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PubMed1979

Computed tomography in the diagnosis of intracranial meningioma.

The CT findings in 53 meningiomas are reported. Based upon the plain and post-contrast CT pattern and density characteristics, the diagnosis of meningioma was accurately predicted in 28 of 35 convexity, parasagittal, subfrontal, middle fossa and sphenoid wing lesions (80%). In 2 calcified nonenhancing meningioma, the diagnosis was suspected by CT findings. CT was extremely accurate in detecting 16 juxtasellar, intraventricular, tentorial and posterior fossa meningiomas, but the CT pattern was less specific such that differentiation from other neoplastic or vascular lesions was not always possible. There were only 2 false negative cases; these occurred when contrast infusion had not been performed.

Brain Neoplasms↗
PubMed2000

The effect of the atrioventricular interval during atrioventricular sequential pacing on the hemodynamics in dynamic obstruction of the left ventricular outflow tract in dogs.

The present study was performed to clarify the mechanism involved in the reduction of the pressure gradient in the left ventricular outflow tract of patients with hypertrophic obstructive cardiomyopathy when treated with atrioventricular (AV) sequential pacing. The effect of AV sequential pacing with variable AV intervals on the hemodynamics and dyssynchronous wall motion was experimentally studied using echocardiography in the dynamic obstruction of the left ventricular outflow tract created by dobutamine infusion in 17 dogs. The pressure gradient of the left ventricular outflow tract decreased with shortening of the AV interval during AV sequential pacing. Also, the dyssynchrony time, defined as the difference in the time between the intraventricular septum and posterior wall during the systolic phase recorded with M-mode echocardiography, increased with shortening of the AV interval during AV sequential pacing. However, very short AV intervals produced a significant decrease in the aortic pressure and increase in the pulmonary capillary wedge pressure. The dyssynchrony time showed a positive liner correlation with the percentage reduction in the pressure gradient of the left ventricular outflow tract (R=0.794, p<0.0001). It was concluded that dyssynchronous wall motion in the left ventricle was produced by pacing from the right ventricular apex and resulted in a reduction in the pressure gradient of the left ventricular outflow tract. Optimization of the AV interval during AV sequential pacing may play an important role in improving the hemodynamics in dynamic obstruction of the left ventricular outflow tract.

Animals↗
PubMedDate not supplied

[The effect of endotoxin on the cardiovascular system].

The dynamics of changes in myocardial contractility and pressure in the left ventricle of the heart and the femoral artery were studied in rabbits before and after intravenous infusion of 2 mg/kg endotoxin. The left ventricle was catheterized. The signal from the left-ventricular pressure transducer was fed into a microcomputer after analog-digital conversion for calculating the maximal rate of increase in intraventricular pressure. All the parameters studied began decreasing as early as the 5th minute after endotoxin administration. A statistically significant decrease (p less than 0.05) of the heart rate was recorded first on the 30th minute, than the left-ventricular pressure and maximal rate of intraventricular pressure increase took place on the 45th minute, and systolic and diastolic pressure in the femoral artery decreased on the 60th minute. The detected disorders of myocardial contractility provoke the appearance of hypotension the main role in the development of which is played by damage to the peripheral vascular network.

Animals↗
PubMed1985

Drug pumps for treatment of neurologic diseases and pain.

Implanted drug pumps provide a new way to infuse medication chronically to the nervous system in a selective fashion. They have been of value in treating pain of cancer and spasticity through spinal subarachnoid catheters. Treatment of Alzheimer's disease is currently being investigated using intraventricular bethanechol.

Alzheimer Disease↗
PubMed1994

Intraventricular application of BDNF and NT-3 failed to protect nucleus basalis magnocellularis cholinergic neurones.

Quantitative analysis of ChAT immunoreactive neurones was used to evaluate the protective potential of BDNF or NT-3 against retrograde changes in nucleus basalis magnocellularis (nbm) cholinergic neurones after unilateral partial devascularization of the rat neocortex. A daily intracerebroventricular dose of 12 micrograms, proven to be effective for NGF and aFGF in the same experimental paradigm, was administered by minipump infusion for a 1-week period. Thirty days after lesioning, neuronal shrinkage and loss of neuritic processes were not prevented by treatment. The results indicate that intracerebroventricularly delivered BDNF and NT-3 are not as effective as NGF and aFGF in protection of nbm cholinergic neurones against lesion-induced changes in adult rat brain.

