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Treatment of nosocomial meningitis due to a multidrug resistant Acinetobacter baumannii with intraventricular colistin.

We report a case of serious nosocomial meningitis due to a multidrug-resistant Acinetobacter baumannii in a 23-year-old woman who had a posterior fossa craniotomy with upper cervical laminectomy for excision of a meningioma at the level of foramen magnum. Post-operatively, she had neck pain with continuous fever and deterioration in the level of consciousness and convulsions. The CSF was turbid and had neutrophil pleocytosis. A multidrug-resistant Acinetobacter baumannii was isolated from the blood and CSF. The patient failed high doses of imipenem, ciprofloxacin and systemic colistin but responded well to intraventricular injections of colistin 125,000 units twice daily for 3 weeks. No apparent side effects were noticed. We have reviewed other similar cases reported in the literature.

Acinetobacter Infections↗

Physiological role of neuropeptide Y (NPY) in control of anterior pituitary hormone release in the rat.

Neuropeptide Y (NPY) is a peptide originally isolated from porcine brain and subsequently shown to be widely distributed in the body of several species, including man. Neuropeptide Y is a circulating peptide; however, blood levels were higher in portal than peripheral blood of anesthesized rats. Earlier studies in ovariectomized and intact male rats have shown that intraventricular injection of NPY inhibits release of growth hormone (GH) and luteinizing hormone (LH) without producing significant modification of plasma follicle stimulating hormone (FSH) and thyrotropin stimulating hormone (TSH). In the male low doses of NPY elevate prolactin (PRL) whereas high doses suppress its release. To assess the physiologic significance of these actions, we injected a highly specific anti-NPY serum (aNPY) into the third cerebral ventricle (3V) of unrestrained male, ovariectomized, and ovariectomized, estrogen progesterone blocked rats and measured plasma GH, PRL, LH and TSH by blood sampling via indwelling jugular catheters. Third ventricular injection of aNPY (2 microliters of 1:10 dilution) caused a significant elevation of plasma GH levels after 3 and 4 h compared to the values in NRS (1:10)-injected rats. To determine if these changes were due to alterations in pituitary responsiveness to somatostatin, the rats were injected intravenously with a challenge dose of somatostatin (0.5 microgram) 2 h after previous injection of aNPY or NRS, and blood samples were taken every 10 min for 30 min. The responses did not differ in both groups which indicated that the antiserum was not acting directly on the pituitary gland.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[The electrical activity of the hippocampus in rats centrally administered GABA agonists and antagonists].

In unrestrained rats, frequency ranges of dorsal hippocampus electrograms were studied after intraventricular injections of the GABA, muscimol, baclofen, bicuculline and picrotoxin. The data obtained corroborates the idea of an interrelationship between the agonists and antagonists of the GABA receptors. A possibility of participation of these receptors in the formation and/or modulation of total electrical hippocampal activity, is discussed.

Animals↗

[The brain catecholamine system in narcotic-dependent rats under the action of oxytocin].

Intraventricular injection of oxytocin exerted a selective effect on catecholamine metabolism in microchondrial fractions of different brain formations of normal and narcotic drug-dependent animals. The drug-dependent group showed a higher level of the brain catecholamines as compared to the controls, oxytocin decreasing the catecholamine level in this group. The oxytocin modulatory role in the processes of narcotic drug-dependence, is discussed.

Animals↗

Fluorocarbon emulsion as a potential contrast medium in the subarachnoid space and brain tissue. Experiments in cats.

Ventriculosubarachnoid perfusion with oxygenated fluorocarbon emulsion has been used in the treatment of severe cerebral ischemia in cats. The perfusion vehicle is prepared mimicking cerebrospinal fluid in terms of electrolyte content, osmolality, pH, glucose and amino acids. Fluorocarbon emulsion is prepared with the vehicle as the external phase and charged with high partial pressures of oxygen. This fluorocarbon emulsion has been well-tolerated by the central nervous system. In addition to delivering oxygen to the ischemic tissues via the ventriculosubarachnoid space, the fluorocarbon emulsion has an absorption coefficient higher than normal brain and cerebrospinal fluid. This property makes it easily detected on the CT scan. Determination of appearance, attenuation, distribution, and absorption of the fluorocarbon has been performed in cats after direct intraventricular injection of the substances and after perfusion of the emulsion. The results of these experiments stress the possibility of using a fluorocarbon emulsion as a potential contrast medium in the brain and subarachnoid space, particularly after brain anoxia.

