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PubMed1980

Estimation of the in vivo concentration of salsolinol and tetrahydropapaveroline in rat brain after the administration of ethanol.

Tetrahydroisoquinolines (TIQs) are not only pharmacologically active, but their intraventricular infusion evokes alcohol drinking in rats. It is not known if salsolinol or tetrahydropapaveroline (THP), the two most commonly studied TIQs, spontaneously form in vivo in brain during chronic or acute consumption of ethanol. A theoretical calculation based on a steady-state assumption was made in order to estimate what could be the upper limit of these compounds in rat brain. The model used was that the rate of formation was equal to the rate of disappearance. The latter term is the rate constant for metabolism times the TIQ concentration. The former was estimated for salsolinol from data obtained from human urine while for THP it was simply the second order rate equation. The values obtained for both concentrations were ca 1 ng/g-brain tissue.

Aldehydes↗

PubMed1995

Selective inhibition of axon outgrowth by antibodies to NGF in a model of temporal lobe epilepsy.

The molecular basis of the axonal reorganization that follows seizure-induced brain injury is unknown. Elevations in neurotrophins following seizures suggest that growth factors may play a role in this process. After pilocarpine-induced seizures, robust axonal sprouting from dentate granule cells and cholinergic forebrain neurons was evident in the inner molecular layer of the dentate gyrus. Intraventricular infusions of an NGF-specific antibody that blocks NGF biological activity in vitro attenuated the cholinergic axonal sprouting and the increases in cell body size of basal forebrain cholinergic neurons that followed seizure-induced injury in vivo. In contrast to its effects on the cholinergic network, the NGF antibody did not decrease the sprouting of dentate granule cell axons into the inner molecular layer. These results suggest that NGF may have a functional and system-specific role in the remodeling of networks that follows repetitive seizures.

Animals↗

PubMed1993

The role of endocardial endothelium in the modulation of myocardial contraction in the isolated whole heart.

Selective damage to the endocardial endothelium in isolated papillary muscle preparations has been shown to produce an abbreviation of contraction, changes which were also observed following an increase in myocardial cyclic GMP in those preparations. In the present study we have investigated the effects of removing the endocardium and increasing myocardial cyclic GMP on contractile parameters in isolated Langendorff perfused ferret hearts, where the myocardial mass underlying the endocardium is much greater. Selective damage to left ventricular endocardial endothelium without damaging the underlying myocardium was achieved by brief exposure to a weak detergent solution (Triton X-100 0.005% v/v). This resulted in a significant abbreviation of the left ventricular pressure-time curve due to the earlier onset of relaxation, but there was little effect on early systole. The direct intraventricular infusion for 15 minutes of 10 microM sodium nitroprusside, a donor of nitric oxide, or of 1 microM substance P, to stimulate release of endothelium-derived relaxing factor, did not increase myocardial cyclic GMP levels or alter left ventricular contractile performance. Myocardial cyclic GMP levels were significantly increased by 15 minute intracoronary infusions of 10 microM nitroprusside and 1 microM substance P, approximately ten-fold and two-fold respectively. Intracoronary nitroprusside induced an abbreviation of the left ventricular pressure-time curve with an earlier onset of relaxation, but contraction was unaltered by intracoronary substance P. These results show that, in the isolated Langendorff perfused ferret heart, both selective removal of endocardial endothelium and an increase in myocardial cyclic GMP cause an abbreviation of left ventricular pressure and an earlier onset of relaxation with little change in early systole.

Animals↗

PubMed1993

Pharmacology of CP-99,994; a nonpeptide antagonist of the tachykinin neurokinin-1 receptor.

