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Results for “Infusions, Intraventricular”

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PubMed1986

Ovarian steroid modulation of norepinephrine action on luteinizing hormone release. Analogous effects in male and female rats.

The modulatory actions of ovarian steroids on the norepinephrine (NE) induced alterations in luteinizing hormone (LH) secretion were examined in male and female rats. Long-term (4 weeks) castrated male and female rats bearing chronic third-ventricle cannulae were implanted with intra-atrial catheters. Animals were bled sequentially at 5- or 15-min intervals for 4-6 h, and plasma LH secretory patterns were determined by radioimmunoassay. After a 2- to 3-hour control bleeding period, castrated unprimed rats received an intracerebroventricular (ICV) infusion of 0.3 mumol of arterenol bitartrate or vehicle. Blood sampling was continued for an additional 2-3 h after infusion. In female rats NE caused a rapid and potent inhibition of episodic LH secretion which was characterized by decreases in mean plasma LH, mean pulse amplitude, and pulse frequency. Similarly, ICV infusion of NE into male rats resulted in decreased mean plasma LH and pulse frequency. In a second series of experiments, castrated male and female rats were primed with estrogen and progesterone 2 days prior to the bleeding/infusion session. Animals were bled sequentially and infused with 0.3 mumol arterenol bitartrate or vehicle during a morning or afternoon session. ICV infusion of vehicle had no effect on plasma LH in either sex regardless of the time of day. NE infusion into estrogen and progesterone primed female rats resulted in significant elevations of plasma LH during both morning and afternoon periods. In estrogen and progesterone primed male rats, NE infusion resulted in a marked facilitation of LH release, similar to that observed in female rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Activity Cycles↗

PubMed2000

[Chronic administration of arginine-vasopressin stimulates insulin's synthesis in beta-cells of pancreas in intact and diabetic rats].

Investigations on the intact and diabetic rats show us that chronic administration of [Arg8]-vasopressin for ten days (intracerebroventricular 24 pg or intraperitoneal 240 ng every day) leads to the increasing of insulin's level in beta-cells of the pancreas in normoglycemic rats to 6.% +/- 0.2% in comparison with the control group, and in hyperglycemic diabetic rats to 25.9% +/- 0.6% at the intracerebroventricular infusions, and to 15.9% +/- 0.8% at the intraperitoneal injections. The administrations of vasopressin in animals with experimental diabetes mellitus leads to the decreasing of glycemia's level in average to 37%, but do not have an influence on the destruction of Langerhans islets. Probably an insulin-stimulating effect of intracerebroventricular infusions of vasopressin is connected with the modulation of functional activity of hypothalamic centres of food behaviour and dorsal motor nucleus of vagal nerve and in peripheral injections vasopressin directly stimulates insulin synthesis.

Animals↗

PubMed1977

Controlled trial of bicarbonate therapy in high-risk premature newborn infants.

Sixty-two high-risk acidemic premature newborn infants, given maintenance intravascular infusions of 10% glucose, were assigned to liberal or restricted sodium bicarbonate treatment groups. Those infants in the liberal group received 5 to 15 mEq bicarbonate/dl 10% glucose, depending on the degree of acidosis. Among infants given bicarbonate, correction of pH was not more rapid and mortality was not decreased. Instead, there was a small increase in the number of deaths, but the incidence of intraventricular hemorrhage was similar to that in infants not given bicarbonate.

Acidosis↗

PubMed1974

Regional cerebral blood flow and intraventricular pressure in acute head injuries.

Twelve patients who were comatose after head injuries were studied with serial determinations of regional cerebral blood flow, jugular PO(2) tension, and intraventricular pressure. These determinations began a few hours after the injury, and were followed throughout the clinical course. Diffuse derangement of cerebral vasomotor regulation is confirmed after severe head trauma, which may contribute to deterioration and poor prognosis, and which indicates a need for therapeutic maintenance of rich oxygenation, hyperventilation with moderate hypocapnia, and steady blood pressure. Continuous recording of IVP (eventually sensitized by fluid infusion or CO(2) inhalation tests) may give an early indication of the subsequent clinical state and may suggest the need to submit the patients to further investigative and therapeutic procedures.