Animals↗

[Predatory aggressiveness of the rat after intraventricular administration of individual brain-specific proteins of the S-100 group and their peptide fragments].

Intraventricular injections to rats of the basic fraction of the brain specific protein S-100 in a concentration of 3 mg/ml, significantly facilitates the formation of their predatory aggression induced by the alimentary deprivation and social isolation, expressed in mice killing. This effect is not produced by fragments of S-100 molecules obtained as a result of treatment of the basic protein fraction by proteolytic enzymes. Administration of the minor S-100 fraction, albumin and rats summate brain proteins did not influence animals predatory aggression.

Aggression↗

[Spontaneous motor activity and radial-maze learning in rats neonatally treated with 6-hydroxydopamine].

6-Hydroxydopamine (6-OHDA: 35 micrograms) was intraventricularly injected twice to rat pups with desmethylimipramine pretreatment (20 mg/kg, sc) at 3 and 6 days of age in order to selectively deplete brain dopamine. At every 3 days from 7 through 31 days of age, the pups were tested for their locomotive activity in the open-field. The locomotive activity was measured by two different methods (counting the number of sections traversed and time-sampling behavioral items such as pivoting, creeping and walking). The results showed that significant increases in the activities by the both methods were produced by the treatment of 6-OHDA throughout the observation days. From 80 days of age the animals were trained 1 trial per day on radial 8-arm maze learning. Rats treated with 6-OHDA took significantly more trials to attain the learning criterion (at least 7 correct choices in the first 8 choices for 5 consecutive trials) as compared with the control animals. This retardation, however, was mainly derived from that of familiarization (habituation) to the apparatus in the beginning of the training. In conclusion, the neonatal treatments with 6-OHDA produced pronounced hyperactivity during the developmental period but little deficit in learning ability during the adult period.

Animals↗

Disrupted retention of the classically conditioned nictitating membrane response in rabbits with aluminum-induced neurofibrillary degeneration.

Rabbits underwent classical conditioning of the nictitating membrane response (NMR) to a tone conditioned stimulus and an air puff unconditioned stimulus until they emitted 90 percent or greater conditioned responses (CRs) for two consecutive days. They then received intraventricular injection of aluminum chloride, hydrochloric acid or saline. Ten days post injection they were tested for retention of the conditioned response. Animals injected with saline or hydrochloric acid emitted an average of greater than 90 percent CRs. Aluminum injected rabbits, in contrast, emitted an average of only about 40 percent CRs. This disruption of retention of conditioning in aluminum treated rabbits could not be attributed to deficits in sensory or motor processes or to illness. Neuropathological analysis revealed widespread neurofibrillary tangle formation in the aluminum treated animals. Furthermore, the degree of neurofibrillary degeneration was significantly negatively correlated with retention of the CR. The results are considered in the context of using the rabbit NMR preparation as a model system for studying age-related conditioning disorders.

Aluminum↗

Application of [125I]iodocyanopindolol to measure 5-hydroxytryptamine1B receptors in the brain of the rat.

