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PubMed1993

[Initial experiences with implantable pump systems for intrathecal therapy of chronic pain conditions].

The therapeutic concept of local administration of opioids into the perimedullar and cerebrospinal fluid is the result of fundamental studies concerning the discovery and localization of specific binding sites. These studies provoked considerable clinical interest, because they suggested a non-destructive and fully reversible method. In our department we have been gathering experience with an implantable pump system for various indications of chronic pain on a sample of 25 patients. The first implantation was performed in February 1987 and the latest included in this study in February 1991. The sample of patients consisted of two groups: (A) Chronic non-malignant pain (13 cases), (B) Chronic pain due to cancer (12 cases). We used two different pump devices: the gas-filled continuous infusion pump (Infusaid, Mod. 400) in 10 cases and the manually tractable micro pump (Cordis) in 15 cases. In 23 cases we decided in favour of an intraventricular drug administration, mainly because of the site of the pain; in each of these a ventricular catheter was placed in the frontal horn of the lateral ventricle. In the remaining two cases, the catheter was placed intraspinally, the catheter tip terminating at thoracic segments. Nine of the patients with cancer-related pain experienced from excellent to acceptable pain relief, as did also 10 patients with chronic non-malignant pain. Side effects were rare. Our findings also indicate that, in carefully selected patients, both malignant and non-malignant pain may be managed satisfactorily with this technique.

Adult↗
PubMed2002

The effects of analgesia in the vulnerable infant during the perinatal period.

Although our knowledge of pain and its management in the perinatal period has increased, little is known about the first hours and days of life when major physiologic transition events occur. Prematurity and critical illnesses further complicate analgesic use during this time. Increased morbidity and mortality have been shown in infants receiving placebo infusions after surgery compared with infants with analgesia, highlighting the negative consequences of pain in infants. Opioids can help promote hemodynamic stability, promote respirator synchrony, and decrease the incidence of grade III & IV intraventricular hemorrhage in ventilated preterm neonates. Long-term follow-up studies suggest improved behavioral and cognitive outcomes in children given morphine infusions during NICU confinement. The necessity of fetal analgesia is dictated by the ability of the fetus to feel pain and by the adverse effects of noxious stimuli on future sensory development. Effects of drugs given to the pregnant woman on the (preterm) newborn might be influenced by decreased or absent transplacental transport, compression of the umbilical cord during delivery, or diminished blood flow in the placenta in pre-eclamptic women, resulting in higher serum concentrations. Pharmacokinetics and drug metabolism change in the last trimester, and pain sensitivity may be altered after 32 weeks of gestation. Consequently, dose and dose interval may vary considerably between neonates and within an individual during the first days of life. This subpopulation is not homogenous, and drug doses in a term neonate with a postnatal age of 2 weeks may be quite different from those at birth and are certainly different from those in a premature neonate. Size must be disentangled from age-related factors when examining developmental pharmacokinetic parameters. There are no longitudinal studies published investigating the pharmacokinetic properties of any analgesic more than once per infant. Polymorphisms of the genes encoding for the enzymes involved in the metabolism of analgesics or in genes involved in receptor expression may contribute to the large interindividual pharmacokinetic parameter variability. Polymorphism of the human mu opioid receptor has not yet satisfactorily explained pharmacodynamic variability.

Analgesia↗
PubMed1998

Effects of nitric oxide synthesis on reperfusion injury and catecholamine responsiveness in a heterotopic rat heart-transplantation model.

Global myocardial ischemia and reperfusion injury play a major role in early postoperative graft dysfunction. In this study, the influence of nitric oxide (NO) on reperfusion injury and catecholamine sensitivity after ischemia was investigated in a heterotopic rat heart-transplantation model. After a 1-h ischemic preservation, reperfusion was started either after application of saline vehicle (control, n = 8) or nitro-L-arginine methyl ester (L-NAME; 10 mg/kg, n = 8) for inhibition of NO synthesis or NO-precursor L-arginine (L-Arg; 40 mg/kg, n = 8), or L-NAME plus L-Arg (n = 8), respectively. After 60 min of reperfusion, continuous dobutamine infusion (5 microg/kg/min) was started. Myocardial blood flow was assessed by the hydrogen-clearance method. An intraventricular balloon was used to measure pressure-volume relations: peak left ventricular pressure, the rate of pressure development (dP/dt), end-diastolic pressure, and isovolumic relaxation constant. Myocardial blood flow was significantly reduced after L-NAME and increased after L-Arg in comparison with control (p < 0.05). The L-NAME group showed decreased systolic and diastolic functional recovery in comparison with control. Simultaneous infusion of L-Arg and L-NAME reversed these effects. L-Arg alone led to a further improvement of cardiac functional recovery. Whereas myocardial blood flow remained unchanged in the L-NAME group with dobutamine infusion, it significantly increased in the control group (p < 0.05). L-Arg antagonized this effect of L-NAME. Dobutamine increased peak left ventricular pressure and dP/dt and shortened the isovolumic relaxation constant in all groups; however, the changes of systolic hemodynamic indices were significantly smaller in the L-NAME group (p < 0.05) and significantly higher in the L-Arg group (p < 0.05). These results indicate that (a) NO production within the graft during reperfusion has a significant beneficial effect on graft function, and (b) NO formation may play an important role in beta-adrenergic responses after heart transplantation.

