SEARCH · PubMed Health

Results for “Infusions, Intraventricular”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,351 records · Page 75Linked to original sources

PubMed1996

Delayed intravenous administration of basic fibroblast growth factor (bFGF) reduces infarct volume in a model of focal cerebral ischemia/reperfusion in the rat.

Basic fibroblast growth factor (bFGF) is a potent neurotrophic and vasoactive peptide. Previous studies have shown that intraventricularly-administered bFGF reduces the size of cerebral infarcts following focal ischemia. In the current study, we tested the effects of intravenously-administered bFGF in a model of focal ischemia/reperfusion. The right middle cerebral artery of mature male Wistar rats was occluded by intraluminal suture. After 2 h of occlusion, the suture was removed and intravenous infusion of bFGF in vehicle (45 micrograms/kg/h) or vehicle alone was begun, lasting 3 h. Animals were weighed and evaluated neurologically until sacrifice 7 days after ischemia. The volume of cerebral infarcts was then determined by H and E staining and image analysis. We found a 40% reduction in infarct volume in bFGF- vs. vehicle-treated rats (n = 11 vs. 11, P < 0.05). Reduction in infarct volume was associated with improved neurological outcome and regained body weight in bFGF-treated animals (both P < 0.05). No change in blood pressure was found during bFGF treatment. These results show that the delayed intravenous administration of bFGF reduces infarct size in this model of focal ischemia/reperfusion. The mechanisms of infarct reduction may include direct cytoprotective and/or vasoactive effects.

Animals↗

PubMed1989

Behavioural and electrocortical effects after injection of two ornithine decarboxylase inhibitors into several areas of the brain in the rat.

The behavioural and electrocortical effects of alpha-methylornithine and alpha-difluoromethylornithine, two ornithine decarboxylase inhibitors, were evaluated after their infusion into several areas of the brain in the rat. Both compounds induced, in dose-dependent manner, similar epileptogenic effects, stereotyped behaviour and postural asymmetry, depending upon the site of injection. Unilateral injection of DFMO into the entopeduncular nucleus or the substantia nigra pars reticulata, caused an increase in locomotor activity. Unilateral injection of DFMO into the caudate nucleus or the substantia nigra pars compacta had no effect on locomotor activity. Among the areas of the brain studied, the most sensitive site from which electrocortical epileptogenic disorders were evoked, was the hippocampus. The GABA agonist muscimol, infused prior to DFMO, resulted in an anticonvulsant action, while DFMO, infused prior to putrescine, increased the convulsant properties of putrescine. In conclusion, these results indicate that DFMO and alpha-methylornithine produced epileptogenic effects after their intracerebral infusion and suggest that may act as analogues of putrescine.

Amygdala↗

PubMed1985

Oxytocin stimulates lordosis behavior in female rats.

Oxytocin, either intraperitoneally injected (200 ng/rat) or intracerebroventricularly infused (1 ng/rat in 4 microliters saline) 60 and 15 min respectively before testing, significantly increased the lordosis response to the mounting male of ovariectomized, estrogen/progesterone treated rats. The intracerebroventricular infusion of oxytocin 0.1 ng/rat had no effect; nor did saline. These results indicate that oxytocin increases female receptivity, the site of action probably being in the central nervous system.

Animals↗

PubMed1984

In vivo release of somatostatin from rat median eminence after local K+ infusion or delivery of nociceptive stress.

The effects of local infusion of a 16 mM K+ solution or of a nociceptive stress on the release of somatostatin (SRIF) from the hypothalamus was measured in unanesthetized male rats implanted with a push-pull cannula in the median eminence. Although the baseline secretion rate of SRIF was increased in animals displaying agitation as a result of handling stress, both treatments induced fast doubling of SRIF release lasting for 15-30 min. Neither an equimolar Na+ infusion into the median eminence nor a similar K+ infusion into the 3rd ventricle had any affect on this release. The possible role of SRIF release in the mechanism of growth hormone inhibition following nociceptive stress is discussed.

Animals↗

PubMed1986

The effect of 6-hydroxydopamine infusion into the third cerebral ventricle on the plasma prolactin levels in anoestrous ewes subjected to prolonged and repeated stress.

