Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 11-year-old girl presented from Villa Azueta, Veracruz, a poor and small town on the Tesechoacan riverside. The Tesechoacan riverside is a tropical area in the south-east of Mexico, between 18 degrees, 04',32" latitude and 95 degrees, 42',23" longitude. Her family consisted of both parents and 12 brothers, all apparently healthy and living in a humble hut, with poor nutrition and hygiene. The main sign was a tumor on her neck that had developed during the previous 6 months. On clinical examination, the patient's temperature was normal and her weight was 27.5 kg. Below the right angle of the jaw a firm-to-hard tumor was noted measuring 5 x 3 cm, it was tender and lobulated (Fig. 1) with a central purulent fistula containing small worms with morphology of Lagochilascans minor (Fig. 2). Iron-deficiency anemia was found with no increase of blood eosinophils and a while blood count of 9000/mm3 with 72% of neutrophils. Roentgenograms of the head and chest were both normal. A stool was negative for parasites; glutamic oxalade and glutamic pyruvate transaminases were normal. Histopathologic examination revealed parakeratosis and mild acanthosis with exocytosis of eosinophils. The superficial dermis showed an inflammatory reaction, mainly composed of eosinophils, plasma cells, and histiocytes, and in the deep dermis an abscess containing different sections of the parasite was seen surrounded by a thin fibrous capsule (Fig. 3). There was no clinical improvement after medical treatment with two courses of thiabendazole (50 mg/kg orally, two 5-day pulses) and praziquantel (400 mg orally for 3 days). Therefore, the growth was extirpated under general anesthesia; however, the clinical condition of the patient did not improve. Eggs, larvae, and adult worms continued to be present in the pus after surgical excision. Finally, the patient asked for a discharge and did not return to the institute.
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PMID:Infestation from Lagochilascaris minor in Mexico. 907 20

Cobalamin (vitamin B12) deficiency is more common in the elderly than in younger patients. This is because of the increased prevalence of cobalamin malabsorption in this age group, which is mainly caused by (autoimmune) atrophic body gastritis. Cobalamin supplementation is affordable and nontoxic, and it may prevent irreversible neurological damage if started early. Elderly individuals with cobalamin deficiency may present with neuropsychiatric or metabolic deficiencies, without frank macrocytic anaemia. An investigation of symptoms and/or signs includes the diagnosis of deficiency as well as any underlying cause. Deficiency states can still exist even when serum cobalamin levels are higher than the traditional lower reference limit. Cobalamin-responsive elevations of serum methylmalonic acid (MMA) and homocysteine are helpful laboratory tools for the diagnosis. The health-related reference ranges for homocysteine and MMA appear to vary with age and gender. Atrophic body gastritis is indirectly diagnosed by measuring serum levels of gastrin and pepsinogens, and it may cause dietary cobalamin malabsorption despite a normal traditional Schilling's test. The use of gastroscopy may also be considered to diagnose dysplasia, bacterial overgrowth and intestinal villous atrophy in healthy patients with atrophic body gastritis or concomitant iron or folic acid deficiency. Elderly patients respond to cobalamin treatment as fully as younger patients, with complete haematological recovery and complete or good partial resolution of neurological deficits. Chronic dementia responds poorly but should, nevertheless, be treated if there is a metabolic deficiency (as indicated by elevated homocysteine and/or MMA levels). Patients who are at risk from cobalamin deficiency include those with a gastrointestinal predisposition (e.g. atrophic body gastritis or previous partial gastrectomy), autoimmune disorders [type 1 (insulin-dependent) diabetes mellitus and thyroid disorders], those receiving long term therapy with gastric acid inhibitors or biguanides, and those undergoing nitrous oxide anaesthesia. To date, inadequate cobalamin intake has not proven to be a major risk factor. Intervention trials of cobalamin, folic acid and pyridoxine (vitamin B6) in unselected elderly populations are currently under way.
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PMID:Age-related changes in cobalamin (vitamin B12) handling. Implications for therapy. 957 92