Adrenergic beta-Agonists↗
PubMed2001

Protecting TPN and lipid infusions from light: reducing hydroperoxides in NICU patients.

The use of total parenteral nutrition (TPN) and intravenous fat emulsions in sick or preterm infants is often required to maintain adequate nutrition, yet recent research has shown that when exposed to light these nutrients are altered and deliver a high load of exogenous toxic hydroperoxides to already compromised infants. Hydroperoxides cause damage at the cellular level unless mediated by the body's antioxidant systems. NICU patients are, by definition, patients at risk. Preterm infants have low antioxidant reserves and, like sick term infants, typically suffer significant oxidative stress. Endogenous hydroperoxides alone may overwhelm defenses. The addition of hyperperoxides from light-exposed TPN or fat emulsions increases the risk of tissue damage. Hydroperoxides have been associated with hypoxic-ischemic encephalopathy, intraventricular hemorrhage, periventricular leukomalacia, chronic lung disease, retinopathy of prematurity, and necrotizing enterocolitis. By protecting these infusates from light, bedside nurses can reduce the amount of hydroperoxides infused and protect NICU patients from the associated risks.

Drug Interactions↗
PubMed1984

Behavioral and electrophysiological manifestations of bombesin: excessive grooming and elimination of sleep.

The effect of bombesin, applied intraventricularly in the rat, was examined with regard to the central control of behavior and arousal. Infusion of 1.0 micrograms bombesin produced stereotypic grooming activity and completely eliminated observable sleep. EEG frequency analysis confirmed the absence of sleep and demonstrated normal waking patterns during behavioral stereotypy. These results support a possible physiologic function for bombesin-like peptides in grooming and the sleep-waking cycle.

Adrenocorticotropic Hormone↗
PubMed1977

Central angiotensin II-induced responses in spontaneously hypertensive rats.

The brain isorenin angiotensin system has been implicated in the development of spontaneous hypertension by several investigators. The experiments reported here were designed to test the responsiveness of unanesthetized spontaneous hypertensive (SH) rats to intracerebroventricular angiotensin II injections compared to Wistar-Kyoto (WK) normotensive controls. The results indicate that there is no difference between SH and WK animals in drinking responses or antidiuretic hormone release to central angiotensin II injections; however, an increased pressor responsiveness to intraventricular angiotensin II in SH as compared to WK was observed. The results of intravenous infusions of pressor substances in these experiments and reports by other investigators suggest that the increased blood pressure effects to central angiotensin are due to three possible factors: 1) increased vascular responsiveness of SH to vasoconstrictor substances in general, 2) increased vascular sensitivity of SH rats to sympathetic outflow, and 3) decreased baroreceptor reflexes to acute increases in blood pressure. We suggest that the brain isorenin-angiotensin system may be involved in spontaneous hypertension by increased production of angiotensin II or by activation of a potentiated sympathetic system, but not by a generalized increased sensitivity of brain receptors to central angiotensin.

Angiotensin II↗
PubMed2005

Clinical decision support systems for neonatal care.