The effect of 6-hydroxydopamine (6-OHDA) infusion into the third cerebral ventricle on the secretion pattern of prolactin in anoestrous sheep, subjected to repeated and prolonged stress-stimuli was followed. On the 12-15 th day after the infusion of 6-OHDA into the third cerebral ventricle and after having tested the effect of this infusion on plasma prolactin concentration, the animals were subjected to mild electric footshocks 9 hrs daily (9 a.m.-6 p.m.) for 3 consecutive days. Infusion of 6-OHDA induced a very high rise of plasma prolactin values by about 3 times as compared to those found before infusion (from 118.2 +/- 39.5 to 338.9 +/- 81.7 ng/ml mesor 24 h). On the other hand, the response of the animals pretreated with 6-OHDA to electric stimulation was characterized by the lack of changes in plasma prolactin concentration; their plasma hormone concentrations were neither raised during stimulation nor decreased after the stimulation and were maintained during all these days nearly at the same level as after the infusion of 6-OHDA. Central mechanisms which could account for the so high and prolonged elevation of plasma prolactin concentration after the infusion of 6-OHDA and for the lack of its rise under conditions of prolonged stress are discussed.

Anestrus↗

PubMed2005

Chronic intracerebroventricular infusion of lipopolysaccharide: effects of ibuprofen treatment and behavioural and histopathological correlates.

Twenty male Wistar rats were trained under an alternating-lever cyclic-ratio (ALCR) schedule of food reinforcement. When responding showed no trends, each subject was subcutaneously implanted with an Alzet osmotic mini-pump, connected to a chronic indwelling cannula extending into the lateral ventricle of the brain. The mini-pumps were primed to infuse 0.25 microl lipopolysaccharide (LPS) (1.0 microg/0.25 ml) or 0.25 microl artificial cerebrospinal fluid (aCSF) per hour and were implanted for 28 days. LPS infusion produced behavioural deficits which chronic ibuprofen treatment (40 mg/kg every 12 h) alleviated. Infusion of LPS induced R 1282-positive amyloid deposits, and activation of microglia and astrocytes. Ibuprofen treatment reduced the numbers of activated microglia, and withdrawal of ibuprofen resulted in an increase in activated microglia; however, ibuprofen treatment had no effect on numbers of activated astrocytes in the LPS-infused subjects.

Amyloid beta-Peptides↗

PubMed1989

Effects of chronic icv infusion of vasopressin on sleep-waking cycle of rats.

The effect of arginine vasopressin (AVP) on the duration and the relative proportion of sleeping and wakeful periods has been investigated. Vigilance states were determined by visual scoring of polygraphic recordings from unrestrained rats. Animals were implanted with a cannula into the third ventricle through which AVP or related drugs, dissolved in artificial cerebrospinal fluid, were infused at a constant rate by an osmotic pump. Polygraphic data were collected 24 h/day from day 4 to day 9. Recordings were continued for 3 additional days during AVP recovery. AVP infusions significantly increased the amount of time spent in waking compared with control or recovery periods (12%). This effect was mimicked by an AVP agonist (2-phenylalanine, 8-ornithine oxytocin). Oxytocin, a peptide structurally close to AVP, induced a mild change in waking time. The infusion of an AVP antagonist, 1-desaminopenicillamine-2-(O-methyl)tyrosine-arginine vasopressin (dPTyr(Me)AVP), or of anti-AVP antibodies significantly decreased duration of waking. The infusion of antioxytocin antibodies did not modify the duration of waking. The effects of structural analogues of AVP relatively specific for each type of peripheral AVP receptor indicated the participation of a V1-like AVP receptor in the action of AVP on waking time. During infusion of anti-AVP antibodies and dPTyr(Me)AVP and during the first days of recovery from AVP infusion, the ultradian rhythmic distribution of sleep and wakefulness was still present, but the amplitude of the circadian rhythm was reduced.

Animals↗

PubMed2000

Effect of intracerebroventricular alpha-MSH on food intake, adiposity, c-Fos induction, and neuropeptide expression.

alpha-Melanocyte-stimulating hormone (alpha-MSH) is a hypothalamic neuropeptide proposed to play a key role in energy homeostasis. To investigate the behavioral, metabolic, and hypothalamic responses to chronic central alpha-MSH administration, alpha-MSH was infused continuously into the third cerebral ventricle of rats for 6 days. Chronic alpha-MSH infusion reduced cumulative food intake by 10.7% (P < 0.05 vs. saline) and body weight by 4.3% (P < 0.01 vs. saline), which in turn lowered plasma insulin levels by 29.3% (P < 0.05 vs. saline). However, alpha-MSH did not cause adipose-specific wasting nor did it alter hypothalamic neuropeptide mRNA levels. Central alpha-MSH infusion acutely activated neurons in forebrain areas such as the hypothalamic paraventricular nucleus, as measured by a 254% increase in c-Fos-like immunoreactivity (P < 0.01 vs. saline), as well as satiety pathways in the hindbrain. Our findings suggest that, although an increase of central melanocortin receptor signaling acutely reduces food intake and body weight, its anorectic potency wanes during chronic infusion and causes only a modest decrease of body weight.

