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PubMed1987

Intracerebroventricular chloride infusion enhances water intake in rats.

Central anionic influences on dipsogenic response was studied in 54 euhydrated rats. Quantity of water consumed following third ventricular infusions of equimolar hypertonic chloride and bicarbonate solutions of sodium, potassium, calcium, and barium was compared. Control group (n = 6) was given artificial cerebrospinal fluid infusion while rats of the remaining 8 groups (n = 6 each) received one of the test solutions. All the chloride solutions, irrespective of the cations to which they were associated, elicited significantly greater dipsogenic response as compared to the control, or the bicarbonate solutions. Response of the bicarbonate solutions was more than the control only in the observation taken 30 min after the infusions. In the later observations, there was no significant difference. Drinking was not affected significantly by the cationic composition of the infusion fluids. Anionic concentration of the solutions has predominantly influenced the dipsogenic response. Enhancement of drinking following infusions of chloride solutions suggests the possibility of the CSF anions exerting active physiological influences over the juxtacerebroventricular sensors.

Animals↗
PubMed1994

Intracerebroventricular injection of bombesin (6-14) restores blood pressure in hemorrhaged rabbits.

Rabbits were intracerebroventricularly (i.c.v.) injected by bombesin (6-14) (100 micrograms) or saline (control group) immediately after acute hemorrhage (28 ml/kg body wt.). Bombesin (6-14) normalized the blood pressure and maintained it at the normal level during 30-40 min but it did not alter the dynamics of heart rate and body temperature. It has been proposed that action on the central regulation of vascular tension by intrathecal injection of bombesin or some active analogs might avoid the need for infusion therapy or minimize the infusion volume.

Animals↗
PubMed1999

Autoradiographical and behavioural effects of a chronic infusion of antisense to the alpha2D-adrenoceptor in the rat.

1. The aims of this study were, firstly to use receptor autoradiography to investigate the effect of antisense oligonucleotides to the alpha2D-adrenoceptor on receptor binding and, secondly to measure behavioural and physiological parameters to determine whether the chronic antisense infusion had any effect on alpha2-adrenoceptor function in vivo. 2. A 3 day infusion of antisense to the alpha2D-adrenoceptor significantly reduced specific [3H]-RX821002 binding in the septum (20 - 30%) and anterior hypothalamic area (20 - 30%). beta-Adrenoceptor expression was unaffected in those brain areas examined, indicating the antisense knockdown was specific to the alpha2-adrenoceptors. 3. On the second day of the infusion, the hypothermic response to UK 14,304 was significantly attenuated in the antisense-treated group compared with both vehicle and mismatch controls. The effect was fully reversible and a similar decrease in body temperature was observed in all the treatment groups 4 days after the end of infusion. 4. During the second day of the infusion, the effects of UK 14,304 on behaviour were reduced in the antisense-treated rats, but were not significantly lower than those of the vehicle and mismatch, UK 14, 304 controls. These trends were not observed 4 days after the end of the infusion. 5. In conclusion, antisense has been shown to selectively knockdown alpha2-adrenoceptor expression in specific brain areas. The consequence of this knockdown is a significant attenuation of UK 14,304-induced hypothermia and a reduction in its sedative actions. These changes were fully reversed 4 days after the end of the infusion.

Animals↗
PubMed1976

[Propafenon, a new anti-arrhythmic drug (author's transl)].

Propafenon, at an initial oral dose of 900 mg, proved an effective anti-arrhythmic drug in 34 patients with frequent ventricular and(or) supraventricular extrasystoles at rest. Long-term ECG monitoring of seven patients revealed that this effect lasted about eight hours. It can be maintained by an oral dose of 300 mg propafenon at eight-hourly intervals, as demonstrated in 21 further patients. Rapid anti-arrhythmic action was achieved in six acute cases with 1.0-1.5 mg propafenon per kg body weight by quick infusion, and lasted for one to one-and-a-half hours. In such cases the drug should, therefore, be given synchronously by the oral route. Side effects related to the gastrointestinal tract, sinus automatism as well as atrio-ventricular and intraventricular conduction, but in no case were very serious.

Administration, Oral↗
PubMed2002

Location and clinical implications of high-degree atrioventricular block during dipyridamole infusion: a case report.

We describe a patient with bifascicular block, who developed transient high-degree atrioventricular block during dipyridamole infusion. This patient was subsequently found to have significant His-Purkinje disease at electrophysiology study, and underwent permanent pacemaker implantation. Spontaneous atrioventricular block was documented during follow-up. This case report raises the issue of dipyridamole safety in patients with intraventricular conduction defects, and contributes an additional mechanism to the possible explanation of dipyridamole-induced atrioventricular block.