Acute Disease↗

PubMed2004

[Three special cases of pregnancy outcome to reflect about].

BACKGROUND: Neonatal alloimmune thrombocytopenia (NAITP) may be a serious condition with prenatal intracranial haemorrhages. Our three cases of serious NAITP raise the question of whether pregnant women should be screened for thrombocyte type and then for HPA-1a antibodies if they are HPA-1bb positive. CASE REPORTS: We present three cases of severe NAITP in which screening and follow up of HPA-1a antibodies prevented serious sequelae in two of the siblings. The first child was a stillbirth with congenital hydrocephalus caused by an intraventricular haemorrhage. In the second pregnancy, the mother was found to be platelet type HPA-1bb with platelet antibodies against HPA-1a. The antibody level was extremely high and an elective caesarean section was performed four weeks before term. The platelet count at birth was 3 and 5 x 10(9)/L and a transfusion of matched platelets was immediately performed followed by infusion of intravenous immunoglobulin. In the third pregnancy, an intracerebral haemorrhage was detected by ultrasound at 27 weeks of gestation. The mother was given steroids to induce foetal lung maturation followed by a caesarean section in week 28. The platelet count was 6 x 10(9)/L. The child was transfused with compatible platelets and given an infusion of intravenous immunoglobulin. OUTCOME: None of the two children have developed any psychomotor sequelae by the age of five and three years, respectively. The importance of screening for platelet type and anti-platelet antibodies and mode of delivery is discussed.

Adult↗

PubMed1984

Timing and antecedents of intracranial hemorrhage in the newborn.

Fifty newborn infants of less than 33 weeks' gestation were followed prospectively from birth to evaluate the temporal relationships of various clinical factors to the onset and progression of intracranial hemorrhage (ICH) in an inborn population given maximal support. ICH was diagnosed and followed with bedside ultrasound every eight hours. The incidence of intraventricular hemorrhage was 30% and of any ICH was 40% with onset from less than 2 hours to 8 days of age. Grades 2, 3, and 4 ICH correlated with Apgar scores of less than 5 at five minutes, vaginal delivery, longer labors, and intrapartum hemorrhage. There was a significant correlation between ICH and both blood pressure fluctuations of greater than 100% and rapid colloid infusions. Slow transfusions of packed red cells did not appear to precipitate episodes of ICH. In a setting of optimal care, ICH appears to be more related to prenatal stresses than to specific postnatal complications.

Apgar Score↗

PubMed1995

Pregastric and postabsorptive inhibitory effects of water on angiotensin-induced Fos in rat brain.

Intraventricularly (ICV)-injected Ang II activates cells in several forebrain structures of rats, including SFO, OVLT, PVN and SON, and produces a spectrum of physiological and behavioral responses. It has been reported that the Fos-like immunoreactivity (FLI; a marker of cell activation) that is induced in PVN and SON by exogenous Ang II is prevented by allowing rats to ingest water after injection. The present study tests whether this inhibitory effect of water is due to either preabsorptive (oral) or postingestive factors, or both. Rats received cerebroventricular injection of Ang II (100 ng) and were killed 1 h later. One group received no water after the injection, another group drank water, a third group drank water but had it drain from a gastric fistula (sham drinking), and a fourth group received an intragastric infusion of water. In confirmation of a previous study, rats allowed to drink water after Ang II showed an almost complete absence of FLI in SON and PVN, compared with those not allowed access to water. Both sham drinking and intragastrically-infused rats showed less FLI in SON and PVN than nondrinkers. The reduction was greater in the infused group than the sham drinkers, but was not as great as in those allowed to drink water and absorb it. This suggests that both orally-mediated as well as postabsorptive factors can inhibit Ang II-induced FLI by impinging upon cells in the SON and PVN. In contrast, Ang II-induced FLI in OVLT and SFO was not affected by any of the oral or gastric water conditions.

Angiotensin II↗

PubMed2004

NMDA receptor blockade attenuates locomotion elicited by intrastriatal dopamine D1-receptor stimulation.

