutive patients referred with a clinical and radiological suspicion of INPH to our out-patient multidisciplinary memory clinic are evaluated. Primary diagnoses and potential concomitant disorders considered of secondary importance for the symptomatologies were established. Abnormal hydrodynamics, demonstrated by intraventricular pressure monitoring and infusion test were mandatory for the diagnosis of INPH. Mean age was 68 years and mean Mini-Mental State Examination (MMSE) score was 22. DSM IV criteria of dementia were fulfilled in 42%. In half of the referred patients (n=36), the suspicion of INPH was already disproved subsequently to the evaluation programme performed in the outpatient clinic. The main primary diagnosis was cerebrovascular disease (CVD) comprising 27% (n=19) of the referrals, whereas INPH was diagnosed in only 20% (n=14). Shunt improvement rate was 72%. The remaining patients were diagnosed as having one of 26 different conditions. A multiplicity of disorders mimics the INPH syndrome, with CVD being the primary differential diagnosis. Evaluating patients with possible INPH in an outpatient multidisciplinary memory clinic is an effective and rational diagnostic approach.

Adult↗

PubMed2001

Vector delivery methods and targeting strategies for gene therapy of brain tumors.

Efficient virus and non-virus vector systems for gene transfer to tumor cells have been developed and tested in cell culture and in animal experiments. With some of the earliest and most comprehensively evaluated vectors, such as retroviruses, advanced clinical trials were performed in tumor patients. Malignant primary brain tumors (gliomas) have been chosen for the first clinical studies on novel gene therapy approaches because these tumors are non-metastatic and develop on the largely postmitotic background of normal glial and neuronal tissue. However, the human cancer gene therapy studies performed so far were not as successful as preclinical animal experiments. Furthermore, the clinical studies did not address major limiting factors for in vivo gene therapy, such as insufficient gene transfer rates to the tumor with the used local delivery modalities, and the resulting inability of a particular transgene-prodrug system to confer permanently eradicating cytotoxicity to the whole neoplasm. Critical evaluation of gene transfer and therapy studies has led to the conclusion that, even using identical vectors, the anatomical route of vector administration can dramatically affect both the efficiency of tumor transduction and its spatial distribution, as well as the extent of intratumoral and intracerebral transgene expression. This review concentrates on different physical methods for vector delivery to malignant primary brain tumors in experimental or clinical settings: stereotactic or direct intratumoral injection or convection-enhanced bulk-flow interstitial delivery; intrathecal and intraventricular injection; and intravascular infusion with or without modification of the blood-tumor-barrier. The advantages and drawbacks of the different modes and delivery routes of in vivo vector application, and the possibilities for tumor targeting by modifications of the native tropism of virus vectors or by using tissue-specific or inducible transgene expression are summarized.

Animals↗

PubMed1981

Inhibition of renin secretion by clonidine after alpha-adrenoceptor blockade in anesthetized dogs.

Dogs anaesthetised with pentobarbital were used to study the effects of the alpha-adrenoceptor antagonists phentolamine and piperoxan on the clonidine-induced suppression of plasma renin activity (PRA). Given alone, clonidine (30 microgram/kg, i.v.) produced an initial rise in mean arterial pressure (MAP) which was followed by a hypotensive response. These changes in blood pressure were accompanied by decreased in PRA and heart rate (HR). Pretreatment with phentolamine, 1 mg/kg i.v. or 3.3 microgram/kg/min infused into the third cerebral ventricle, or piperoxan, 20 microgram/kg stat. + 5 microgram/kg/min infused either i.v. or intraventricularly, did not modify the clonidine-induced falls in PRA, MAP or HR. All pretreatment regimes, with the exception of intraventricular phentolamine, virtually abolished the initial pressor response to clonidine. These results demonstrate that the renin-lowering action of clonidine in the dog is not inhibited by two classical alpha-adrenoceptor antagonists.

Adrenergic alpha-Antagonists↗

PubMed1990

[Acute propafenone poisoning. Description of a case].

The paper reports a case of a 16-year-old girl who was admitted to hospital in a state of shock having attempted to commit suicide by taking ten 300 mg pills of propafenone (Rytmonorm). The patient showed severe atrio-ventricular and intraventricular conduction disorders; an infusion of bicarbonate if soda and dopamine was immediately given and a temporary heart electro-stimulator was inserted. Conduction disorders gradually disappeared over the course of 36 hours and the patient was discharged with sinusal rhythm and good hemodynamic balance on the third day after admittance.

Acute Disease↗

PubMed1997

Failure of fibrinolytic endoventricular treatment to prevent neonatal post-haemorrhagic hydrocephalus. A case-control trial.