Aged↗
PubMed1999

Interventional MRI-guided stereotactic aspiration of acute/subacute intracerebral hematomas.

Surgical interventions for hypertensive intracerebral hematomas are still controversial. Many believe only hyperacute intervention is of any real utility. The majority of present interventions require a formal craniotomy with standard neurosurgical techniques. There are, however, a few reports on CT-guided stereotactic aspiration of these hematomas with favorable results. We report 10 patients treated with frameless fiduciless stereotactic means using an intraoperative MRI scanner (GE 0.5 T Signa SP). These patients were initially diagnosed as having hypertensive intracerebral hematoma and operated on within 1-34 days after hemorrhage. The actual operating time averaged less than 120 min, including intraoperative imaging. Clot volumes ranged from 2.5 to 75 cm(3) with a mean of 31 cm(3). There were 2 thalamic hematomas and 8 basal gangliar hematomas. Three patients had intraventricular hematoma extension and all 3, as well as an additional patient, required extraventricular drainage. However, no patients required permanent posthemorrhage ventriculoperitoneal shunting. Aspiration was successful in all cases to 70-90% of clot removal. Two cases utilized intrahematoma t-PA infusion with subsequent 80-90% clot removal. There were no complications or rehemorrhages. All patients showed some form of improvement that included either improved blood pressure control, speech or cognitive abilities. We conclude that using an intraoperative MRI scanner to perform frameless, fiduciless stereotactic aspiration of acute/subacute intracerebral hematoma is a safe and potentially effective means of treating intracerebral hematomas.

Acute Disease↗
PubMed2000

Intravenous midazolam infusion for sedation of infants in the neonatal intensive care unit.

BACKGROUND: The need for sedation for neonates undergoing uncomfortable procedures in the neonatal intensive care unit (NICU) has often been overlooked. Proper sedation may reduce stress and avoid complications during procedures such as mechanical ventilation. Midazolam is a short acting benzodiazepine that has been increasingly used in the NICU. However, the effectiveness of intravenous midazolam as a sedative in neonates has not been systematically evaluated. OBJECTIVES: To determine whether intravenous midazolam infusion is an effective sedative, as evaluated by behavioural and/or physiologic measurements, for critically ill neonates undergoing intensive care, and to assess clinically significant short and long term adverse effects associated with its use. SEARCH STRATEGY: Literature search according to the Cochrane Neonatal Collaborative Review Group search strategy. Randomized and quasi-randomized controlled trials of intravenous midazolam use in neonates were identified by searching MEDLINE, EMBASE, the Cochrane Controlled Trials Register, reference lists of published studies, personal files, and abstracts published in Pediatric Research from 1990-1999. SELECTION CRITERIA: Randomized controlled trials of intravenous midazolam infusion in infants </= 28 days of age for sedation during mechanical ventilation or radiologic investigations were selected for review. Studies on midazolam use as an anesthetic or an anticonvulsant were excluded. Studies involving neonates and older infants and children were excluded if data for neonates could not be extracted. DATA COLLECTION AND ANALYSIS: Data regarding the primary outcome of level of sedation (as evaluated by behavioural scales or physiologic parameters) were abstracted. Secondary outcomes including intraventricular hemorrhage (IVH), periventricular leukomalacia (PVL), death within 28 days of age, adverse effects associated with midazolam (hemodynamic and neurologic), days of ventilation, days of supplemental oxygen use, pneumothorax, length of NICU stay, and long term neurodevelopmental outcome were assessed. When appropriate, meta-analyses were performed using relative risk (RR), risk difference (RD), along with their 95% confidence intervals (95% CI) for categorical variables and weighted mean difference (WMD) for continuous variables. MAIN RESULTS: Two trials were eligible for inclusion in the review. Data on level of sedation from the two trials could not be combined because of differences in tools used to measure sedation levels. One study (Jacqz-Aigrain 1994) showed statistically a significant higher level of sedation in the midazolam group compared to the placebo group. The other study (Anand 1999) comparing midazolam to morphine and placebo found no statistically significant difference in sedation level among the three groups, but statistically significantly higher level of sedation was found in the midazolam group compared with the placebo group during the treatment infusion. However, since the sedation scales used in both studies have not been validated in preterm infants, the effectiveness of midazolam as a sedative in this population could not be ascertained based on the findings of these two studies. In the study by Jacqz-Aigrain (1994), blood pressures were statistically significantly lower in the midazolam group than in the placebo group on days 1 and 2, although there was no statistically significant difference in the incidence of hypotension requiring albumin or vasoactive drugs between groups. The study by Anand (1999) showed a statistically significant higher incidence of adverse neurologic events (death, grade III-IV IVH, PVL) in the midazolam group compared with the other groups. In addition, the midazolam group had a statistically significantly longer duration of NICU stay compared to the placebo group (WMD 5.4 days, 95%CI 0.4, 10.5). (ABSTRACT TRUNCATED)

