[Postherpetic neuralgia--therapeutic approaches].
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Biomedical subjects
Publications and source records attributed to E Geller.
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CT examination of the abdomens of two children demonstrated sites of high attenuation in the stomach, which were revealed to be bubble gum. Investigation of the CT appearance of samples of chewing gum showed that it consistently has high attenuation (178-345 HU). The attenuation of gum base, which contains calcium carbonate, was 476 HU. In addition, examination of a volunteer who had swallowed bubble gum confirmed the CT appearance.
The direct cardiac effects of volatile anesthetics following cardioplegic ischemia were investigated in isolated, paced rat hearts. In one series of experiments, the hearts were perfused with oxygenated Krebs Henseleit solution for a 15-minute stabilization period and then the effect of the volatile anesthetic was tested. In another series of experiments, after the stabilization period, the hearts were subjected to cardioplegic (KCl 20mEq/L) ischemia at 30 degrees C for 30 minutes and then the effect of the volatile anesthetic was tested. Halothane, enflurane or isoflurane was introduced to the Krebs Henseleit solution at 0.7 and 1.4 minimal alveolar concentration. All the volatile anesthetics decreased myocardial contractility in a dose dependent manner both before and after cardioplegic arrest. Halothane decreased coronary flow, while isoflurane and enflurane increased coronary flow in both the cardioplegic and non-cardioplegic hearts. The influence of the anesthetics was transient and ceased once they were withdrawn. Ischemic cardioplegia did not affect the response to volatile anesthetics.
A 22 year old male was admitted with haemoptysis. A chest X-ray showed bilateral confluent alveolar infiltrates. Bronchoscopy revealed blood oozing from all bronchopulmonary segments. Open lung biopsy disclosed bilateral effusions and large necrotizing nodules with pleural adhesions. Histological examination showed tumour cells, which were negative to epithelial and embryogenic markers but positive to factor VIII. This confirmed the diagnosis of an epithelioid haemangioendothelioma. This rare tumour, usually has an indolent course, whereas in our case it was complicated by alveolar and intrapleural bleeding.
The popularity and widespread availability of benzodiazepines (BZD) has led to their frequent abuse in intentional drug poisoning. Although mortality from pure BZD overdose is usually small, in elderly, debilitated patients, or when BZD are combined with other CNS depressant drugs, morbidity increases significantly and outcome may be fatal. Drug overdose is therefore a medical emergency necessitating close observation and support of vital functions. Recently, the specific BZD antagonist flumazenil (Anexate) has become clinically available and much experience in its usefulness has accumulated. The present review summarizes a total of 30 studies and reports published to date, involving approximately 760 intoxicated patients. Flumazenil was evaluated both in prehospital use as well as in emergency rooms or in intensive care units. The age of patients ranged from 4-90 years and doses of flumazenil varied between 0.3-10 mg, approximately 1 mg being the most frequently used. All patients intoxicated with only BZD returned to full consciousness within minutes after the injection of flumazenil. When a mixture of BZD and other CNS depressants was abused, a range of effects was observed. This varied from no change to a return to full orientation, depending on the contribution of the BZD to the state of unconsciousness. Re-sedation occurred in about 65% of flumazenil treated patients, usually within 0.5-3 h after the first dose, the shorter interval being associated with mixed-drug poisoning. Repeated doses of the antagonist (0.2-2 mg), sometimes followed by continuous infusion (0.1-0.5 mg/h), were effective in maintaining patients fully oriented.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic fenfluramine treatment reduced whole blood serotonin and CSF 5-hydroxyindoleacetic acid, but increased aggressive and locomotor behavior, in adult male vervet monkeys (Cercopithecus aethiops sabaeus). Following a drug-free washout period to monitor the drug recovery course, we initiated a second period of fenfluramine treatment in the same animals. When whole blood serotonin concentrations were reduced by about 40% from predrug baseline levels, we examined 11 cortical and subcortical brain regions for their content of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid, norepinephrine, and dopamine. We observed correspondence between the reduction in whole blood serotonin and the reduction in brain 5-hydroxytryptamine. Similarly, there was a correspondence between the reduced 5-hydroxyindoleacetic acid levels observed in CSF and brain. No alterations were noted in the concentrations of norepinephrine or dopamine. These observations suggest that the behavioral effects observed in monkeys after chronic fenfluramine treatment result from reduced central serotonin.
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Flumazenil, the first specific benzodiazepine (BZD) antagonist, is one of the most innovative drugs to become available within the last few years. Flumazenil is indicated for the reversal of the centrally depressant effects of BZDs, in BZD-induced anaesthesia, in BZD sedation in intensive care and in patients comatose after drug overdoses including BZDs. A conference of experts experienced in the treatment of mixed drug overdoses by various means, including flumazenil, was held in order to try to reach a consensus regarding the safe use of flumazenil in this indication. From the knowledge and experience gained to date, it was concluded that flumazenil may be useful and safe in the treatment of suspected BZD and mixed drug overdoses, provided that the appropriate precautions are observed.