Each of a diverse array of compounds, at concentrations reported to effect general anesthesia, when added to liver microsomes, forms a complex with cytochromes P450 to generate, with reference to a cuvette containing microsomes only, a characteristic absorbance-difference spectrum. This spectrum results from a change in the electron-spin state of the heme iron atom induced upon entry by the anesthetic molecule into the enzyme catalytic pocket. The difference spectrum, representing the anesthetic-P450 complex, is characteristic of substances that are substrates for the enzyme. For the group of compounds as a whole, the magnitudes of the absorbance-difference spectra vary only about twofold, although the anesthetic potencies vary by several orders of magnitude. The dissociation constants (Ks), calculated from absorbance data and representing affinities of the anesthetics for P450, agree closely with the respective EC50 (concentration that effects anesthesia in 50% of individuals) values, and with the respective Ki (concentration that inhibits P450 catalytic activities half-maximally) values reported by us previously. The absorbance complex resulting from the occupation of the catalytic pocket by endogenous substrates, androstenedione and arachidonic acid, is inhibited, competitively, by anesthetics. Occupation of and perturbation of the heme catalytic pocket by anesthetic, as monitored by the absorbance-difference spectrum, is rapidly reversible. The presumed in vivo consequences of perturbation by general anesthetics of heme proteins is suppression of the generation of chemical signals that determine cell sensitivity and response.
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PMID:Occupation of the cytochrome P450 substrate pocket by diverse compounds at general anesthesia concentrations. 980 68

The development of transgenic mice has led to an increase in the use of mice as models for human disease. We hypothesized that the degree of brain damage sustained by animals in a neonatal mouse model of hypoxia-ischemia depends on the strain used. We compared three strains of mice commonly used to generate transgenic strains (C57Bl/6, 129Sv and CD1), as well as three hybrids of these strains (C57Bl/6x129Sv, CD1xC57Bl/6, and CD1x129Sv). At postnatal day 7 (P7), pups were subjected to a modified Vannucci procedure for hypoxia-ischemia as follows: permanent ligation of right common carotid artery under halothane anesthesia, 2-h recovery period, exposure to 8% oxygen at 37 degreesC for varying durations (30, 60 or 90 min). After 5 days, animals were perfused with 4% paraformaldehyde, brains were removed, postfixed and examined histologically with cresyl violet and Perl's iron stain to assess the degree of damage. Damage was assessed blindly using a score ranging from 0 (none) to 3 (infarct) in eight regions (ant-, mid-, and post- cortex, CA1, CA2, CA3 and dentate gyrus of the hippocampus, and striatum). We found significant differences in susceptibility to brain damage and mortality depending on the strain used. While determining the maximal degree of injury with the least amount of mortality for each strain, it was found that some strains (CD1) are particularly susceptible to brain damage in this model, while others (129Sv) are resistant.
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PMID:Strain-related brain injury in neonatal mice subjected to hypoxia-ischemia. 981 71

Heme oxygenase-1 (HO-1, HSP32) is an early gene that is responsive to an array of pathological conditions including, but not limited to, hypoxia and cerebral ischemia. HO-1 cleaves the heme molecule and produces carbon monoxide (CO) and biliverdin (an antioxidant) and is essential for iron homeostasis. The purpose of this study was to investigate, using transgenic (Tg) mice, whether overexpression of HO-1 in the brain augments or attenuates cellular injury caused by ischemic stroke. Homozygous HO-1 Tg mice that overexpress HO-1 under the control of the neuron-specific enolase promoter (characterized previously) were used. Under halothane anesthesia and normothermic conditions, wild-type nontransgenic (nTg; n = 22) and HO-1 Tg (n = 24) mice were subjected to middle cerebral artery occlusion (MCAo). Six hours after induction of ischemia, Tg and nTg mice developed infarcts that were 39 +/- 6 and 63 +/- 9 mm3, respectively (p < 0.01). No significant difference between the two strains was observed in the values of brain edema (11.3 +/- 4% in Tg vs. 14.6 +/- 5% in nTg; p < 0.1). At 24 h after MCAo, Tg mice exhibited significant neuroprotection as determined by the stroke volumes (41 +/- 2 mm3 in Tg vs. 74 +/- 5 mm3 in nTg; p < 0.01) and values of ischemic cerebral edema (21 +/- 6% in Tg vs. 35 +/- 11% in nTg; p < 0.01). Data suggest that neuroprotection in Tg mice was, at least in part, related to the following findings: (a) constitutively up-regulated cyclic GMP and bcl-2 levels in neurons; (b) inhibition of nuclear localization of p53 protein; and (c) antioxidant action of HO-1, as detected by postischemic neuronal expression of ferritin, and decreases in iron staining and tissue lipid peroxidation. We suggest that pharmacological stimulation of HO-1 activity may constitute a novel therapeutic approach in the amelioration of ischemic injury during the acute period of stroke.
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PMID:Overexpression of heme oxygenase-1 is neuroprotective in a model of permanent middle cerebral artery occlusion in transgenic mice. 1003 92