Humans↗
PubMed1994

Therapy of B-cell acute lymphoblastic leukaemia in childhood: the BFM experience.

In 1981 the BFM group introduced a new treatment strategy for B-ALL based on two alternating 5-day courses of chemotherapy delivered in short intervals up to a total of eight. The therapy courses were composed of fractionated cyclophosphamide, MTX 0.5 g/m2 (24-h infusion), i.t. MTX therapy, and ara-C/VM26 alternating with doxorubicin. The development of the therapy strategies during the subsequent two studies was characterized by shortening treatment duration from eight to six courses, and intensification of CNS chemotherapy in study ALL-BFM-83, and the introduction of HD-MTX (5 g/m2, 24-h infusion) in study ALL-BFM-86. In study ALL-BFM-81, CNS therapy consisted of ID-MTX in combination with i.t. MTX and RX. CNS-positive patients received complete neuroaxis irradiation. In study ALL-BFM-83, CNS chemotherapy was intensified by adding dexamethasone, while MTX/ara-C were administered intraventricularly. Spinal irradiation for CNS-positive patients was omitted. In study ALL-BFM-86, i.t. MTX/ara-C/prednisolone therapy was introduced in combination with HD-MTX but the intraventricular route of drug administration was no longer used. Radiotherapy was omitted completely. In all, 87 patients were enrolled, 22 (eight CNS positive) in study ALL-BFM-81, 24 (seven CNS positive) in study ALL-BFM-83, and 41 (none CNS positive) in study ALL-BFM-86. The estimated 5-year duration of EFS was 40% in study ALL-BFM-81, 50% in study ALL-BFM-83, and 78% in study ALL-BFM-86 (minimal follow-up 36 months). Nineteen of 24 relapses occurred while on therapy or shortly thereafter. In study ALL-BFM-81, the CNS was the most frequent site of failure. In ALL-BFM-83 there were no isolated CNS relapses but more BM relapses occurred. In ALL-BFM-86 localized manifestations were the predominant site of failure, no isolated BM relapses occurred, and only one CNS relapse was diagnosed. No single parameter exerted a consistent influence on outcome with one exception. The presence of residual disease after the first two courses was correlated with an increased risk of therapy failure. Our conclusions from the three studies are listed below. An intensive, short-pulse therapy delivered within a 4 month period is highly effective in the treatment of B-ALL. Prolonged therapy duration is of no value. In addition to fractionated cyclophosphamide-ifosfamide, a 24-h infusion of HD-MTX5 g/m2 in conjunction with an i.t. therapy is a very important component for prevention of both systemic and CNS relapses.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1999

Selective inhibition of kindling development by intraventricular administration of TrkB receptor body.

Recent work has shown that neurotrophin gene expression is increased after seizures evoked in the kindling model of epilepsy, but whether neurotrophins regulate kindling development is as yet unclear. In this study, we attempted to block selectively the activation of distinct neurotrophin receptors throughout kindling development in the rat via chronic intracerebroventricular administration of trk receptor bodies. The efficacy and selectivity of the trk receptor bodies were established by inhibition of neurotrophin-induced trk receptor phosphorylation in pheochromocytoma (PC12) cells and primary cultures of cortical neurons. The intracerebroventricular infusion of trkB receptor body (trkB-Fc) inhibited development of kindling in comparison with that seen with saline or human IgG controls, trkA-Fc, or trkC-Fc. These results imply that activation of trkB receptors contributes to the development of kindling, a form of activity-dependent behavioral plasticity in the adult mammalian brain.

Animals↗
PubMed1985

Risk factors for neonatal hyperglycemia associated with 10% dextrose infusion.