Previous behavioral studies suggest that the striatum mediates a hyperactive response to systemic NMDA receptor antagonism in combination with systemic D1 receptor stimulation. However, many experiments conducted at the cellular level suggest that inhibition of NMDA receptors should block D1 receptor-mediated locomotor activity. Therefore, we investigated the consequences of NMDA receptor blockade on the ability of striatal D1 receptors to elicit locomotor activity using systemic and intrastriatal injections of the NMDA antagonist MK-801 combined with intrastriatal injections of the D1 full agonist SKF 82958. Following drug treatment locomotor activity was measured via computerized activity monitors designed to quantify multiple parameters of rodent open-field behavior. Both systemic (0.1 mg/kg) and intrastriatal (1.0 microg) MK-801 pretreatments completely blocked locomotor and stereotypic activity elicited by 10 microg of SKF 82958 directly infused into the striatum. Further, increased activity triggered by intrastriatal SKF 82958 was attenuated by a posttreatment with intrastriatal infusion of 1 microg MK-801. These data suggest that D1-stimulated locomotor behaviors controlled by the striatum require functional NMDA channels.

Animals↗

PubMed1996

Facilitation of ethanol consumption by intracerebroventricular infusions of corticosterone.

Male Wistar rats bearing intracerebroventricular (ICV) cannulae and with simultaneous access to 6% ethanol and water were subjected to adrenalectomy (ADX) or sham surgery. ADX decreased ethanol intake. Starting a few days later, the animals received ICV infusions with 100 micrograms corticosterone acetate (CORT) with 2-to 3-day intervals for 2 weeks. ICV CORT, but not SC CORT at the same dose, restored ethanol consumption in ADX rats to preoperative levels, whereas vehicle infusions (propylene glycol) did not. Adrenally intact animals, which normally consumed moderate amounts of ethanol (approximately 0.5 g/kg per day), also showed a robust effect of ICV infusions of CORT, whereas this facilitatory effect was not observed in high consumers (approximately 3.0 g/kg per day). The suppressive effect of ADX on ethanol intake was not reproduced by concurrent and repeated ICV infusions of intracellular mineralocorticoid (RU 28318) and glucocorticoid (mifepristone) receptor blockers. It is concluded that CORT stimulates alcohol consumption by acting in the brain, probably by way of neuronal membrane mechanisms.

Adrenalectomy↗

PubMed1983

Area postrema lesions disrupt food intake induced by cerebroventricular infusions of 5-thioglucose in the rat.

The present experiment assesses the contribution of the area postrema (AP) to glucoprivic feeding in the rat. Lateral ventricular infusions of 5-thioglucose increased pelleted food intake in sham animals but not in animals with AP lesions. Drinking in response to infusion of angiotensin II into the lateral ventricle was not reduced by AP lesions. The data suggest that the AP is part of the brainstem circuitry underlying glucoprivic feeding.

Animals↗

PubMed1994

Chronic cerebroventricular galanin does not induce sustained hyperphagia or obesity.

Acute central administration of galanin has been reported to increase fat consumption. These experiments were designed to test the hypothesis that repeated injections of galanin would elicit hyperphagia and weight gain and that this response would depend on the available diet. Male Sprague-Dawley rats were fed high (56% energy) or low (10% energy) fat diets. Galanin (300 pmol) or saline vehicle was injected into the third ventricle twice daily for 7 days and three times daily for another 6 days. On both the high-carbohydrate and high-fat diets, twice daily galanin increased daytime food intake, but there was a compensatory decrease in nighttime intake. The addition of a third, nighttime injection of galanin was ineffective in producing an increase in total 24-h intake. There was no significant increase in body weight during galanin treatment in rats eating either diet although animals eating the high-fat diet gained more weight as reflected by a significant increase in epididymal fat pad weight. Galanin treatment had no effects on serum insulin, glucose or corticosterone concentrations, measured at the end of the experiment. However, animals fed the high-fat diet had significantly higher insulin concentrations at the time of sacrifice. Although repeated central infusions of galanin reliably stimulated daytime intake of both diets, they failed to increase total daily energy intake or body weight.

Animals↗

PubMed2004

A novel melatonin derivative modulates sleep-wake cycle in rats.