Adipose Tissue↗

PubMed1989

Central administration of aldosterone increases blood pressure in rats.

Experiments were designed to determine whether hypertension in rats caused by a central infusion of aldosterone requires supplemental sodium and uninephrectomy. Group 1 was uninephrectomized and received an intracerebroventricular (i.c.v.) infusion of aldosterone (9 ng/h) plus 1M NaCl, dissolved in 0.01% ethyl alcohol-artificial cerebrospinal fluid (vehicle). Group 2 received the same infusion but was not uninephrectomized. Group 3 received an i.c.v. infusion of aldosterone alone in vehicle. Group 4 received an i.c.v. infusion of vehicle with intravenous (i.v.) infusion of aldosterone plus NaCl. All rats received a diet of standard Purina rat chow and tap water ad libitum. Systolic blood pressure of groups 1 and 2 was significantly increased. Rats treated with i.c.v. aldosterone alone also showed a significant increase in blood pressure on day 21. However, i.v. infusion of the same dose of aldosterone did not change blood pressure. The results show that hypertension induced with chronic central infusion of aldosterone does not require uninephrectomy. We conclude that aldosterone may act directly within the central nervous system to increase blood pressure.

Aldosterone↗

PubMedDate not supplied

Release of oxytocin and substance P-like peptides from the rat posterior pituitary lobe incubated in situ after infusion of hypertonic solution into the third cerebral ventricle.

Release of oxytocin and Substance P-like peptides from the rat posterior pituitary lobe incubated in situ after infusion of hypertonic solution into the third cerebral ventricle. Acta Physiol. Pol., 1978, 29 (1): 9-16. The experiments were carried out on male rats. Under general urethane and chloralose anaesthesia the ventral surface of the hypothalamus and the pituitary gland were exposed by a transpharyngeal approach and the anterior pituitary lobe was entirely removed. The posterior lobe with the remaining neural and partially vascular connections with the hypothalamus was incubated in situ. Oxytocin and Substance P-like peptides were assayed biologically in six 20-min samples of the fluid outflow from the posterior pituitary lobe incubated in situ. At the beginning of collection of the fourth sample a hypertonic solution was infused into the third ventricle through a micropipette. This infusion increased significantly the release of oxytocin and insignificantly that of Substance P-like pepides from the posterior pituitary lobe into the incubation fluid.

Animals↗

PubMed1983

Correction of CSF HCO-3 after its experimental increase in normocapnia: inhibition by acetazolamide.

In anaesthetized normocapnic dogs CSF [HCO-3] was increased to ca 33 mmol/l by perfusing the brain ventricles for 45 min with a mock CSF containing a high [HCO-3] which in addition contained 2.5 mg/ml acetazolamide to inhibit central carbonic anhydrase. In dogs with normal plasma [HCO-3], CSF [HCO-3] fell by 5.4 mmol/l in 2 h following the end of the perfusion. Lowering plasma [HCO-3] to 11 mmol/l by infusing HCl intravenously increased the CSF [HCO-3] fall to 7.5 mmol/l. Increasing plasma [HCO-3] to 36 mmol/l completely impeded the fall in CSF [HCO-3]. It is concluded that in these experiments clearing of HCO-3 from the CSF is critically dependent on plasma [HCO-3]. When the data are compared to those of comparable experiments without intraventricular administration of acetazolamide (Weyne et al. 1982), they indicate that acetazolamide impedes clearing of HCO-3 from CSF at high and at normal plasma [HCO-3] but not at low plasma [HCO-3]. The experiments therefore suggest a dual contribution for the clearing of HCO-3 from the CSF after its experimental increase: diffusion along the CSF-plasma gradient for HCO-3 and a carbonic anhydrase dependent clearing of HCO-3.

Acetazolamide↗

PubMed1980

The role of the lymphatic system in drainage of cerebrospinal fluid and aqueous humour.