As part of an intensive drug surveillance program, we identified rates and associated risk factors for hyperglycemia related to intravenous 10% dextrose solution in a population of 1,157 newborns in two neonatal intensive care units. Hyperglycemia related to 10% dextrose solution was observed in 64 exposed infants (5.5%), a rate similar to that observed for hypoglycemia (6.7%) in this population. There was a highly significant trend toward an increasing risk of hyperglycemia with decreasing body weight, such that the risk of hyperglycemia among infants weighing less than 1,000 g was 18 times greater than the risk among infants weighing more than 2,000 g. The risk of hyperglycemia also increased with increasing dextrose dose. The effects of weight and dose were independent. Certain measures of disease severity also were associated with increased risks of hyperglycemia. Because increases in blood glucose levels may affect renal function or possibly lead to intraventricular hemorrhage, it is important that glucose levels in neonates receiving 10% dextrose solution be carefully monitored, and the total dextrose dose be adjusted accordingly.

Birth Weight↗
PubMed1991

Simultaneous and continuous measurement of choroid plexus blood flow and cerebrospinal fluid production: effects of vasoactive intestinal polypeptide.

Using laser-Doppler flowmetry during ventriculocisternal perfusion with inulin-[14C]carboxylic acid, choroid plexus blood flow (CPBF) and CSF production were measured simultaneously in rats during periods of 3 h. Blood flow and CSF production decreased only slightly during control experiments. The effect of vasoactive intestinal polypeptide (VIP) was studied at different concentrations of the peptide given either intraventricularly or intravenously. Intraventricular administration of VIP (10(-9) or 10(-7) M) resulted in a decrease in CSF production of up to 30%, while CPBF increased by 20%, also demonstrating that CSF production and blood flow are not directly coupled in the choroid plexus. When infused intravenously, VIP (10 or 100 pmol/kg/min) increased CPBF, an effect partly antagonized at higher concentrations owing to a VIP-induced systemic hypotension. No effect of VIP on CSF production could be seen with intravenous administration.

Animals↗
PubMed1996

[Anesthetic problems in a very low birth weight infant with Kasabach-Merritt syndrome].

Kasabach-Merritt syndrome is characterized by thrombocytopenia and bleeding tendency leading to disseminated intravascular coagulation with giant hemangiomas. We present a very low birth weight infant with this syndrome who underwent four operations. A male baby (1179 g, 37 cm) was born at a gestational age of 28 weeks and 6 days by caesarean section. A large hemangioma, 7 x 8 cm in size, was recognized on the left thigh. As associated consumption coagulopathy (Kasabach-Merritt syndrome) was diagnosed with platelet count 5.1 +/- 10(4) mm-3 and fibrinogen 49 mg.dl-1. Despite treatment with liniac X-ray radiation, systemic steroid and component transfusion, coagulopathy became worse with extremely low platelet count of 1.1 x 10(4) mm-3. Infusion of dopamine and dobutamine was necessary for high output cardiac failure. On day 9, PDA ligation was performed. Cerebro-ventricular drainage, ventricuro-peritoneal shunt and shunt revision were required on day 15, 49 and 88, respectively, for hydrocephalus due to intraventricular hemorrhage. Main anesthetics used were fentanyl and sevoflurane. Major problems encountered by anesthetists were: bleeding tendency, water and electrolyte management, body temperature control, and immaturity and fragility of premature infant. Coagulopathy in Kasabach-Merritt syndrome must be a risk factor for intraventricular hemorrhage, which is a characteristic complication of a very low birth weight infant.

Anesthesia, General↗
PubMed1992

[Effect of intraventricular administration of histamine and its receptor agonists on pentagastrin-induced gastric acid secretion in rats].

The present study shows the dual effects of intraventricularly injected histamine (0.25-2.0 micrograms/5 microliters) on pentagastrin-induced gastric acid secretion. Male Wistar rats weighing 200-300 g were anesthetized with intraperitoneal sodium pentobarbital. Gastric acid was continuously washed out with 37 degrees C saline solution by means of a perfusion pump. On the background of continuous intravenous infusion of pentagastrin [7.5 micrograms/(kg.h),] histamine (0.25 microgram/5 microliters) or 2-pyridylethylamine (PEA, 10 micrograms/5 microliters), a H1-receptor agonist, was injected into the third ventricle through a chronically implanted canula. The acid output decreased 10 min after injection and did not recover at 90 min. When the dose of histamine was increased to 1.0 micrograms or 2.0 micrograms, dual effects appeared. The acid output decreased respectively in 73% or 50% of the animals, while in the rest 27% and 50% of the animals, the acid output increased. H2-receptor agonist dimaprit (10 micrograms/5 microliters, i.c.v.) or impromidine (0.1 micrograms/5 microliters, i.c.v.) had no pronounced effect on pentagastrin-induced acid secretion. Pretreatment with diphenhydramine (16 micrograms/0.2 ml or 32 micrograms/0.2 ml, i.m.) abolished the inhibitory effect of histamine and PEA on acid secretion. These results suggest that histamine may be involved in the central regulation of gastric acid secretion, and the inhibitory effect may be mediated by H1-receptors in the brain. The mechanism underlying the production of the dual effects of histamine is unknown.