The aim of this study was to evaluate, in comparison with melatonin (MLT), the effects of a novel 2-melatonin derivative, having a 2-trifluoromethyl group (MLTD) on the sleep-wake cycle in freely behaving rats. Doses of MLTD (100, 300 and 500 nmol/100 microl saline) or MLT (500 nmol/100 microl saline) replaced the i.c.v. infusion of saline during the diurnal infusion period (7:00-17:00). Diurnal infusion of MLTD significantly (P < 0.05) increased NREM sleep at doses of 300 and 500 nmol during the second 4-h time interval of the light period and the lowest dose showed delayed effects on NREM sleep in the third 4-h time interval. However, REM sleep was only increased significantly at the dose of 500 nmol. The infusion of MLT did not have effects on REM sleep but significantly increased NREM sleep. These findings support the notion that MLTD diurnal infusion into the third ventricle produces soporific effects dose-dependently and more potently than MLT. Thus, MLTD may play an important role in studies of sleep.

Animals↗

PubMed2002

Sympathetic ingrowth to the trigeminal ganglion following intracerebroventricular infusion of nerve growth factor.

The objective of the present study was to examine the remodeling of uninjured sympathetic axons in the adult rat trigeminal ganglion following a 2-week in vivo intracerebroventricular infusion of NGF. The accumulation of infused NGF in the trigeminal was assessed using ELISA and sympathetic fibers were localized immunohistochemically with an antibody to tyrosine hydroxylase (TH). In addition, high performance liquid chromatography coupled with electrochemical detection (HPLC-ECD) allowed for biochemical measurements of the catecholamines norepinephrine (NE) and dopamine (DA). Increased NGF protein in the trigeminal ganglion was paralleled by a significant increase in sympathetic fibers and pericellular plexuses (i.e. baskets) in the cell body regions. Some ganglia showed elevated NE following NGF infusion, yet the 88% increase in mean NE did not reach significance. Following bilateral removal of the sympathetic superior cervical ganglia (SCG), a significant reduction was observed in overall NE levels and in TH-immunoreactive (-ir) fibers in the cell body regions and peripheral branches, suggesting the SCG as the origin of the sympathetic ingrowth. However, mean DA levels as well as TH-ir fibers within the trigeminal central branch were unaffected by NGF infusion or removal of the SCG and likely resulted from intrinsic dopaminergic cell bodies. In conclusion, our data provide evidence that the increased availability of NGF in the young adult rat trigeminal ganglion observed following in vivo NGF infusion enhanced sympathetic associations with the sensory neurons in the trigeminal, supporting a role for NGF in the regulation of sympathosensory interactions.

Adrenergic Fibers↗

PubMed1998

Propentofylline improves learning and memory deficits in rats induced by beta-amyloid protein-(1-40).

We have reported that continuous infusion of beta-amyloid protein-(1-40) into the cerebral ventricle produces learning and memory deficits in rats. Propentofylline has potent stimulatory effects on nerve growth factor (NGF) synthesis/secretion in mouse astrocytes in vitro and increases cerebral NGF content in aged rats. In the present study, we examined the effects of propentofylline on learning and memory deficits in beta-amyloid protein-infused rats. The rats were given propentofylline orally once a day throughout the period of behavioral examination. In the beta-amyloid protein-infused rats, spontaneous alternation behavior in a Y-maze, and performance in water maze and passive avoidance tasks were significantly impaired compared to sham-operated rats. Propentofylline prevented these behavioral deficits, but did not change the reduction of the activity of choline acetyltransferase in the hippocampus in the beta-amyloid protein-infused rats. These results suggest that propentofylline is useful for the treatment of patients with Alzheimer's disease.

Administration, Oral↗

PubMedDate not supplied

Nerve growth factor preserves behavioral visual acuity in monocularly deprived kittens.

Recent electrophysiological and anatomical experiments in rats and cats have shown that treatment with the neurotrophic factor-nerve growth factor (NGF)-prevents the effects of monocular deprivation (MD) at the level of visual cortex and lateral geniculate nucleus. We tested whether NGF treatment was effective in preventing MD effects on visual behavior of monocularly deprived kittens. Behavioral visual acuity was measured in kittens that had been monocularly deprived and treated intraventricularly with NGF for 2 weeks during the critical postnatal period. The detrimental effects of MD on behavioral visual acuity were found to be largely prevented by NGF treatment.