Animals↗
PubMed1985

Efficacy and tolerance of intravenous lorcainide in patients with normal and impaired intraventricular conduction.

The effectiveness and safety of intravenous lorcainide was evaluated in 14 patients with normal (QRS less than 110 ms) and in 9 patients with prolonged QRS duration (QRS greater than or equal to 110 ms) showing chronic high frequency premature ventricular complexes (mean value of PVCs 17 min-1). Lorcainide was infused intravenously by intermittent bolus at 10 mg every minute to a total dose of 160 mg with exception of 5 patients with a prolonged QRS duration who only received 100 mg. The overall reduction of PVCs 1 hour after administration of the drug was 86% (p less than 0.05) in the patients with normal QRS duration and 98.5% (p less than 0.05) in the patients with a prolonged QRS duration. The mean plasma drug level achieved 1 h after treatment was 280 +/- 60 ng/ml in the patients with QRS less than 110 ms and 170 +/- 40 ng/ml in the patients with a QRS greater than or equal to 110 ms. Heart rate and blood pressure did not change but a significant increase (p less than 0.05) in QRS duration (+37%) was observed 30 min after the infusion of 160 mg lorcainide in the patient group with normal QRS duration. Lorcainide was well tolerated. Mild adverse effects were observed in five patients including: warmth sensation, vomiting, paresthesias, transient hypotension and the development of a junctional escape rhythm. Therefore lorcainide appears to be a safe and effective drug, that can even be administered to patients with a prolonged QRS duration.

Adult↗
PubMed1995

Alterations in sensitivity to intracerebral vasopressin and the effects of a V1a receptor antagonist on cellular, autonomic and endocrine responses to repeated stress.

We have shown previously that repeated restraint stress results in differential adaptation at both macrophysiological and cellular levels. Chronic stress accentuates vasopressinergic control of adrenocorticotropic hormone secretion in the pituitary. The present work determined whether endogenous vasopressin plays a role in response to repeated restraint. The first experiment explored changes in the response of repeatedly stressed animals to intracerebral vasopressin infusions. The second determined the effect of pretreating rats with a vasopressin V1a receptor antagonist on the way that they adapted to repeated restraint. Experiment 1: rats were subjected either to daily 60-min restraint for 10 days or transferred to the testing room where restraint sessions took place (controls). On the 11th day, they were infused with either artificial cerebrospinal fluid or 250 pmol vasopressin. The behavioural response to vasopressin was unaltered by previous stress. Plasma corticosterone was lowered in vasopressin-treated rats only after previous stress. Sixty minutes after vasopressin infusion, the central amygdala, locus coeruleus, the nucleus of the solitary tract and the dorsal vagal nucleus expressed increased levels of c-fos, and there were significant two-way interactions between stress and infusion for dorsal paraventricular nucleus, locus coeruleus and dorsal vagal nucleus. One-way analysis suggested that previous stress also reduced the c-fos response to vasopressin in the nucleus of the solitary tract. These results show that previous stress causes differential alterations in behavioural, endocrine and cellular responses to vasopressin. Experiment 2: rats were implanted with a transmitter which monitored heart rate and core temperature and a lateral cerebroventricular cannula. For 10 days, either artificial cerebrospinal fluid or 2500 pmol V1a antagonist, [d(CH2)1(5)-O-Me-Tyr2-Arg8]-vasopressin were infused i.c.v. 10 min prior to a 60-min restraint session. On the 11th day, no infusions were carried out, but rats received the usual period of restraint. The vasopressin antagonist was followed by motor responses (freezing, grooming and burrowing), more evident during the third and fifth days of stress. Core temperature responses were altered by the antagonist: stress-induced hypothermia was greatly reduced. Reduced baseline core temperatures, observed in controls as successive stress proceeded, were absent in antagonist-treated rats. By contrast, there were no significant effects of vasopressin antagonism on stress-induced tachycardia, nor in the way that this adapted to repeated restraint. On the 11th day (no i.c.v. infusions), hypothermic responses were no different in rats previously receiving either antagonist or control vehicle, but secondary hyperthermia was greater in the first group. Corticosterone levels were not altered by previous i.c.v. infusions.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Physiological↗
PubMed1993

Intracerebroventricular infusion of glycine stimulates vasopressin release in conscious sheep.