Post-haemorrhagic hydrocephalus is assumed to result from obstruction of the cerebrospinal fluid (CSF) pathways by blood clots and subsequent chronic infiltration with collagen. The aim of this work was to evaluate the possibility of preventing permanent shunt dependence by enhancing the endoventricular fibrinolysis by means of an endoventricular streptokinase infusion in babies affected by posthaemorrhagic ventricular dilation. A case-control trial was carried out in 12 neonates affected by intraventricular haemorrhage and subsequent progressive ventriculomegaly. Six of them were treated with 20,000 U/day of streptokinase infused over 96 h through a percutaneous ventricular catheter. Our results show that the percentage of shunted babies was identical in treated and control patients despite the enhancement of endoventricular fibrinolysis obtained in all treated patients. On the basis of our results we do not recommend intraventricular streptokinase infusion for routine use in post-haemorrhagic ventricular dilatation.

Case-Control Studies↗

PubMed1981

Intraoperative assessment of the reconstructed mitral valve using a low pressure crystalloid infusion.

A technique to intraoperatively assess mitral valve function after reconstruction is described. Cold cardioplegic solution is infused into the left ventricle at low intraventricular pressure (less than 15 mm-Hg) via the cardioplegia infusion line. The infusion of a crystalloid solution, instead of blood, clearly demonstrates residual leaks. Additional pump lines are not required and hypothermic cardioplegic arrest is maintained, thus allowing for repeated testing and additional repair. In combined aortic and mitral valve procedures, a Foley catheter is used to seal the aortic annulus and to infuse the crystalloid solution into the left ventricle. This method has been found to simplify mitral valve testing after reconstruction in a series of 25 patients since September 1979. Testing prompted additional repair in 4 patients and subsequent valve replacement in 2 patients.

Adolescent↗

PubMed1988

Electrophysiologic effects of propranolol in intraventricular conduction disturbance.

Sixteen patients underwent electrophysiologic studies before and after intravenous infusion of propranolol, 0.1 mg/kg. All of them had intraventricular conduction disturbances. A significant (p less than 0.01) increase occurred after propranolol in the mean spontaneous cycle length (mean change 122 ms) and the AH interval (mean 28 ms). The HV interval did not change significantly. The effective refractory period of the His-Purkinje system increased in 4 of 5 patients (mean net change 44 ms, p greater than 0.10). In 7 patients with phase 3 infranodal block, the longest cycle length for producing block increased after propranolol in 5 and remained unchanged in 2 (mean increase 40 ms, p less than 0.02). Two patients showed phase 4 atrioventricular block. Propranolol increased the critical cycle length by an average of 120 ms. Propranolol-induced bradycardia restored stable atrioventricular conduction in 2 patients with intermittent 2:1 block but facilitated the occurrence of high grade infranodal block in 1 patient. Thus, propranolol can impair His-Purkinje conduction in patients with preexisting infranodal abnormalities.

Aged↗

PubMed1992

Lidocaine has a narrow antiarrhythmic dose range against ventricular arrhythmias induced by programmed electrical stimulation in conscious postinfarction dogs.

The aim of the present study was to investigate the dose-dependent antiarrhythmic efficacy of lidocaine against electrically induced tachycardias in conscious, chronically instrumented postinfarction dogs. Programmed electrical stimulation (PES) was performed in 16 dogs 8 to 21 days after a 4 h occlusion of the left anterior descending coronary artery (LAD). Infusion of saline in 8 control animals with sustained ventricular tachycardia (SVT) inducible at baseline did not affect subsequent inducibility. In the treatment group 7 of 8 animals responded with SVT and one exhibited ventricular fibrillation at baseline. After an initial bolus of 1 mg/kg lidocaine intravenously (i.v.), the drug was infused at infusion rates of 40, 80 and 120 micrograms/kg/min (i.v.). During 80 micrograms/kg/min lidocaine (mean plasma level 3.5 micrograms/ml) 7 out of 8 animals displayed an antiarrhythmic response; both the lower and the higher infusion rate were associated with a smaller antiarrhythmic efficacy (3 of 8 animals responded to 40 micrograms/kg/min and 4 of 8 to 120 micrograms/kg/min). Licocaine did not affect ventricular refractory periods, but induced an increase in intraventricular conduction time at all infusion rates, from 66.2 ms at baseline to 67.7 ms (p less than 0.05), 67.7 ms (p less than 0.05), 70.0 ms (p less than 0.01) respectively. In conclusion the present study demonstrates that lidocaine is of considerable value in the management of PES-induced ventricular arrhythmias in the postinfarction phase. However there is only a small optimal therapeutic plasma level range, where lidocaine exhibits its antiarrhythmic efficacy against this type of arrhythmia; this makes a carefully titration of the drug necessary both in the experimental and in the clinical setting.

Animals↗

PubMed1975

Effect of intraventricular glutamate on ACTH release.

Sodium glutamate infused into the 3rd ventricle is a potent stimulus of ACTH release, as shown by the rise in plasma corticosterone levels. Glutamate failed to consistently increase the plasma corticosterone level in rats with deafferentation of the medial basal hypothalamus (MBH). We suggest that intraventricular glutamate interferes with central nervous function outside the MBH and stimulates ACTH release via afferent neural pathways.

Adrenocorticotropic Hormone↗