Animals↗

PubMed1997

Oxytocin neurone autoexcitation during morphine withdrawal in anaesthetized rats.

We investigated whether release of oxytocin into the supraoptic nucleus is involved in morphine-withdrawal excitation of oxytocin neurones. Retrodialysis of naloxone into the supraoptic nucleus of morphine-dependent rats increased intranuclear oxytocin release by 56.5p +/- 12.7% whereas no change was seen in vehicle-treated dependent rats. In another experiment, in morphine-dependent rats given intravenous (i.v.) naloxone, intracerebroventricular (i.c.v.) oxytocin receptor antagonist injection reduced the increase of plasma oxytocin concentration (to 28-fold) compared with i.c.v. vehicle (62-fold increase). Finally, the increase in oxytocin neurone firing rate following morphine-withdrawal in the presence of i.c.v. oxytocin antagonist infusion was 28% of the steady state firing rate (15-20 min later) and this was lower (p < 0.05) than the percentage increase in i.c.v. vehicle-infused rats (89%). Thus, central endogenous oxytocin may be involved in withdrawal excitation of oxytocin neurones.

Action Potentials↗

PubMed1994

Assessment of left ventricular stiffness and compliance.

Invasive and non-invasive methods exist to assess left ventricular compliance (LVC). This work has two parts, one experimental and one clinical. We estimated left chamber stiffness in dogs by using volume data from radionuclide ventriculography (RNV) and left ventricular pressure data, synchronized with a gating system to the intraventricular dp/dt max to obtain volume and pressure data from a mean cardiac cycle. In five dogs after acute experimental ischaemia, the modulus chamber stiffness Kp rose from 30.2 +/- 4.4 to 55.4 +/- 5.9 (P < 0.01). In 10 dogs with experimental infarction after intra-aortic balloon pumping, Kp decreased from 33.7 +/- 5.0 to 15.5 +/- 3.9 (P < 0.01) and in five dogs with experimental infarction, after intravenous infusion of sodium nitroprusside, Kp decreased from 41.4 +/- 5.5 to 22.2 +/- 2.8 (P < 0.01). In eight normal volunteers and in 20 postmyocardial infarction patients, we estimated a parameter reflecting the LVC by using volume data with blood flow velocity at the mitral valve annulus. Assuming that the mitral flow-velocity variation reflects LV pressure changes, the formula LVC = (dv/dt)/(dp-dt) becomes (dv/dt)/(df/dt) = dv/df. Values obtained in normals were 0.841 +/- 0.295 m-1s and after myocardial infarction 0.331 +/- 0.10 m-1s. Both methods allow clear separation in groups of animals or patients according to the expected changes in LVC or stiffness.

Adult↗

PubMed1987

Centrally administered atrial natriuretic factor increases renal water excretion.

The effects of intracerebroventricular (ICV) infusion of atrial natriuretic factor (ANF; atriopeptin III) on renal function, plasma concentrations of antidiurectic hormone, aldosterone, and plasma renin activity (PRA) were examined in anesthetized rats and sodium-depleted conscious sheep. The results were compared with those obtained by intravenous infusion of the same dose of ANF. In both rats and sheep, urine volume was increased four- to sixfold over basal values by ICV infusion of ANF. The response was not associated with increased excretion of sodium or potassium. However, urine osmolality was decreased, and free water clearance increased. Intravenous infusion of the same dose of ANF was without effect. Neither mean arterial blood pressure nor heart rate was changed by the ICV infusion of ANF. In the sheep, renal plasma flow showed no significant changes and glomerular filtration rate was unaltered with the exception of a single experimental period out of four periods of ICV ANF infusion. Plasma concentration of ADH was decreased and PRA increased, whereas aldosterone levels remained unchanged as a function of ICV ANF. In the rat, the diuretic response to ANF was prevented by continuous intravenous infusion of a subpressor dose of ADH. These results suggest that ANF within the central nervous system inhibits secretion of ADH.

Aldosterone↗