We have previously observed that elevation of the plasma glycine concentration stimulates vasopressin (AVP) release in man and sheep. In the present study we show that this effect of glycine can be elicited directly via a cerebral site of action in conscious sheep. Intracerebroventricular infusions of 0.05 and 0.15 M glycine solutions increased the plasma AVP concentration by 6 and 50 times, respectively, while no effect on water intake was observed. Hyperhydration did not block the stimulation of AVP release. No behavioural side effects, or changes in blood pressure, were observed in response to the infusions.

Analysis of Variance↗
PubMed1995

Effect of central infusion of benzamil on Dahl S rat hypertension.

The effect of continuous central infusion of benzamil, a Na+ channel-selective amiloride analogue, on the salt-induced hypertension in inbred Dahl salt-sensitive (SS/jr) rats was assessed. The continuous intracerebroventricular or subcutaneous infusion of benzamil at doses which have no effect when infused systemically was started at the same time or 2 wk after saline was substituted for drinking water, when the rats' blood pressures had become significantly elevated. Within 13 days, drinking saline caused a similar and significant increase in the blood pressures of rats receiving the vehicle intracerebroventricularly and 1 microgram/h of benzamil subcutaneously, which persisted throughout the 4-wk experiment. The intracerebroventricular infusion of 1 or 0.3 microgram/h benzamil, started at the same time the salt challenge was instituted, significantly deterred the increase in blood pressure over 4 wk. The intracerebroventricular, but not the subcutaneous, infusion of benzamil at 0.5 microgram/h arrested the increase in blood pressure in rats that were already hypertensive after 12 days on saline. Within 3 days the pressures in the intracerebroventricular and subcutaneous benzamil groups became significantly different, due to the further increase of the blood pressure in those animals receiving the intracerebroventricular vehicle with subcutaneous benzamil. There was no significant difference in weight gain throughout the experiment or in 24-h urine volumes and urinary Na(+)-to-K+ ratio at days 5 and 12 of benzamil infusion between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed2003

Leptin signaling in the hypothalamus during chronic central leptin infusion.

Using a rat model of chronic central leptin infusion in which neuropeptide Y neurons develop leptin resistance, we examined whether leptin signal transduction mechanism in the hypothalamus is altered during central leptin infusion. Adult male rats were infused chronically into the lateral cerebroventricle with leptin (160 ng/h) or vehicle via Alzet pumps for 16 d. In the leptin-infused group, the initial decrease in food intake was followed by a recovery to their preleptin levels by d 16, although food intake remained significantly lower than in artificial cerebrospinal fluid controls; and body weight gradually decreased reaching a nadir at d 11 and remained stabilized at lower level thereafter. Phosphorylated leptin receptor and phosphorylated signal transducer and activator of transcription-3 (p-STAT3) remained elevated in association with a sustained elevation in DNA-binding activity of STAT3 in the hypothalamus throughout 16-d period of leptin infusion. However, phosphorylated Janus kinase-2 was increased during the early part of leptin infusion but remained unaltered on d 16. Although hypothalamic suppressors of cytokine signaling-3 (SOCS3) mRNA levels were increased throughout leptin infusion, SOCS3 protein levels were increased only on d 16. This study demonstrates a sustained elevation in hypothalamic leptin receptor signaling through Janus kinase-STAT pathway despite an increased expression of SOCS3 during chronic central leptin infusion. We propose that an alteration in leptin signaling in the hypothalamus through pathways other than STAT3 and/or a defect in downstream of STAT3 signaling may be involved in food intake recovery seen after an initial decrease during chronic central leptin infusion.

Adipose Tissue↗
PubMed1997

Lack of effect of antenatal indomethacin on fetal cerebral blood flow.