The specific benzodiazepine antagonist flumazenil is currently under intense study. Despite much clinical experience, no detailed invasive hemodynamic studies of its use in cardiac patients have been published. In the present study, hemodynamic and respiratory variables were measured in 10 cardiac patients undergoing catheterization of the right and left sides of the heart, before and after sedation with intravenous diazepam, and after reversal of sedation with flumazenil. A sleep dose of diazepam (12.2 +/- 5.1 mg, mean +/- SD) caused only slight decreases in mean arterial pressure (103 +/- 12 to 98 +/- 14 mm Hg; P less than 0.05), pulmonary capillary wedge pressure (13.2 +/- 6.3 to 11.7 +/- 6.6 mm Hg; P less than 0.05), and left ventricular end-diastolic pressure (20.8 +/- 7.5 to 17.3 +/- 10.0 mm Hg; P less than 0.05), with no significant changes in respiratory gas homeostasis. Intravenous flumazenil (0.22 +/- 0.07 mg) resulted in spontaneous awakening and return to full orientation, yet caused no significant alteration in either hemodynamic or respiratory variables measured. Reversal of diazepam-induced sedation by flumazenil in cardiac patients appears safe and effective.
Spinal cord ischemia complicating resuscitative aortic occlusion is reported in a patient requiring emergency thoracotomy and aortic cross-clamping following a stab wound to the heart. Paraparesis and ischemic myelopathy were documented in the absence of associated injury. The possible contribution of systemic hypotension to spinal cord ischemia following aortic occlusion is suggested.
The purpose of this study was to determine the effects of reversal of sedation with flumazenil (F), in the presence or absence of opiates, on arterial oxygen saturation (SaO2) and end-tidal CO2 (ETCO2). Twenty-four patients undergoing surgery and epidural anaesthesia were studied. Twelve patients (Group A) were orally premedicated with diazepam and 0.1 mg.kg-1 morphine i.m. Intraoperative sedation consisted of midazolam 0.1 mg.kg-1 and pethidine 0.7 mg.kg-1 i.v. Twelve patients (Group B) were premedicated with diazepam and sedated intraoperatively with 0.1 mg.kg-1 midazolam. In the recovery room, six patients in each group were randomly allocated to receive 1 mg of flumazenil while the others were allowed to awaken spontaneously (control). Sedation (eyes open vs closed), SaO2, ETCO2, respiratory rate, blood pressure and pulse were non-invasively monitored for 90 min. Administration of flumazenil resulted in a statistically significant increase in the number of patients with eyes open in both groups at 5 min, lasting 15 min in Group A and 30 min in Group B patients. An increase in SaO2 from 15-45 min after injection of flumazenil was observed only in Group B. No significant difference between groups in any other parameter was found. We concluded that reversal of benzodiazepine (BZ) sedation with flumazenil improved SaO2 in patients sedated with only BZ; in the presence of BZ and opiates, flumazenil did not affect respiratory parameters.
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We examined in the rat several possible relationships between the pineal gland and the hypothalamus-pituitary-thyroid axis. The pineal gland, the retina, and the hypothalamus exhibited a diurnal rhythm in thyrotropin-releasing hormone (TRH) content with peak values occurring around 1200 h. This rhythm in the hypothalamus was abolished by constant light but was not affected by pinealectomy. Nor did pinealectomy affect hypothalamic TRH content, pituitary content of thyroid-stimulating hormone (TSH) or prolactin; serum levels of (TSH), triiodothyronine (T3), or thyroxine (T4), or serum free-thyroxine index; or free-triiodothyronine index. Melatonin did not affect TSH or prolactin release from the anterior pituitary or TRH release from the hypothalamus in vitro. Isoproterenol did not affect the TRH content of pineal glands in vitro; nor did TRH or T3 affect basal or stimulated activities of serotonin N-acetyltransferase, the presumed controlling enzyme in melatonin production. We found no evidence for significant interactions between the pineal gland and the hypothalamus-pituitary-thyroid axis.
Administration of corticosteroids to rat pups within the first several days of life results in retardation of several behavioral, neurophysiological, and biochemical developmental patterns. At 25 days of age, animals treated neonatally with 1.0, 0.5, or 0.1 mg hydrocortisone acetate showed dose-dependent decreases in plasma ACTH following 2.5 min continuous exposure to ether. On day 20, plasma corticosterone values did not differ between these groups 15 min after ether stress, but lower values were seen 60 min after ether in animals treated at birth with 0.5 mg hydrocortisone. At 45--48 days of age, hydrocortisone-treated animals exposed to one of 2 different stressors showed decreased plasma corticosterone response to stress; females had lower corticosterone levels following both stressors, while males showed suppressed corticosterone levels following exposure to the mild (novelty) but not to the intense (ether) stress. These data demonstrate that neonatal exposure to hydrocortisone results in decreased CNS-pituitary responsivity to stress at 20--25 days of age, and that the adrenocortical response to stress in impaired at 45--48 days of age.
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The intravenous administration of chlorpromazine in 12 patients with acute myocardial infarction and altered pump function was followed by a significant reduction in systemic vascular resistance (28.4%) and an increased cardiac index (23.0%). The drug also produced a significant decline in mean pulmonary capillary wedge pressure (38.2%), while the heart rate and mean stroke work index did not change significantly. Although the mean blood pressure decreased by 18.3%, the transymocardial pressure gradient was not affected. A significant reduction in the major determinants of myocardial oxygen consumption, such as arterial blood pressure and left ventricular wall tension, suggested a decrease in myocardial demand for oxygen. Improvement of left ventricular performance was associated with a sedative effect in most of the patients. Intravenous administration of chlorpromazine proved to be of benefit in patients with moderate to severe congestive heart failure and cardiogenic shock.