BACKGROUND: Clinical decision support systems (CDSS) are computer-based information systems used to integrate clinical and patient information to provide support for decision-making in patient care. They may be useful in aiding the diagnostic process, the generation of alerts and reminders, therapy critiquing/planning, information retrieval, and image recognition and interpretation. CDSS for use in adult patients have been evaluated using randomised control trials and their results analysed in systematic reviews. There is as yet no systematic review on CDSS use in neonatal medicine. OBJECTIVES: To examine whether the use of clinical decision support systems has an effect on 1. the mortality and morbidity of newborn infants and 2. the performance of physicians treating them SEARCH STRATEGY: The standard search method of the Cochrane Neonatal Review Group was used. Searches were made of the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 1, 2004), MEDLINE (from 1966 to August 2004), EMBASE (1980-2004), CINAHL (1982 to August 2004) and AMED (1985 to August 2004). SELECTION CRITERIA: Randomised or quasi-randomised controlled trials which compared the effects of CDSS versus no CDSS in the care of newborn infants. Trials which compared CDSS against other CDSS were also considered. The eligible interventions were CDSS for computerised physician order entry, computerised physiological monitoring, diagnostic systems and prognostic systems. DATA COLLECTION AND ANALYSIS: Studies were assessed for eligibility using a standard pro forma. Methodological quality was assessed independently by the different investigators. MAIN RESULTS: Two studies fitting the selection criteria were found for computer aided prescribing and one study for computer aided physiological monitoring.Computer-aided prescribing: one study (Cade 1997) examined the effects of computerised prescribing of parenteral nutrition ordering. No significant effects on short-term outcomes were found and longer term outcomes were not studied. The second study (Balaguer 2001) investigated the effects of a database program in aiding the calculation of neonatal drug dosages. It was found that the time taken for calculation was significantly reduced and there was a significant reduction in the number of calculation errors.Computer-aided physiological monitoring: one eligible study (Cunningham 1998) was found which examined the effects of computerised cot side physiological trend monitoring and display. There were no significant effects on mortality, volume of colloid infused, frequency of blood gases sampling (samples per day) or severe (Papile Grade 4) intraventricular haemorrhage. Published data did not permit us to analyse effects on long-term neurodevelopmental outcome. AUTHORS' CONCLUSIONS: There are very limited data from randomised trials on which to assess the effects of clinical decision support systems in neonatal care. Further evaluation of CDSS using randomised controlled trials is warranted.

Decision Making, Computer-Assisted↗
PubMed1996

Buflomedil poisoning: five cases with cardiotoxicity.

OBJECTIVE: To report cardiotoxicity of buflomedil. SETTING: Medical intensive care unit of a university hospital. PATIENTS: Five patients admitted to the hospital since 1985 for buflomedil poisoning. The amount ingested was known for only three patients (3-10.8 g). RESULTS: The five young women were admitted to the hospital because of generalized seizures or myoclonic jerks. Cardiac arrest (asystole) occurred for two of them on admission, 1 and 3 h after ingestion. Electrocardiogram revealed atrio-ventricular and intraventricular conduction abnormalities, increased QT interval and flattened T wave, decreasing after sodium bicarbonate infusion in two cases. The patients received mechanical ventilation, gastric lavage, oral activated charcoal, and clonazepam or valproic acid for convulsions or myoclonic jerks. Epinephrine was administered for cardiac arrest. Sodium bicarbonate was infused in one patient on the basis of slightly prolonged QRS duration and in two patients due to cardiac arrest. Clinical outcome was good and without sequelae for all five patients after a few days in the intensive care unit. CONCLUSION: Clinical and electrocardiographic symptomatology of buflomedil poisoning suggests direct cardiotoxicity, which could be related to possible sodium antagonist properties.

Adolescent↗
PubMed1988

Use of an in vitro model for studying the eradication of catheter colonisation by Staphylococcus epidermidis.

Silicone rubber catheters were experimentally colonised with three different strains of Staphylococcus epidermidis sensu stricto. The catheters were then perfused with brain-heart infusion broth by means of an in vitro apparatus which simulates the pharmacokinetics of intraventricular administration of antimicrobial agents. When colonisation was established, vancomycin was administered to the dosing chamber three times daily so as to give peak concentrations of 16, 32, 64 and 128 mg/l. Each experiment was performed in triplicate. Samples of fluid taken from each catheter were cultured before treatment and at intervals thereafter during perfusion for 4 weeks or until recolonisation became apparent. Those catheters not showing evidence of recolonisation were examined by scanning electron microscopy for the presence of organisms. Colonisation was eradicated (as judged by cultural examination) in 37% catheters but eradication did not bear any clear relationship to drug concentrations. Electron microscopical examination of all catheters showing eradication by cultural means revealed the presence of organisms.

Catheterization, Central Venous↗
PubMed2002

Effects of melanocortins on cardiovascular regulation in rats.