(+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine (CP-99,994) binds selectively and with high affinity (Ki = 0.25 nM) to neurokinin (NK)-1 tachykinin receptors in a human cell line and in guinea pigs where it acts as an antagonist as evidenced by its blockade of substance P-induced excitation of locus coeruleus neurons in vitro. Subcutaneously administered CP-99,994 antagonized locomotor activity in guinea pigs induced by intraventricular infusion of [Sar9,Met(O2)11]-substance P (50 micrograms) with an ID50 = 0.59 mg/kg, indicating that CP-99,994 penetrates into the central nervous system. Orally administered CP-99,994 potently blocked (ID50 = 4 mg/kg) the leakage of Evans blue dye into trachea and bronchi elicited by exposure of guinea pigs to aerosol capsaicin (1 mM). CP-99,994 has reduced affinity (IC50 = 3 microM) for the L-type calcium channel in contrast to CP-96,345 (IC50 = 27 nM) an earlier nonpeptide antagonist. Thus, CP-99,994 represents an important pharmacological tool for investigating the physiological role of substance P and a potentially novel therapeutic agent for treating a variety of diseases.

Animals↗

PubMed1994

[Studies on the isolation of endogenous sleep factors from Tupaia Belangeri Chinensis (TBC) after sleep deprivation].

The present study was undertaken to explore endogenous sleep factors isolated from 48-72 h sleep deprived (SD) male Tupaia belangeri chinensis (TBC). Only drink ad libitum (10% glucose) was available within 24 h before collection of urine. Controlled "clean" urinary samples were pooled and stored at 20 C. Fraction I-V from the urine were determined after ultrafiltration and Sephadex-G15. Amino-acid analysis of each fraction was automatically done by a 835 Amino-acid Analyzer, respectively. Bioassay was performed in 40 adult rabbits weighing 2.5-3.5 kg of either sex. Experiments were undertaken via the mesodiencephalic intraventricular infusion. Results show that S2C (Fraction-III) (50 micrograms/rabbit, i.c.v.) exhibited significant delta-enhancing effect compared to the controls. Further purification was done with Sephadex G-25 and Sephadex LH-20. The more purified S4B (50 micrograms/rabbit, i.c.v.) also exhibited significant delta-enhancing effect compared to the controls. The amino-acid analysis of Fraction-III revealed that the compositional contents of S2C and S4B are different from what have been known with Factor S, DSIP and SPS.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed1977

Synthesis of the tripeptide L-Trp-L-Ser-L-Glu. Comparison of its biological activity with that of the delta-sleep-inducing-peptide (DSIP).

In order to test the specificity of the natural Delta-Sleep-Inducing-Peptide (DSIP), a tripeptide with the same N-terminal amino acid was synthesized. The synthesis of the new tripeptide L-Trp-L-Ser-L-Glu was carried out by the method of the mixed anhydride. Protecting groups were all oxygen-bound benzyl groups. The physical-chemical data of the newly synthesized peptides are reported. The biological activity of the tripeptide was assayed by intraventricular infusion in the rabbit under the same conditions as for the DSIP. The effects of the tripeptide on the EEG could not duplicate those of DSIP which induced a marked increase of delta activity, typical for orthodox 'Slow Wave Sleep' (SWS).

Animals↗

PubMed1998

[Intracerebral neurosurgery in the treatment of chronic pain].

Brain surgery is generally considered a treatment of last resort for chronic pain resistant to all other therapeutic measures. The neurosurgical treatment of pain may be either destructive (e.g., thalamotomy) or augmentative (e.g., electrical stimulation through an electrode connected to an implanted neurologic pacemaker). For pain of the neurogenic type (neuropathic or deafferentation pain), the preferred target is either the sensory nucleus of the thalamus, at a site corresponding somatotopically to the location of the pain, or the precentral cortex. For somatic (nociceptive) pain, stimulation of the periventricular or periaqueductal gray matter, or intraventricular infusion of morphine, may be useful. These operations are now indicated only in exceptional cases, as will be explained with reference to the author's long experience.

Brain Mapping↗

PubMed1998

Protease inhibitor coinfusion with amyloid beta-protein results in enhanced deposition and toxicity in rat brain.

