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PubMed1989

Effects of intraventricular infusion of corticotropin-releasing factor on VMH-lesioned obese rats.

Corticotropin-releasing factor (CRF) has been administered into the third ventricle of sham-operated and ventromedial hypothalamic (VMH)-lesioned rats in acute and chronic experiments. After a single 5-microgram injection of CRF, there was an acute reduction of food intake in both sham-operated and VMH-lesioned rats that persisted for 3 h. The effect was still present in the VMH-lesioned rats between 3 and 6 h but had dissipated in the sham-operated controls. Guanosine 5'-diphosphate (GDP) binding to mitochondria from interscapular brown adipose tissue was used as an index of thermogenic activity in this tissue. In 21-h food-deprived rats, GDP binding was significantly lower in VMH-lesioned than in sham-operated animals. Although the mean increase in sham-operated animals was increased, this was not significantly different from saline-injected controls. In the VMH-lesioned rats, however, CRF acutely increased GDP binding to values not different than those of the sham-operated controls. Serum corticosterone was significantly lower in the VMH-lesioned rats, but both groups showed a significant stimulation by CRF during a 7-day infusion of CRF (4.8 micrograms/day) into the third ventricle. Food intake was significantly depressed in the VMH-lesioned animals that received CRF, from values of 35 g/day to approximately 25 g/day. Body weight showed a slow steady decrease, having fallen by nearly 15 g at the end of the 7-day infusion period. In contrast the mean value in the VMH-lesioned controls had significantly higher in CRF-infused animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed1980

Effects of intraventricular infusions of 6-hydroxydopamine (6-OHDA) on pituitary LH release and ovulation in the rabbit.

Repeated infusions of 6-hydroxydopamine (6-OHDA) into the third ventricle of the rabbit brain in dosages shown to depress hypothalamic norepinephrine (NE) by more than 80% failed to block the copulation-induced ovulatory surge of LH release from the adenohypophysis in estrogen-primed, multiparous New Zealand White does. Only when infusion of the neurotoxin produced a basal hypothalamic lesion did it intercept the coital stimulus and prevent LH release. In 5 rabbits the initial infusion of 6-OHDA stimulated an LH surge presumably by activating NE release from noradrenergic nerve endings. The failure of chronic depletion of hypothalamic NE to prevent coitally-induced LH release suggests that the transmitter may normally play only a modulatory role in hypothalamopituitary activation in the reflex ovulator, as has also been proposed for its function in cyclic ovulation in the rat. The results suggest that alternative systems may be brought into play to subserve reproductive mechanisms when hypothalamic NE is chronically depleted.

Animals↗
PubMed1978

The delta EEG (sleep)-inducing peptide (DSIP). XI. Amino-acid analysis, sequence, synthesis and activity of the nonapeptide.

A peptide which induces slow-wave EEG (sleep) after intraventricular infusion into the brain has been isolated from the extracorporeal dialysate of cerebral venous blood in rabbits submitted to hypnogenic electrical stimulation of the intralaminar thalamic area. It was shown by amino-acid analysis and sequence determination to be Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu and named "Delta Sleep-Inducing Peptide" (DSIP). This compound was synthesized as well as 5 possible metabolic products (1--8, 2--9, 2--8, 1--4 and 5--9), 2 nonapeptide analogues (with one and two amino-acids exchanged) and a related tripeptide (Trp-Ser-Glu). All 9 synthetic peptides were infused intraventricularly in rabbits (6 nmol/kg in 0.05 ml of CSF-like solution over 3.5 min) and tested under double-blind conditions. A total of 61 rabbits including controls were used. The EEG from the frontal neocortex and the limbic archicortex were subjected to direct fast-Fourier transformation and analyzed by an 1108 computer system. A highly specific delta and spindle EEG-enhancing effect of the synthetic DSIP could be demonstrated. The mean increase of EEG delta activity reached 35% in the neocortex and limbic cortex as compared to control animals receiving CSF-like solution or any of the other 8 peptides. The final chemical characterization of the synthetic DSIP revealed that only the pure alpha-aspartyl peptide is highly active in contrast to its beta-Asp isomer. A neurohumoral modulating and programming activity was suggested.

Amino Acid Sequence↗
PubMed2004

[Structural characteristics of astrocytes from the rat hippocampus in postischemia].