OBJECTIVE: Our purpose was to investigate fetal cerebral blood flow and the incidence of intraventricular hemorrhage in patients undergoing tocolysis with either indomethacin or magnesium sulfate at < 30 weeks' gestation. STUDY DESIGN: Consenting patients at < 30 weeks' gestation with preterm labor were randomized to receive indomethacin or magnesium sulfate tocolysis. Magnesium sulfate was administered intravenously with an 8 gm loading dose given over the first hour, 4 gm over the second hour, and then a maintenance infusion of 2.5 gm per hour. The infusion was continued for approximately 12 hours after the cessation of uterine contractions. Patients randomized to receive indomethacin were given an initial dose of 50 to 100 mg orally or per rectum, followed by 25 to 50 mg orally every 4 to 6 hours for 24 to 48 hours. Oral tocolytic agents were not used after successful tocolysis. Betamethasone was administered to all patients. Patients underwent fetal cerebral Doppler studies during tocolytic therapy and at least 24 hours after completion of the treatment. RESULTS: Twelve patients were randomized to receive indomethacin and twelve patients were randomized to receive magnesium sulfate. Twenty-one fetuses underwent cerebral Doppler studies in triplicate during and after therapy. The mean gestational age at tocolysis was 27.5 +/- 1.9 weeks for the indomethacin group and 26.4 +/- 1.6 weeks for the magnesium sulfate group (p = 0.14). The middle cerebral artery resistance index for fetuses during indomethacin treatment was 0.73 +/- 0.09, whereas the resistance index after therapy was 0.75 +/- 0.05 (p = 0.49). The resistance index during magnesium sulfate tocolysis was 0.79 +/- 0.04 and after therapy it was 0.76 +/- 0.04 (p = 0.18). There was no significant difference in the resistance index between the groups on or off therapy. In addition, the incidence of intraventricular hemorrhage was similar in both groups. CONCLUSION: These results suggest that indomethacin does not significantly affect fetal cerebral blood flow. If antenatal indomethacin in the preterm fetus increases the risk of intraventricular hemorrhage, it would appear to be by another mechanism.

Adolescent↗
PubMed1997

Impact of corticotropin-releasing hormone on extracellular norepinephrine in prefrontal cortex after chronic cold stress.

We have previously demonstrated that exposing rats to cold (5 degrees C) for 3-4 weeks potentiates the increase in extracellular norepinephrine (NE) in the medial prefrontal cortex produced by acute tail shock. In the present study, we used microdialysis to determine the duration of cold exposure required to produce this sensitization and explored the mechanism of the phenomenon. Tail shock elicited a twofold greater increase in extracellular NE in the medial prefrontal cortex of rats exposed to cold for 2 weeks than in naive control rats or in rats exposed to cold for 1 week and tested either immediately or after a 2-week delay. Local infusion of 10 microM D-amphetamine or 30 mM K+ increased extracellular NE in the medial prefrontal cortex (approximately 350 and 190%, respectively) comparably in control rats and rats exposed to cold for 3 weeks. In contrast, intraventricular administration of 3.0 microg of corticotropin-releasing hormone increased extracellular NE in the medial prefrontal cortex by 65% in rats exposed to cold for 2 weeks, but only 35% in control rats. These results indicate that an enhanced responsiveness of noradrenergic neurons to acute tail shock (1) requires approximately 2 weeks of cold exposure to develop and (2) may be mediated by a change at the level of the noradrenergic cell bodies rather than the nerve terminals.

Adrenergic Agents↗
PubMed1986

Effects of intraventricular methotrexate on cerebrospinal fluid monoamine metabolites in rhesus monkeys.

Previous work suggested that methotrexate (MTX) may cause encephalopathy by inhibiting biosynthetic pathways for dopamine and serotonin in the brain. We examined this issue by measuring the neurotransmitter metabolites homovanillic acid and 5-hydroxyindoleacetic acid in the lumbar CSF of rhesus monkeys receiving continuous intracerebroventricular infusions of MTX or dichloromethotrexate. Infusion of the lowest dose (0.05 mg/day) produced a large (300%) rise in homovanillic acid levels and a modest elevation in 5-hydroxy-indoleacetic acid. During higher dose infusion, which was associated with clinical encephalopathy, the biogenic amine metabolites fell from their previous elevated levels. In one encephalopathic monkey, an injection of 1 mg of leucovorin produced a marked elevation in CSF monoamine metabolites within 1 hour and rapid clinical recovery. In contrast, leucovorin produced no change in monoamine metabolites in control animals. The data suggest that MTX may block egress of monoamine metabolites from CSF at the lower doses and suppress neurotransmitter turnover at toxic doses which cause encephalopathy. Serial measurements of CSF monoamine metabolites deserve further investigation as biochemical markers for toxic effects of MTX on neuronal metabolism in the CNS.