Amyloid beta-protein, Abeta, is normally produced in brain and is cleared by unknown mechanisms. In Alzheimer's disease (AD), Abeta accumulates in plaque-like deposits and is implicated genetically in neurodegeneration. Here we investigate mechanisms for Abeta degradation and Abeta toxicity in vivo, focusing on the effects of Abeta40, which is the peptide that accumulates in apolipoprotein E4-associated AD. Chronic intraventricular infusion of Abeta40 into rat brain resulted in limited deposition and toxicity. Coinfusion of Abeta40 with the cysteine protease inhibitor leupeptin resulted in increased extracellular and intracellular Abeta immunoreactivity. Analysis of gliosis and TUNEL in neuron layers of the frontal and entorhinal cortex suggested that leupeptin exacerbated Abeta40 toxicity. This was supported further by the neuronal staining of cathepsin B in endosomes or lysosomes, colocalizing with intracellular Abeta immunoreactivity in pyknotic cells. Leupeptin plus Abeta40 caused limited but significant neuronal phospho-tau immunostaining in the entorhinal cortex. Intriguingly, Abeta40 plus leupeptin induced intracellular accumulation of the more toxic Abeta, Abeta42, in a small group of septal neurons. Leupeptin infusion previously has been reported to interfere with lysosomal proteolysis and to result in the accumulation of lipofuscin, dystrophic neurites, tau- and ubiquitin-positive inclusions, and structures resembling paired helical filaments. Coinfusion of Abeta40 with the serine protease inhibitor aprotinin also increased diffuse extracellular deposition but reduced astrocytosis and TUNEL and was not associated with intracellular Abeta staining. Collectively, these data suggest that an age or Alzheimer's-related defect in lysosomal/endosomal function could promote Abeta deposition and DNA fragmentation in neurons and glia similar to that found in Alzheimer's disease.

Alzheimer Disease↗

PubMed2005

Intraventricular or lumbar infusion test in adult communicating hydrocephalus? Practical consequences and clinical outcome of shunt operation.

BACKGROUND: To investigate the therapeutic consequences of restricting the CSF dynamic evaluation to a lumbar infusion test (LIT), as opposed to our formerly applied intraventricular assessment (VIT), in patients with communicating hydrocephalus (CH). METHOD: All patients over 18 years of age referred with clinical and radiological indication of treatment-requiring secondary CH (n = 50) or idiopathic normal-pressure hydrocephalus (INPH, n = 33) were subjected to a LIT. Subsequently, a combination of the results of the LIT (mainly the resistance to CSF outflow) and the clinical presentation determined whether to proceed with (a) VIT before a decision about shunt surgery, (b) shunt surgery or (c) no further diagnostic investigation or surgery. FINDINGS: In 88 percent of the patients with secondary CH and 80 percent of the patients with INPH the decision on shunt surgery was made after performing exclusively a LIT. The shunting success rate was 90 percent in patients with secondary CH and 82 percent in patients with INPH, which however in the latter group decreased to 76 percent, when including the patients undergoing an additional VIT. The achieved shunt success rates are equal or better, compared to the results from previous studies using intraventricular assessment. CONCLUSIONS: LIT and VIT are equally reliable for selecting shunt responsive patients with CH, using clinical improvement rate as the main criterion for comparison. The practical and economic consequences are substantial: the LIT can be performed in an outpatient setting, whereas VIT necessitates hospitalisation for 1-2 days including occupation of the neurosurgical theatre and postoperative neuro-intensive monitoring.

Adult↗

PubMed1978

Relationship of intravenous sodium bicarbonate infusions and cerebral intraventricular hemorrhage.

The incidence of cerebral intraventricular hemorrhage was determined by computed tomography in 100 infants with birth weights less than or equal to 1,500 gm. A comparison of IVH with serum sodium concentrations and the amount of intravenous sodium bicarbonate administered did not reveal a significant relationship. Analysis of the method of infusion of sodium bicarbonate indicated that the rapid infusion of hyperosmolar (M to M/12) sodium bicarbonate is associated with a significantly increased incidence of IVH.