The aim of this investigation was to study the distribution and structural organization of rat hippocampal astrocytes containing immunoreactive glial fibrillary acidic protein (GFAP) after ischemic damage of the brain in the animals treated with intraventricular infusion of creatine as a neuroprotective drug, and in those which received no treatment. Using the methods of light microscopy and immunocytochemistry, the brain of 26 mature Sprague-Dawley (Koltushi) rats was studied. Some animals were narcotized and subjected to general brain ischemia (lasting for 12 min) followed by a reperfusion (for 7 days). Creatine was infused intraventricularly to 11 animals using an automatic Alzet osmotic minipump. It was found that GFAP-immunoreactive hippocampal astrocytes were concentrated within two major areas (stratum lacunosum-moleculare CA1 and fascia dentata stratum polymorphae). As a result of neuroprotective effect of creatine, moderate ischemic damage of the hippocampus was not followed by the changes in the zones of activated astrocyte localization. Redistribution of GFAP-positive astrocytes in postischemic period was caused by the loss of pyramidal neurons in cytoarchitectonic field CA1. Complete loss of pyramidal neurons in this hippocampal area resulted in a qualitatively new level of astrocyte activation--their proliferation.

Animals↗
PubMed1995

Urokinase infusion for severe intraventricular haemorrhage.

The purpose of this study was to explore in patients with intraventricular haematomas the effectiveness and complication rate of a treatment protocol including standard ventriculostomy and application of urokinase via the catheter. Our series includes 16 patients with severe CT-diagnosed intraparenchymal and predominantly intraventricular haemorrhages. In all cases, ventricular drainage was performed. Urokinase treatment was started immediately with intraventricular infusions of 10,000 U urokinase in 5 ml sterile physiological saline every 12 hours. Twelve patients had an excellent outcome, three good and one poor. There were no complications related to urokinase therapy. Side effects of the infusion volume were profuse sweating and headache which were present at 10 ml total infusion volume, but disappeared after reduction to 5 ml. A group of five patients with comparable lesions treated only with ventriculostomy served as controls. Two of them had a good outcome, two a poor one and one died. The late results in the urokinase-treated group were also favourable. Only one of the patients developed hydrocephalus and was shunted. In the control group, two patients required shunting for delayed hydrocephalus. We conclude that this protocol for urokinase treatment is safe and effective and can be used in almost all patients with intracerebroventricular haemorrhage.

Adult↗
PubMedDate not supplied

Implanted system for intraventricular drug infusion in central nervous system tumors.

We have developed a totally implanted drug delivery system capable of maintaining constant cerebrospinal fluid (CSF) drug levels through continuous intraventricular infusion in outpatients. This system was used to infuse methotrexate (MTX) intraventricularly in seven patients with incurable CNS malignancies. One patient with meningeal diffuse histiocytic lymphoma, five patients with grade III--IV astrocytomas, and one patient with melanoma metastatic to the brain were treated with this system for 4--40+ weeks. The system consists of an Infusaid pump (Metal Bellows Corp, Sharon, MA), implanted subcutaneously in the infraclavicular fossa, which delivers a drug-containing solution at a set rate (3--5 mg/day) through a subcutaneous silastic catheter to a Rickham ventriculostomy reservoir and into a lateral ventricle. System placement and maintenance were readily tolerated. Constant MTX infusion at rates of 0.5--10 mg/day generated corresponding constant CSF drug levels in the range of 2--30 microM. Simultaneous serum MTX levels were undetectable (less than 0.01 microM), indicative of a 200- to 3000-fold selective regional concentration advantage for this approach. CNS toxic effects included transient meningism and fever (four patients), transverse myelitis (one), and the development of a diffuse hypodensity of the white matter on computerized tomographic scan which was not associated with any neurologic deficit (two). The usual systemic toxic effects (myelosuppression and mucositis) of MTX were not seen. The patient with meningeal lymphoma has had a complete remission of meningeal disease continuing past 10 months. Computerized tomography showed that three of the five high-grade astrocytomas had 25% size reductions in tumors lasting 2--6 months. This system may provide a means for improved treatment of meningeal tumor although its role in the treatment of intraparenchymal brain tumors is less clear. Of greater consequence, however, is the demonstrated ability of this system to maintain a controlled CSF drug level which should prove useful in many areas of therapeutic research.

Adult↗
PubMed2004

Treatment of transmissible spongiform encephalopathy by intraventricular drug infusion in animal models.