1. The jugular lymphatic trunks were cannulated in anaesthetized rabbits and cats. Over 6-8 hr, the mean lymph flow was 2.3 microliters min-1 in the rabbit (one side only) and 5.0 microliters min-1 in the cat (sum of both sides). 2. After a single injection of radio-iodinated albumin into a lateral cerebral ventricle without significant rise in pressure, a mean of 14.4% of the radioactivity was recovered in deep cervical lymph of one side in the rabbit and of 12.9% in that of both sides in the cat. 3. During slow infusion of [125I]albumin and fluorescent dextran of 150,000 mol. wt. into a lateral ventricle of the cat at 20 microliters min-1, radioactivity and fluorescence reached plateaus in deep cervical lymph at 47.4 and 50.0% of their concentrations in cisternal c.s.f. respectively. 4. No significant radioactivity, other than from blood, was detected in superficial cervical lymph after intraventricular injection of radio-iodinated albumin in the cat. 5. No significant radioactivity, other than from blood, was detected in deep cervical lymph of the rabbit or in deep and superficial cervical lymph of the cat within 6 hr after injection of radio-iodinated albumin into the aqueous humour or orbital fat. 6. Gradients of radioactivity in tissues within the orbit suggested that there is a small flow of c.s.f., 0.05-0.15 microliters min-1 in the rabbit, passing centrifugally along the subarachnoid space of the optic nerve, through the posterior part of the globe and into the orbital tissue. Also a small proportion of aqueous humour, 1-2% or more, drains through the anterior sclera into the surrounding tissue. 7. A substantial quantity of cerebrospinal fluid drains into the deep cervical lymphatic system of the rabbit, 30% or more, and of the cat, 10-15% or more. The small component of aqueous humour drainage passing through the wall of the glove does not enter cervical lymph within 6 hr, if at all.

Animals↗

PubMed1985

Fluid intake, distribution, and excretion during lateral ventricular infusions of carbachol in rats.

Infusion of carbachol into the lateral ventricles of rats at rates of 400 or 2000 ng/h for 6 h produced dose-related natriuresis, kaliuresis, and water drinking but no consumption of hypertonic NaCl solution. Electrolyte excretion and water intake were maximal during the first 2 h, and no further increases occurred after 4 h. Sodium losses were estimated as 15-30% of total extracellular sodium. Continuous infusion of 2000 ng/h carbachol for 6 days produced a chronic increase of water intake but no increased consumption of saline. Sodium balances were negative during the first day of infusion, but gradually returned to normal over 6 days. Plasma volume, hematocrit, and plasma sodium and potassium concentrations were normal in carbachol-infused animals on the 6th day. Cholinergic stimulation of the brain thus appeared to interfere with the usual salt appetite following sodium loss.

Animals↗

PubMed1985

Cerebrospinal fluid sodium concentration and salt appetite.

Infusion into a lateral brain ventricle (IVT) of different hypertonic (0.7 M) saccharide solutions decreased [Na+] of cerebrospinal fluid (CSF). Increased Na appetite of moderately Na-deplete sheep was observed during infusion of mannitol, L-glucose or L-fucose, while no change was observed during infusion of D-glucose, D-fucose, D-mannose, 2-deoxy-D-glucose, 3-O-methyl-glucose or fructose. In other experiments, increased Na appetite was observed during infusion of 2.3 mM phlorizin (a relatively specific blocker of Na-coupled glucose transport into cells) or 2.3 mM phlorizin plus 0.7 M D-glucose. In addition, phlorizin eliminated the characteristic decrease in Na appetite but did not affect the increase in water intake caused by IVT infusion of hypertonic NaCl which increased [Na+] of CSF. The results suggest that: (a) there are sensors within the neuropil which respond to change of [Na+] and influence Na appetite, and that these changes of [Na+] are induced deep within the neuropil by those saccharides which do not cross the blood-brain barrier or enter cells; change of CSF[Na+] alone is not sufficient to alter appetite but a change in brain extracellular fluid (ECF)[Na+] is probably necessary; (b) the theory is advanced that the stimulus for altered Na intake could be altered brain ECF[Na+] producing a change in cerebral intracellular fluid (ICF)[Na+] of the sensors; and (c) phlorizin, in reducing or blocking Na-coupled glucose transport, could increase Na appetite by producing a fall in ICF[Na+] of the specific neurones subserving sodium appetite or prevent a decrease in Na appetite caused by IVT infusion of hypertonic NaCl by preventing an increase in ICF[Na+] of this same neuronal system.