Bicarbonates↗

PubMed1980

Diuretic effect of intraventricular and intravenous infusions of noradrenaline in conscious sheep.

Infusion of noradrenaline at rates between 32-160 nmol.min-1 for 30 min into one lateral cerebral ventricle of conscious sheep caused a diuresis which was accompanied by negative solute-free water reabsorption and which lasted for 90-120 min. The range of noradrenaline infusion rates used reflects differences between individual animals in the rate of infusion necessry to cause diuresis. Intracerebroventricular (ICV) infusion of noradrenaline at half the diuretic rate caused no significant changes in urine flow. The diuresis induced by ICV noradrenaline infusion was prevented by concurrent ICV administration of the alpha-adrenergic antagonist, phentolamine, but was not prevented by concurrent ICV administration of the beta antagonist, propranolol, or by concurrent intravenous infusion of phentolamine. Intravenous infusion of noradrenaline at rates that were diuretic by ICV infusion caused a diuresis of approximately 30 min duration which coincided with the period of intravenous noradrenaline infusion. This diuresis was prevented by concurrent intravenous infusion of phentolamine. These results were interpreted as indicating that the higher rates of ICV infusion of noradrenaline caused the prolonged water diuresis by acting at a site in the brain and, thereby, inhibiting the release of endogenous vasopressin. ICV infusion of noradrenaline at all rates was followed by a reduction in mean arterial blood pressure and pulse pressure with variable changes in heart rate and by depression of the rates of renal clearance of PAH, potassium and total solute.

Animals↗

PubMed2005

Intraventricular nerve growth factor infusion: a possible treatment for neurological deficits following hypoxic-ischemic brain injury in infants.

OBJECTIVE AND IMPORTANCE: Hypoxic-ischemic brain injuries in childhood are associated with poor neurological outcome. Unfortunately, no new therapeutic approaches have been proposed. Recently, animal studies show that nerve growth factor (NGF) can reduce neurological deficits following hypoxic-ischemic brain injuries. The objective of this study is to demonstrate the therapeutic effects of intraventricular NGF infusion in severe post-ischemic damage. CLINICAL PRESENTATION: Two infants, aged 9 and 8 months, with hypoxic-ischemic brain damage, secondary to prolonged cardiorespiratory arrest and stabilized after the conventional treatment, were treated with intraventricular NGF infusion. Before the therapy both infants were comatose with asymmetrical tetraparesis; their Glasgow Coma Scale (GCS) was 4 and 5, respectively. One month after the treatment, their GCS was 8 and 9, respectively. EEG examinations performed after the NGF infusion showed an increased alpha/theta ratio. MRI showed a reduction of malacic areas in the brain. A SPECT study, performed only in one infant, demonstrated that the NGF treatment resulted in an improvement of regional cerebral perfusion in right temporal and occipital cortices. INTERVENTION: The drug utilized was 2.5S NGF purified and lyophilized from male mouse submaxillary glands. NGF infusion was started about 30 days after the hypoxic-ischemic brain injury. 0.1 mg NGF was administered via the external drainage catheter into the right cerebral ventricle once a day for 10 days consecutively. CONCLUSION: Our observations are interesting, but further studies are necessary to confirm the effects of NGF in hypoxic-ischemic brain injuries in infants.

Cerebral Ventricles↗

PubMed1975

Interaction of estradiol and LHRH on LH release in rhesus females: evidence for a neural site of action.