The therapeutic efficacy of direct drug infusion into the brain, the target organ of transmissible spongiform encephalopathies, was assessed in transgenic mice intracerebrally infected with 263K scrapie agent. Pentosan polysulfate (PPS) gave the most dramatic prolongation of the incubation period, and amphotericin B had intermediate effects, but antimalarial drugs such as quinacrine gave no significant prolongation. Treatment with the highest dose of PPS at an early or late stage of the infection prolonged the incubation time by 2.4 or 1.7 times that of the control mice, respectively. PPS infusion decreased not only abnormal prion protein deposition but also neurodegenerative changes and infectivity. These alterations were observed within the brain hemisphere fitted with an intraventricular infusion cannula but not within the contralateral hemisphere, even at the terminal disease stage long after the infusion had ended. Therapeutic effects of PPS were also demonstrated in mice infected with either RML agent or Fukuoka-1 agent. However, at doses higher than that providing the maximal effects, intraventricular PPS infusion caused adverse effects such as hematoma formation in the experimental animals. These findings indicate that intraventricular PPS infusion might be useful for the treatment of transmissible spongiform encephalopathies in humans, providing that the therapeutic dosage is carefully evaluated.

Animals↗
PubMed1983

The effects of intraventricular prolactin infusions on pituitary responsiveness to thyrotropin-releasing hormone, 5-hydroxytryptophan or morphine in rhesus monkeys.

The effects of intraventricular infusions of ovine prolactin (oPrl) on both endogenous prolactin levels in serum, and upon the release of prolactin and cortisol in response to treatment with either TRH, 5-HTP or morphine were studied in rhesus monkeys. A single injection of oPrl (10.8 micrograms) into the lateral ventricles of castrated males resulted in CSF levels of around 350 ng/ml 60 min later, but no oPrl could be detected in the blood. Endogenous (rhesus) prolactin levels in serum fell during this time to about half their initial values in oPrl-treated animals but not in the bovine serum albumin (BSA)-injected controls. Ovine prolactin was infused continuously into either the lateral or third ventricles of ovariectomized, estrogen-treated females for 6 days from an osmotic minipump (2.7 micrograms/h). CSF levels of oPrl were about 250 ng/ml though none was found in the serum. The release of endogenous prolactin by TRH (1 microgram) was greatly reduced compared with BSA-treated controls. 5-HTP (2.5 mg/kg together with carbidopa pretreatment) also stimulated much less prolactin release in females chronically infused with oPrl and there was some evidence for a similar effect in males following a single intraventricular injection. CSF levels of 5-HTP itself, and of 5-HIAA and HVA were similar throughout this experiment in both oPrl and BSA-infused animals. Finally, prolactin released by morphine (5 mg) was highly attenuated in females receiving oPrl intraventricularly. In contrast to those on serum prolactin, the effects of these various treatments on serum cortisol were unaltered by intraventricular oPrl. These results suggest that the primate brain contains a neural system which is directly responsive to prolactin, and which can modulate this hormone's release under either basal conditions or following treatment with substances that stimulate its release by acting either directly on the pituitary or upon the neural systems regulating pituitary function. These results are compatible with the presence of increased dopamine in the portal blood, though this was not measured in these experiments.

5-Hydroxytryptophan↗
PubMed1999

Intraventricular lactate infusion attenuates the transactivational effects of the glucose antimetabolite, 2-deoxy-D-glucose, on hypothalamic vasopressinergic neurons.

Glucopenia stimulates neurohypophyseal arginine vasopressin (AVP) secretion and expression of the transcription factor, Fos, by paraventricular (PVN) and supraoptic (SON) magnocellular neurons. Recent studies suggest that central compensatory responses to glucose substrate imbalance are initiated by regulatory signals of periventricular origin. Since the glycolytic endproduct, lactate, is a preferred substrate for central neuronal respiration, we investigated whether intracerebroventricular (i.c.v.) infusion of this monocarboxylate fuel attenuates transactivational effects of glucoprivation on PVN and SON AVP neurons. Continuous intraventricular infusion of sodium lactate (1.0 or 10.0 microM/h) or vehicle was initiated before intraperitoneal (i.p.) injection of the glucose antimetabolite, 2-deoxy-D-glucose (2DG), or saline. Anterior hypothalamic tissue obtained 2 h after systemic injections was processed for colocalization of cytoplasmic AVP- and nuclear Fos-immunoreactivity (Fos-ir). Fos-ir was absent from the PVN and SON of rats treated by i.c.v. infusion of vehicle or either dose of lactate. Intraventricular administration of 10.0 microM lactate/h, but not the lower dose, significantly decreased mean numbers of colabeled AVP neurons in each structure in glucoprivic animals. These data suggest that Fos stimulus-transcription cascade is activated in these cells by decreased central availability of this monocarboxylate fuel, and that cellular sources of regulatory signaling of lactate utilization exist within the periventricular CNS.