Animals↗

PubMed1987

Intracerebroventricular arginine vasopressin causes intracranial pressure to rise in conscious goats.

The effects of intracerebroventricular (i.c.v.) infusion of arginine vasopressin (AVP) on intracranial pressure (ICP), blood pressure (BP) and plasma AVP were investigated in conscious goats. The animals were implanted with ventricular (V) and cisternal (C) cannulae under halothane anaesthesia and allowed to recover prior to experimentation. After 30 min infusion of 20 microliter/min artificial cerebrospinal fluid (CSF) alone, to allow the animals to settle, ICP (estimated at both C and V cannulae), BP and plasma AVP were measured. Then the animals were infused with either artificial CSF alone or 1 or 10 pmol/min AVP for a further 150 min. One pmol/min AVP i.c.v. resulted in significant ICP increases of +2.2 cm CSF (C) and +3.1 cm CSF (V) when compared with artificial CSF alone. Ten pmol/min AVP also led to significant ICP rises of +3.2 cm CSF (C) and +4.2 cm CSF (V). There were no significant changes of BP or plasma AVP during the infusions. We conclude that central infusion of AVP leads to elevated ICP in conscious goats by a mechanism that does not involve BP alteration or changes in plasma AVP.

Animals↗

PubMed1996

The olfactory bulb: a critical site of action for oxytocin in the induction of maternal behaviour in the rat.

Expanding on research showing that oxytocin originating in the hypothalamic paraventricular nucleus acts to decrease olfactory processing at the level of the olfactory bulb, we explored the importance of oxytocin acting on the olfactory bulb for the onset of maternal behaviour in Wistar rats. Experiment I was designed to test whether spontaneous maternal behaviour following natural delivery is blocked by bilateral infusions of a low dose (5 fmol) of the oxytocin antagonist d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)]ornithine-vasotocin into the olfactory bulb immediately after the delivery of the first pup and again just before a test for maternal behaviour. Intrabulbar infusions of the antagonist markedly delayed the occurrence of all components (retrieval, licking, nest building, crouching) of maternal behaviour, whereas intracerebroventricular infusions of the antagonist were without effect on any component as compared with intrabulbar infusions of saline. Experiment 2 was undertaken to determine whether infusions of oxytocin into the bulb induce a rapid onset of maternal behaviour in virgin rats. Forty-eight hours before pup presentation virgins were ovariectomized and treated with oestradiol benzoate. Immediately before pup presentation a low dose (20 pmol) of oxytocin or saline was infused bilaterally into the bulb or lateral ventricle. Intrabulbar infusions of oxytocin induced full maternal behaviour in half of the animals tested within 2 h of pup exposure, in contrast to the ineffectiveness of intracerebroventricular infusions of oxytocin and intrabulbar infusions of saline. These results suggest that the olfactory bulb is a critical site where oxytocin acts to induce a rapid onset of maternal behaviour.

Animals↗

PubMed2004

Septal infusions of glucose or pyruvate with muscimol impair spontaneous alternation.

This experiment examined the effects of co-infusing the GABA agonist muscimol (0.5 nmol) with 33 nmol of glucose, pyruvate, fructose or sorbitol into the medial septum on spontaneous alternation. Only co-infusions of muscimol with glucose or pyruvate impaired spontaneous alternation performance; none of the other infusions had any significant effects. The findings suggest that glucose metabolism rather than hyperosmolarity is involved in the memory-impairing interaction between glucose and muscimol.

Animals↗

PubMed2000

Treatment of refractory complex-partial status epilepticus with propofol: case report.

PURPOSE: We report a case of a 65-year-old woman who had a subarachnoid and intraventricular hemorrhage secondary to rupture of an anterior communicating artery aneurysm and developed nonconvulsive status epilepticus of the complex-partial type, refractory to phenytoin (PHT), phenobarbital (PB), valproate (VPA), and lorazepam (LZP). METHODS: Three weeks after diagnosis of nonconvulsive status epilepticus, general anesthesia was induced with propofol and titrated to burst suppression on the electroencephalogram (EEG). RESULTS: During propofol infusion, the serum VPA level declined markedly, and despite >3 g daily doses, did not return to the therapeutic range, until several days after propofol was discontinued. Continuous propofol infusion was stopped after 7 days, and the patient recovered consciousness. Despite further complications, she gradually regained normal function and was discharged home 4 months after surgery. CONCLUSIONS: This is the first case of nonconvulsive status epilepticus successfully treated with propofol.

Aged↗