The effects on LH release of infusing luteinizing hormone-releasing hormone (LHRH 80 mug/20 min) into the third ventricle, the pituitary, and the peripheral circulation were compared in spayed rhesus monkeys. Within 30 min after iv administration, serum LH concentrations increased to twice to preinfusion levels, and by 120 min declined to original values. Intraventricular or intrapituitary infusions of LHRH resulted in similar LH increments, but the peaks occurred somewhat later (70 to 90 min) and the elevations persisted beyond 200 min. Estradiol-17beta (E2) administered by a sc silastic capsule caused a 5-fold increase in serum E2 within 1 h and reduced serum LH levels by 65% within 4 h. The LH release caused by intrapituitary LHRH was significantly suppressed by maintaining for 72 h E2 concentrations near 100 pg/ml, a level inadequate for stimulating an LH surge. A comparable E2 treatment before intraventricular infusion of LHRH, however, did not inhibit LH release. This difference between the effects of intrapituitary and intraventricular LHRH was demonstrable only in E2-treated monkeys. Moreover, the release of LH after intraventricular infusion of LHRH in E2-treated females was blocked (P less than 0.001) by a single iv injection (90 min before LHRH) of haloperidol (1 mg/kg BW) or phentolamine (5 mg/kg), but was not altered by phenoxybenzamine (3 mg/kg) or propranolol (5 mg/kg). Without E2 pretreatment, LH release after intraventricular LHRH was enhanced by each drug. Phentolamine, injected into both E2- and non-E2-treated monkeys 90 min before an intrapituitary infusion of LHRH had no demonstrable effects on the patterns of serum LH. Our interpretation of these data is that E2 at a concentration below the level that triggers an LH surge has a dual action on LHRH-induced LH release in monkeys: an inhibitory effect exerted directly on the pituitary and a stimulatory effect on the brain. Furthermore, the paradoxical effects of the drugs with and without E2 are due to the involvement of two distinct neuronal systems. The postulated neural effects of both E2 and these drugs can be explained either by an increase in the quantity of injected or secreted LHRH which ultimately binds to LH-secreting cells or by the release of additional endogenous LH-stimulating agents together with ventricular LHRH.

Animals↗

PubMed1987

Continuous intraventricular morphine- or peptide-infusion for intractable cancer pain.

The continuous intraventricular administration of small daily doses of morphine by means of an implantable pump is an effective method of obtaining considerable pain reduction for patients suffering from otherwise untractable carcinoma pain. We consider this method of treatment to be an excellent alternative to the epidural and intrathecal application. Particularly in cases with obstruction of the spinal canal or in cases suffering from untractable pain in the face, neck or upper thoracic area. During the period of treatment, none of the patients involved in the study developed tolerance to morphine or specific opiate side effects. The programmable pump allows precise dosage which is adjusted to the requirements of the individual patient. The high cost of a pump is a justifyable investment in patients in good general condition with a life expectancy longer than 3 months. In most cases the patient may be cared for at home, making further hospitalization unnecessary.

Adult↗

PubMed1976

Central effect of beta adrenergic blocking agents on arterial blood pressure.

dl-Sotalol, dl-pindolol, d-propranolol and dl-propranolol were evaluated for central hypotensive activity in chloralose-anesthetized vagotomized cats. Blood pressure and average evoked potentials recorded from one postganglionic renal nerve were measured during intraventricular (lateral ventricle) or intravenous (radial vein) infusion of each agent. Potentials were evoked in the sympathetic nerve by single shocks to the sciatic nerve. Three concentrations (1, 3, 5 mM) of each compound were infused consecutively for 20 minutes per concentration. The decrease in blood pressure after intraventricular infusion of 1 mM pindolol, 5 mM d-propranolol and 3 mM dl-propranolol was significantly greater than the decrease after intravenous infusion of the same concentrations of each agent. The decrease in the average evoked potential after intraventricular infusion of the 5 mM concentration was greater than the response after intravenous infusion. Consecutive (1, 3, 5 mM) intraventricular or intravenous infusions of sotalol did not significantly change either parameter. During intraventricular infusion of 3 mM dl-propranolol blood pressures was markedly decreased at a time when the average evoked potential was unchanged; however, parallel changes were observed during infusion of the drug in vagotomized cats in which the carotid sinus baroreceptors were also denervated. The results indicate a) that intraventricular administration of d-propranolol, dl-propranolol and dl-pindolol, but not of dl-sotalol, decreased blood pressure and discharge evoked in the postganglionic renal nerve by an action on central sympathetic structures, and b) that baroreceptor activity during hypotension can overcome the depressant effect of dl-propranolol on potentials evoked reflexly in the renal nerve.