Animals↗
PubMed1992

[Ambulatory epidural analgesia in patients with tumors. An outmoded technique?].

In 35 of 316 patients suffering from severe cancer pain, an epidural catheter was placed for continuous morphine application. Indications for epidural opiates included failure of pain relief with oral morphine, severe side effects with oral administration, and contraindications for oral morphine, e.g., ileus. METHODS. The epidural catheter was inserted in the lumbar, thoracic or cervical region, according to the main localization of pain. A silicon catheter with a Dacron cuff (4.2 F Broviac Davol, Cranston, R.I.) was connected and tunneled subcutaneously to a distant exit on the lateral chest wall (Fig. 2). A portable morphine pump (CADD-PCA Pharmacia Deltec) was connected to the externalized catheter. The morphine was infused continuously at a basic rate. It could be increased to a programmed limit by additional boli determined by the patients themselves. Thirty patients were treated as outpatients. RESULTS. The mean duration of treatment was 101 (10-333) days. The daily dose of morphine ranged from 9 to 200 (33) mg at the beginning of therapy, and from 20 to 288 (88) mg at the end of treatment. In 27 patients (77%) epidural morphine administration proved to be a valuable method of pain control (Fig. 3). Even in most cases of tolerance to oral morphine, especially in patients suffering from pain of neuropathic origin, pain control was adequate. There were no cases of continuous loss of effectiveness of continuous loss of effectiveness or development of tolerance (Fig. 5). The epidural morphine dosage depended on the character and intensity of pain and its responsiveness to epidural opiates. Technical complications were noticed in 6 patients (17%), and fairly mild side effects of epidural morphine occurred in 20% of the patients for a limited time. CONCLUSIONS. The technique described is a simple and convenient method for long-term treatment of cancer patients with epidural morphine. There was no need for more invasive procedures, such as intrathecal or intraventricular morphine administration, in this group of patients in whom no pain relief had been achieved with oral morphine administration.

Adult↗
PubMed1994

Effects of hormonal treatment and history on scopolamine inhibition of lordosis.

The muscarinic receptor blocker, scopolamine, inhibits the display of lordosis behavior in female rats but its effectiveness depends on hormonal conditions. In these experiments, systemic administration of scopolamine (0.031-4 mg/kg) inhibited lordosis in ovariectomized rats brought into receptivity by treatment with a low dose of estradiol benzoate (EB, 0.25 micrograms for 3 days) with progesterone (P, 500 micrograms for 1 day), or a high dose of EB (25 micrograms for 3 days) with and without P. However, the effectiveness of scopolamine was reduced at the high dose of EB and with the addition of P. Furthermore, scopolamine failed to inhibit lordosis in females treated on a second week with the high dose of EB with or without P, unless an interval of at least 3 weeks separated the two sets of steroid treatments. The reduced effectiveness of scopolamine cannot be explained by peripheral mechanisms because its inhibitory effect on lordosis also was reduced following repeated hormonal exposure even when scopolamine was infused directly into the lateral ventricles.

Acetylcholine↗
PubMed1990

Lack of pressor response to intracerebroventricular infusion of aldosterone in sheep.

1. Studies in the rat and the dog have shown that infusion of aldosterone for several weeks into the cerebral ventricles (ICV) can produce hypertension at doses that do not have an effect when infused systemically. We have previously shown that a high physiological dose of aldosterone infused intravenously at 10 micrograms/h in sheep produces an increase in blood pressure of 7 mmHg within 2 days. 2. In this paper we report the effects of ICV infusion of aldosterone at 2 micrograms/h for 6 days in conscious sheep. 3. Neither blood pressure nor heart rate were altered, and there were no consistent changes in any of the metabolic parameters measured. 4. These results do not support a role for central effects of aldosterone in the hypertension produced by systemic infusion of the steroid in sheep.

Aldosterone↗