1. Of the melanocortin peptides, gamma(2)-melanocyte-stimulating hormone (MSH) has been attributed a cardiovascular effect, inducing an increase in blood pressure and heart rate. Although still controversial, this effect, based on pharmacological blockade experiments, is supposed to be mediated through sympathetic activation. 2. The aims of the present study were to identify the N-terminal pro-opiomelanocortin (N-POMC) fragments and melanocortins that influence blood pressure and heart rate and to investigate the real-time changes in baroreflex sensitivity and in sympathetic and vagal modulation underlying cardiovascular effects in conscious rats without the use of pharmacological blockade. 3. Intracerebroventricular administration of different melanocortins and N-POMC induced a long-lasting dose- dependent pressor response from 1 nmol onwards, with only a small initial bradycardic response with the highest dose. 4. Coinciding with this pressor response, an elicitation of the low-frequency (LF) component was observed in spectral analysis of both blood pressure variability (BPV) and heart rate variability (HRV), followed by the high-frequency (HF) component in at least BPV. Baroreflex sensitivity remained unchanged. 5. After intravenous administration, gamma(2)-MSH produced a short-lasting dose-dependent pressor and cardioaccelerator response with very rapid onset with concentrations from 1 nmol onwards. 6. Continuous infusion of gamma(2)-MSH depressed baroreflex sensitivity and simultaneously increased both components of BPV, with a radical reduction of the LF component and a preserved vagal HF component in HRV. 7. Of all the intravenously administered melanocortins, only gamma(2)-MSH was active. The central effect is likely to depend on an increase of (alpha-)sympathetic outflow. 8. For the peripheral effect, gamma(2)-MSH appeared to act as a baroreceptor reflex-blocking agent, being compatible with a role in the acute stress response.

Animals↗
PubMed1976

An autoradiographic analysis of [3H]alpha-bungarotoxin distribution in the rat brain after intraventricular injection.

Purified alpha-bungarotoxin was isolated by chromatography and made radioactive with tritium ([3H]acetamidino-alpha-bungarotoxin). Infusions of [3H]alpha-bungarotoxin alone or preceded by tubocurarine or atropine were given into the third ventricle. 2. 12, or 24 h after injection the brains were prepared for autoradiography. Injections of alpha-bungarotoxin (radioinert) in buffer, or of [3H]parathyroid hormone in buffer, served as controls. The various patterns of labeling suggest the presence of nicotinic-cholinergic neurons within the arcuate and basolateral regions of the hypothalamus including the supraoptic and suprachiasmatic nuclei and, in addition, the central nucleus of the amygdala.

Amygdala↗
PubMed1993

Effects of midazolam and flunitrazepam on the release of dopamine from rat striatum measured by in vivo microdialysis.

We have studied the effects of midazolam and flunitrazepam on extracellular concentrations of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in rat striatum in freely moving animals using in vivo microdialysis. I.v. injections of midazolam 0.075 and 0.15 mg kg-1 decreased striatal dopamine concentrations in a dose-dependent manner without affecting the concentrations of DOPAC and HVA. Flunitrazepam 0.015 and 0.03 mg kg-1 also decreased striatal dopamine concentrations in a dose-related manner, but the reductions in DOPAC and HVA were not significant. Flumazenil 6 micrograms kg-1 alone did not affect striatal concentrations of dopamine, DOPAC and HVA, but it prevented the effects of midazolam and flunitrazepam. Flunitrazepam 10 mumol litre-1 also decreased striatal dopamine release when infused through a dialysis probe placed into the striatum, but it failed to affect striatal dopamine release when infused into the ipsilateral substantia nigra. Central administrations of midazolam were effective only when the drug was infused into both sites simultaneously (10 and 100 mumol litre-1) or given by intraventricular injection (0.5 and 1 micrograms). These results suggest that midazolam and flunitrazepam affect striatal dopamine release in a different manner.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Hemodynamic and behavioral effects of angiotensin II in conscious sheep.

Intracerebroventricular (ivt) angiotensin II (ANG II) at 0.4, 2, 10, and 50 ng.kg-1.min-1 increased arterial pressure in conscious sheep in a dose-related manner (26 mmHg, P less than 0.05, at 50 ng.kg-1.min-1). Total peripheral resistance (TPR) and right atrial pressure also increased. Heart rate, stroke volume, and cardiac output did not change. Pressor responses to ivt ANG II were not caused by leakage of ANG II into the periphery, because plasma concentrations of ANG II did not change from control (31 +/- 7 pg/ml) at the highest dose of ANG II infused. In contrast, intravenous (iv) ANG II, 10 and 50 ng.kg-1.min-1, increased arterial pressure 29 and 47 mmHg, respectively (P less than 0.05), and decreased heart rate. ANG II, 10 ng.kg-1.min-1 iv, increased plasma ANG II levels from 36 +/- 6 to 354 +/- 69 pg/ml (P less than 0.05). Intracarotid (ic) ANG II, 10 ng.kg-1.min-1, increased arterial pressure 31 mmHg (P less than 0.05) but did not alter heart rate. ANG II ivt caused a dose-related drinking response, with a positive correlation between the amount of water drunk during ivt ANG II infusion and the increase in arterial pressure. Infusions of ANG II at 50 ng.kg-1.min-1 ivt were associated with decreased plasma osmolality and potassium concentration and increased plasma vasopressin concentration.