Animals↗
PubMed1987

Prolongation of hibernation bout duration by continuous intracerebroventricular infusion of melatonin in hibernating ground squirrels.

Melatonin was infused intracerebroventricularly into hibernating golden-mantled ground squirrels (Citellus lateralis) maintained at 5 degrees C in darkness. Continuous infusion at a rate of 0.5 microliter/h was accomplished using an osmotic minipump. The effect of melatonin on hibernation bout duration was determined with reference to the natural trend in bout duration for each animal. At doses of 200 and 400 ng/h, melatonin produced a dose-related increase in bout duration. No effect was observed following control infusions of artificial cerebrospinal fluid or lower doses of melatonin.

Animals↗
PubMed1995

Antisense oligodeoxynucleotide complementary to oxytocin mRNA blocks lactation in rats.

The posterior lobe peptide oxytocin (OT) is known to control lactation and parturition, as well as maternal and sexual behavior. An antisense oligodeoxynucleotide (ODN) directed against the mRNA of OT was injected intracerebroventricularly 6 times in 12 hour intervals to manipulate the transcriptional message of OT in lactating rats. OT immunoreactivity in magnocellular hypothalamic nuclei and in the posterior lobe of the pituitary was reduced in antisense treated animals in comparison to ODN with scrambled base composition and vehicle controls. This decline in OT levels was associated with a decrease of pup weight. Our results demonstrate that central infusions of antisense ODN significantly reduce OT expression in vivo.

Animals↗
PubMed1997

Adrenalectomy prevents the obesity syndrome produced by chronic central neuropeptide Y infusion in normal rats.

Neuropeptide Y (NPY) in the hypothalamus plays an important role in the regulation of food intake and body weight and seems to be implicated in the etiology of obesity. When intracerebroventricularly (ICV) infused for 6 days in normal rats, NPY resulted in hyperphagia, increased body weight gain, hyperinsulinemia, hypercorticosteronemia, and hypertriglyceridemia compared with vehicle-infused control rats. NPY infusion also resulted in an insulin-resistant state in muscles and in a state of insulin hyperresponsiveness in white adipose tissue, as assessed by the measurement of the in vivo glucose utilization index of these tissues during euglycemic-hyperinsulinemic clamps. All of these hormono-metabolic effects produced by chronic central NPY infusion were completely prevented when rats were adrenalectomized before NPY administration. Adrenalectomy per se had no effect on any of the parameters mentioned above. The levels of mRNA for the obese gene were increased in white adipose tissue after 6 days of ICV NPY infusion in normal rats, and white adipose tissue weight was also increased. These effects of ICV NPY infusion were markedly decreased by prior adrenalectomy, although NPY infusion was able to somewhat enhance the low white adipose tissue obese mRNA levels and tissue weight of adrenalectomized rats. In conclusion, intact adrenal glands, and probably circulating corticosterone in particular, are necessary for the establishment of most of the hormonal and metabolic effects induced by chronic ICV infusion of NPY in normal rats.

Adipose Tissue↗
PubMed1999

The effect of intraventricularly administered GnRH on plasma beta-endorphin levels of the rat.

This study investigates the effects of intraventricularly administered gonadotropin-releasing hormone (GnRH) on plasma beta-endorphin levels in female proestrous rats. Adult female Wistar rats (220-250 g) were implanted with an indwelling cannula in the third ventricle. Approximately 20 days later, the animals which had established a regular 4-day cycle were implanted with two indwelling catheters, one intracarotid and one intrajugular, on the morning of proestrus. A single injection of 100 ng GnRH dissolved in 5 microliters distilled water or 5 microliters of saline (control) was infused slowly through the cannula in the third ventricle. Blood was withdrawn via the intracarotid catheter just before the infusion (12.30 h) and at 14.00, 15.30, 16.30 and 17.30 h for the determination of plasma beta-endorphin levels. The results indicated that intracerebroventricular infusion of GnRH causes a significant decline of plasma beta-endorphin levels at all time points. It is postulated that GnRH possibly causes desensitization of GnRH receptors, due to the continuous GnRH supply to the pituitary via the blood circulation.

Animals↗