Animals↗

PubMed1993

Neurotropism of nerve growth factor for adult rat septal cholinergic axons in vivo.

Nerve growth factor (NGF) can induce sprouting of axotomized adult rat medial septum cholinergic neurons and promote their regeneration into septohippocampal nerve grafts and hippocampal formation. This study investigated the potential neurotropic (chemotactic/attracting) action of NGF in the adult rat cholinergic septohippocampal regeneration model. (i) Some animals received sciatic nerve grafts between the disconnected septum and hippocampal formations on each side. A 4-week infusion with NGF into the rostral portion of the lateral ventricle induced sprouting of cholinergic fibers in the dorsolateral septum with a gradient toward the lateral ventricle. However, the number of cholinergic axons entering the nerve bridge was only one-third that observed in vehicle-infused animals, suggesting that NGF had diverted many of the regrowing axons away from the nerve toward the ventricle. (ii) In animals implanted with nerves for 2 weeks and concurrently infused with NGF into the fornix, proximal to the lesion and grafts, cholinergic sprouting occurred in the mediodorsal septum, i.e., was oriented toward the infused fornix. Essentially no fibers had entered the nerve bridge, suggesting that all regrowing fibers had remained near the NGF source. (iii) When animals with a unilateral fimbria-fornix transection (but no nerve graft) were infused with NGF into the lateral ventricle on the opposite side, cholinergic sprouting was oriented toward the midline of the septum. (iv) Infusion of low doses of NGF directly into the (lesioned) septum induced a sprouting response localized around the infusion site. (v) No sprouting occurred when intraventricular NGF infusion was applied to normal (nonlesioned) animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1997

Intraventricular urokinase for the treatment of posthemorrhagic hydrocephalus.

This case series pilot study assessed the safety of intraventricular urokinase administration, alternating with cerebrospinal fluid (CSF) drainage. A secondary objective was to comment on whether this therapy achieves fibrinolysis, and whether this fibrinolysis is sufficient to prevent progression of hydrocephalus to requirement for ventriculoperitoneal shunt. Six preterm infants with progressive posthemorrhagic hydrocephalus requiring treatment with a ventricular drain received an infusion of intraventricular urokinase alternating with CSF drainage for 3 days. Of the 6 treated patients, the median gestation at birth was 26.5 weeks and the median age at treatment was 30 days. One patient had an elevation in CSF erythrocyte count most likely due to successful clot lysis. One patient had an elevated CSF leukocyte count consistent with transient meningeal irritation. No other side effects were noted. Fibrinolysis was achieved in the CSF, as documented by markedly elevated D-dimer levels. Clot size diminished ultrasonographically. However, all 6 patients eventually required a ventriculoperitoneal shunt. We conclude that intermittent infusion of intraventricular urokinase alternating with periods of CSF drainage is probably a safe way to achieve a fibrinolytic state. However, when administered at the relatively late point in the neonatal course when a ventricular drain is required, this fibrinolytic state is not sufficient to decrease the requirement for ventriculoperitoneal shunt.

Age of Onset↗

PubMed1975

Computer-assisted analysis of intraventricular pressure after mannitol administration.

The effect of prolonged mannitol infusion upon intraventricular pressure was investigated with the aid of a specially-designed automatic digital recording system; the data recorded were processed off-line by a minicomputer. The character of the pressure curves is thought to result from interaction between the mannitol effect and the observed system's shifting equilibrium position, which is caused by other factors. The character of the pressure curves prior to mannitol infusion must be taken into consideration in estimating the actual effect of the drug; the authors suggest that in certain cases it might be possible to decrease further the rate of mannitol administration. The advantages of statistical approach to the evaluation of intracranial pressure variations are discussed.

Analysis of Variance↗