In this study, [125I]iodocyanopindolol ([125I]ICYP), in the presence of isoproterenol, was used to label 5-hydroxytryptamine1B (5-HT1B) receptors in homogenates of the cortex, substantia nigra and caudate-putamen of the rat. The determination of the appropriate concentrations of isoproterenol required to block optimally beta adrenoceptors whereas producing minimal occupancy of 5-HT1B receptors was achieved by generating isotherms for isoproterenol at multiple concentrations of [125I]ICYP. When different concentrations of isoproterenol were used with increasing concentrations of [125I]ICYP, a linear Scatchard transformation of the saturation curve was achieved, even with ligand concentrations about 6-fold greater than the KD for [125I]ICYP. Competition for [125I]ICYP (100 pM) labeled binding sites by 15 serotonin agonists or antagonists was adequately described by a single site model, and the affinity of these drugs for the site labeled by [125I]ICYP was similar to that determined previously when using indirect methods to label 5-HT1B receptors. Serotonin itself showed high affinity for this binding site as did two antagonists, metergoline and methiothepin. By contrast, drugs thought to be selective for the 5-HT1A receptor (e.g., 8-hydroxy-2-(di-n-propylamino)tetralin, buspirone and spiperone) showed very weak affinity for the binding site labeled with [125I]ICYP. The effect of nucleotide regulation on [125I]ICYP binding at 5-HT1B receptors also was evaluated. It was determined that GTP had little effect on the binding of [125I]ICYP, reducing total binding by only 15% and shifting the displacement curve of 5-HT by a factor of less than two. The regulation of 5-HT1B receptors, labeled by [125I]ICYP, also was evaluated. Intraventricular injections of 5.7-dihydroxytryptamine increased significantly the number of 5-HT1B receptors in the caudate-putamen; this treatment had no effect on 5-HT1B binding sites either in the cortex or substantia nigra. The regulatable binding site for [125I]ICYP in the caudate-putamen had a pharmacological profile very similar to that of the 5-HT1B binding site in the cortex. [125I]ICYP appears to be a useful ligand to measure 5-HT1B receptors in the brain of the rat. The localized increase in 5-HT1B receptors in the caudate-putamen after destruction of central serotonergic neurons might indicate that the majority of 5-HT1B receptors in this area of brain are not located on serotonergic nerve terminals.

5,7-Dihydroxytryptamine↗

The barrier systems in the choroidal plexuses of the chick embryo studied by means of horseradish peroxidase.

The development of the blood-cerebrospinal fluid (CSF) and cerebrospinal fluid-blood barriers, and the differentiation of the choroidal vessel wall, have been ultrastructurally investigated in the choroidal plexuses of the lateral ventricles of 10, 15, 18 and 21 day chicken embryos, fixed in normal conditions and also after intracardial and intraventricular injection of horseradish peroxidase. In all the analyzed developmental stages the choroidal epithelial cells seem able to endocytose and degradate, in their lysosomal apparatus, the tracer molecules reaching their ventricular and basolateral sides. The intravascularly injected horseradish peroxidase can enter the ventricular cavity by interepithelial route only at 10th incubation day, when the tight intercellular junctions are not formed everywhere, while a transepithelial transport is always hindered. The marker injected into the ventricular cavity reaches the subepithelial compartment and the blood stream, at 10th incubation day by interepithelial as well as transepithelial route and, successively, by transepithelial vesicular transport alone. The differentiation processes undergone by the choroidal blood vessels consist in a progressive thinning of the endothelial cells, appearance of pores, already numerous at 15th incubation day, and formation of the endothelial basement lamina, the final event in vessel wall maturation.

Animals↗

Transport of diphenhydramine in the central nervous system.

The transport and metabolism of diphenhydramine was studied in vitro in the isolated rabbit choroid plexus and in vivo in New Zealand white rabbits and Sprague-Dawley rats. In vitro, [14C] diphenhydramine was accumulated by a saturable, energy-requiring system in choroid plexus. In vivo, 20 min after intraventricular injection into rabbits, [14C]diphenhydramine was cleared from cerebrospinal fluid much more rapidly than [3H]sucrose, a molecule transported in the central nervous system by simple diffusion. In vivo, employing the in situ rat brain perfusion technique, [14C]diphenhydramine was cleared from the cerebral perfusion fluid as rapidly as [14C]diazepam. However, the clearance of [14C]diphenhydramine, but not [14C]diazepam, was inhibited by the addition of 10 mM unlabeled diphenhydramine to the perfusate. These in vivo and in vitro results show that diphenhydramine, unlike diazepam, is transported between blood, brain and cerebrospinal fluid, in part, by saturable, carrier-mediated transport processes at both the blood-brain and blood-cerebrospinal fluid barriers.