Angiotensin II↗
PubMed1981

[Immediate effects of intravenous acetazolamide on intracranial pressure (author's transl)].

Nineteen patients with hydrocephalus or head injury were subjected to a continuous intraventricular pressure monitoring and received acetazolamide. Seven mg per Kg body-weight were infused intravenously in one minute. Three patterns of reactions were recorded: 1. a sharp and large rise in cerebrospinal fluid pressure 2. a moderate rise 3. no significant change in C.S.F. pressure. The mechanisms of these responses are investigated: metabolic CO2, which is normally converted rapidly to HCO3- through mediation of carbonic anhydrase within erythrocytes, builds up to produce an immediate effect of cerebral vasodilatation and increases C.S.F. pressure of patients with disturbed compensatory mechanisms. Intravenous acetazolamide may be used as a functional test in patients with ventricular enlargement and normal intracranial pressure. This technique provides useful data about the remaining compensatory capacity for further increases in intracranial volume.

Acetazolamide↗
PubMed1983

Deoxycytidine transport and metabolism in the central nervous system.

The mechanisms by which deoxycytidine enters and leaves brain, choroid plexus, and CSF were investigated by injecting [3H]deoxycytidine intraarterially, intravenously, and intraventricularly. After intracarotid injection of deoxycytidine (1.0 microM) into rats, deoxycytidine did not pass through the blood-brain barrier at a faster rate than sucrose. [3H]Deoxycytidine, either alone or together with unlabeled deoxycytidine, was infused at a constant rate into conscious adult rabbits. At 130 min, [3H]deoxycytidine readily entered CSF, choroid plexus, and brain. In brain, approx. 60% of the nonvolatile radioactivity was attributable to [3H]deoxycytidine phosphates. The addition of 0.22 mmol/kg unlabeled deoxycytidine to the infusion syringe decreased the phosphorylation of [3H]deoxycytidine in brain by approx. 50%; the addition of 2.2 mmol/kg of unlabeled deoxycytidine to the infusion syringe decreased the relative entry of [3H]deoxycytidine into CSF and brain by approx. 50 and 75%, respectively. Two hours after the intraventricular injection of [3H]deoxycytidine, [3H]deoxycytidine was rapidly cleared from CSF, in part, to brain, where approx. 65% of the [3H]deoxycytidine was converted to [3H]deoxycytidine phosphates. The intraventricular injection of unlabeled deoxycytidine with the [3H]deoxycytidine decreased the phosphorylation of [3H]deoxycytidine in the brain significantly and also decreased the clearance of [3H]deoxycytidine from the CSF. These results were interpreted as showing that the entry of deoxycytidine from blood into CSF occurs by a saturable transport system within the choroid plexus. Once within the CSF, the deoxycytidine can enter brain, undergo phosphorylation to deoxycytidine phosphates, and subsequently be incorporated into DNA.

Animals↗
PubMed2000

Intraventricular administration of substance p increases the dendritic arborisation and the synaptic surfaces of Purkinje cells in rat's cerebellum.

Substance P was infused in the lateral ventricles of twenty Lewis rats for twenty days. On the twentieth day the animals were sacrificed and the cerebellar cortex was processed for electron microscopy. The ultrastructural morphometric analysis revealed that the Purkinje cell dendritic arborisation and the number of the synapses between the parallel fibres and the Purkinje cell dendritic spines were much higher than in control animals. Numerous unattached spines of the secondary and tertiary dendritic branches of the Purkinje cells were also seen in the molecular layer either free or surrounded by astrocytic sheath. The increased number of synapses between the Purkinje cell dendrites and the parallel fibres in the animals, which received substance P intraventricularly, in correlation to control animals, supports a neurotrophine-like activity of the substance P in the mammalian cerebellum, enforcing the pre-programmed capability of the Purkinje cells to develop new synaptic surfaces.

Animals↗