Animals↗
PubMed1998

Intraventricular streptokinase infusion in acute post-haemorrhagic hydrocephalus.

Neonatal post-haemorrhagic hydrocephalus is a clinical condition with a high mortality and long-term morbidity. Its clinical management is difficult and not well standardized. We describe the case of a term baby suffering from acute intracranial hypertension caused by an intraventricular and thalamic haemorrhage. In this case, the external ventricular drain inserted to control intracranial pressure was ineffective because of repeated obstructions due to blood clots. Continuous intraventricular infusion of streptokinase of 20,000 U/day allowed quick lysis of the clots, drainage of the cerebrospinal fluid and relief from the coma. Although it did not prevent a permanent ventriculoperitoneal shunt, we obtained reabsorption of the intraventricular haemorrhage without rebleeding complications. We suggest the use of low-dose fibrinolytic infusion through an external drain for the treatment of acute intracranial hypertension following intraventricular haemorrhage in term infants.

Acute Disease↗
PubMed1991

Muscarinic receptor subtypes and sexual behavior in female rats.

Cholinergic muscarinic systems are involved in the regulation of female sexual behavior in rats and hamsters. This series of experiments was designed to determine whether sexual behavior in female rats is controlled preferentially by one of the traditional muscarinic receptor subtypes. Intraventricular infusion of the muscarinic antagonist scopolamine (10 micrograms bilaterally) which binds with high affinity to both M1 and M2 subtypes inhibited sexual behavior, as indicated by the incidence of lordosis, in ovariectomized rats treated with estrogen and progesterone. In contrast, the M1-selective antagonist pirenzepine failed to reduce the incidence of lordosis following intraventricular infusion (10 to 80 micrograms bilaterally). Biochemical analyses revealed that intraventricular infusion of scopolamine (10 micrograms bilaterally) inhibited both M1 and M2 binding in brain tissues while intraventricular infusion of pirenzepine (10 micrograms bilaterally) completely inhibited M1 binding without affecting M2 binding. Intraventricular infusions of the acetylcholinesterase inhibitor physostigmine (10 micrograms bilaterally), the cholinergic agonist carbachol (1 microgram bilaterally), and the muscarinic agonist oxotremorine-M (0.1 micrograms bilaterally) activated lordosis in ovariectomized females primed with low doses of estrogen. In contrast, the putative M1 agonist McN-A-343 failed to significantly increase lordosis following intraventricular infusions (1, 10, 20 micrograms bilaterally). According to biochemical results, the ability of these agents to activate lordosis in female rats was related to their affinities for M2 binding sites not M1 binding sites. In a final experiment, estrogen treatment of ovariectomized rats did not alter muscarinic subtype binding in several brain areas as measured by the M1-selective ligand [3H] pirenzepine and the M2-selective ligand [3H] oxotremorine-M. The results of these experiments confirm that muscarinic systems contribute to the regulation of lordosis in female rats and indicate that M2 binding sites rather than M1 binding sites may be a critical component of this regulation.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1980

A microstereotactic approach to small CNS lesions. Part II; Adjuvant therapy. Clinical potential and toxicity of intraventricular lymph infusion.

A technique is described for adjuvant therapy of small central nervous system tumors after their removal. The feasibility of direct application of lymphocytes from the thoracic duct to the ventricular system of cats has been explored. Reduction of the antigenic mass by techniques described in part I of this paper is probably crucial. Patients with gliomas are known to have circulating tumor-specific lymphocytes which may not have direct access to the CNS. This study demonstrated no toxicity from the chronic intraventricular infusion of thoracic duct lymph in cats.

Animals↗
PubMed1980

Evidence for a cholecystokinin gut-brain axis with modulation by bombesin.

The relationship between cerebrospinal fluid and plasma cholecystokinin (CCK) levels was investigated by simultaneous withdrawal of CSF and blood from anesthetized mongrel dogs and measurement of CCK immunoreactivity by radioimmunoassay. A significant correlation occurred between CSF and plasma levels of CCK. During a CCK IV infusion, a statistically significant inverse correlation was noted between CSF and plasma values, while no significant relationship was noted during a bombesin (BBS) IV infusion. When infusion data were analyzed together with the appropriate baseline data, polynomial analysis revealed significant biphasic relationships for both CCK and BBS infusion studies. Intraventricular infusion of CCK did not alter plasma levels. These data suggest that existence of a mechanism relating CSF to plasma CCK levels (a gut to brain axis) with possible modulation or suppression by BBS.

Animals↗