Animals↗

[Inherent behavioral activity of rats administered different fractions of brain-specific S-100 proteins].

The intraventricular injection of brain specific S-100 proteins leads to the prolonged heterochronous changes of the inherent rat behaviour forms during the period of water and food needs restitution. The effects of various doses of S-100 proteins fractions on the behavioural activity differs in the degree of expression and in time of their onset. The specific influence of some S-100 proteins fractions on duration of the different inherent forms of rat behaviour can be explained by plurality of molecular mechanisms of their effects.

Animals↗

On the mechanism of central effect of thyroxine on body temperature in dogs.

The effect of intraventricular injection of thyroxine 1 microgram/animal on body temperature was studied in dogs under resting conditions: at normal ambient temperature, at high ambient temperature (35 degrees C) and during administration of pyrogen. Besides, changes in body temperature were elucidated in dogs performing physical exercise following I.V. T4 injection in the same dose. Thyroxine exerted its central action on body temperature only in dogs performing physical exercise.

Animals↗

Short- and long-term effects of intraventricular 6-hydroxydopamine in rats pretreated with a monoamine oxidase inhibitor.

Bilateral intraventricular injections of high dose (2 X 250 microgram) of 6-hydroxydopamine to rats pretreated with nialamide produced a pronounced hyperactivity persisting for several hours and induced permanent aggressiveness. Only 50% rat survived the treatment for longer than a week, the explorative activity of the survivors was inhibited for over 2 months. The brain catecholamine content was depressed for at least 15 months, while no long-term changes of serotonin level were observed. The hyperactivity, aggressiveness and hypothermia produced by apomorphine were enhanced in centrally chemosympathectomized rats, while the hyperactivity produced by D-amphetamine or amantadine remained inaffected. The results confirm the development of dopamine receptor supersensitivity following central chemosympathectomy, and indicate a possibility of employing the supersensitivity model for distinguishing between pre- and postsynaptic action of dopaminergic stimulants.

Aggression↗

Inhibitory effect of intraventricularly applied D-galactosamine on incorporation of labelled precursors into RNA and protein of rat hippocampus.

Ten mumoles of intraventricularly injected D-galactosamine (GalN) inhibited the incorporation of [(3)H]-guanosine and [(3)H]-leucine into RNA and protein of the rat hippocampus, respectively. The inhibition of guanosine incorporation of appr. 80% occurred during the first 30 min after GalN treatment and lasted at least 4 h. The incorporation of leucine was inhibited by appr. 30% only; this effect occurred not earlier than 90 min after GalN injection. The results demonstrate a similar effect of GalN on brain macromolecular syntheses as already observed in the liver suggesting the same mechanism of action, namely trapping of uridine phosphates. The results are discussed with regard to the amnesic effect of GalN observed on the retention of a brightness discrimination in rats.

Animals↗

[Influence of renin on the effects of electric stimulation on the ventromedial hypothalamus].

The influence of intraventricular injection of different doses of renin on the effects of electrical stimulation of the ventromedial hypothalamus was studied. Injection of renin (10 micrograms/kg) into the lateral ventricles of the brain of experimental animals elicited a prolonged elevation of arterial pressure and a decrease of the heart rate, while given in doses of 20 and 30 micrograms/kg it also provoked arrhythmias and ventricular extrasystoles, and a lowering of the threshold of ventromedial hypothalamus stimulation. It was found that under the central action of renin, a short-term stimulation of the ventromedial hypothalamus provoked ventricular extrasystoles.

Animals↗

[Role of central and peripheral serotoninergic mechanisms].

In male Wistar rats overheated by an infrared lamp, intraperitoneal serotonin administration led to a more rapid overheating than in control, the effect of serotonin being dose-dependent and reduced after i.p. administration of cyproheptadine. Stimulation of the brain serotonin receptors did not affect the development of hyperthermia, whereas the blockade of brain serotonin receptors by intraventricular injections of cyproheptadine or the depletion of brain serotonin by p-chlorophenylalanine resulted in significantly more obvious hyperthermia than in control.

Animals↗