Gauges are old measures of thickness. They originated in the British iron wire industry at a time when there was no universal unit of thickness. The sizes of the gauge numbers were the result of the process of wire-drawing and the nature of iron as a substance. Gauges were measured and described in fractions of an inch during the 19th century. In the UK, one gauge was standardised and legally enforced as the Standard Wire Gauge. One important reason for the standardisation of the gauge was the convenience of craftsmen. In the 20th century, the gauge was to be replaced with the introduction of the International System of Units. However, within the field of anaesthesia at the threshold of the 21st century, the gauge seems hard to remove from the minds of craftsmen like anaesthetists.
Anaesthesia 1999 Jun
PMID:The story of the gauge. 1040 73

This is the first report on increased neuronal levels of biliverdin reductase (BVR) in response to ischemic brain injury. BVR is an oxidoreductase, and is unique among all enzymes characterized to date in having dual pH/dual cofactor requirements--NADH and NADPH at 6.7 and 8.7, respectively. BVR catalyses the final step in the heme metabolic pathway and reduces the heme degradation product, biliverdin, to bilirubin. Bilirubin can be both a neurotoxicant and an antioxidant depending on its ratio to protein and concentration. Bilirubin also has immunomodulatory activity. Other biologically active heme degradation products are iron and CO. This study assessed time-dependent changes in the level of BVR, following permanent middle cerebral artery occlusion (MCAo). It also examined correlation of the change in BVR expression with display of indices of ischemic tissue injury. Under halothane anesthesia and normothermic conditions, 72 DNX inbred mice were subjected to MCAo. A time-dependent enlargement of an ischemic lesion over the course of 24 h was observed and measured 55 +/- 5 mm3 at 6 h, 63 +/- 6.7 mm3 at 12 h, and 73 +/- 5 mm3 at 24 h. Six hours after MCAo, increased immunoreactivity for BVR was noted in neurons in the peri-ischemic areas, intraischemic cortical layers 3 and 5, as well as in neurons in regions distant from the borders of vascular distribution of the MCA, such as those in substantia nigra, in the Purkinje layer of the cerebellum and in the central nucleus of inferior colliculus. Twenty-four hours after MCAo, immunoreactivity for BVR remained increased in the peri-ischemia areas. At all time points staining for BVR was decreased in the ischemic core. At the 24 h time point there was an increase in Fe staining in the perimeter of the lesion and an increase in Schiff's staining for lipid peroxidation at the rim of the lesion. In situ hybridization analysis demonstrated a time dependent increase in BVR mRNA labeling in neurons of the peri-ischemic area. In the ischemic hemisphere, when compared with the contralateral hemisphere, neither measurable decreases in BVR mRNA or total protein levels nor a decrease in NADH-dependent BVR activity at pH 6.7 were observed. As judged by Northern and Western blots and activity analysis, despite the apparent loss of BVR from the ischemic core, and its increase in the peri-ischemic region, when compared with the contralateral hemisphere, the overall capacity of the ischemic hemisphere to catalyze the reduction of biliverdin was unchanged throughout the experiment. Should, in the case of ischemia, the conditions favor the antioxidant activity of bilirubin, then we suggest that increase in BVR expression in ischemic penumbra may present a cellular defense mechanism against free radical-mediated neuronal damage. Furthermore, we interpret the apparent tightly regulated expression of BVR in the ischemic hemisphere as an important factor in protection against bilirubin neurotoxicity. Data suggest that pharmacological modulation of BVR expression is a possible new direction for protecting neurons against ischemic injury and oxidative stress.
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PMID:Enhanced neuronal expression of the oxidoreductase--biliverdin reductase--after permanent focal cerebral ischemia. 1062 43

Oligemic episodes and increased iron concentration have both been proposed as being involved in neurodegenerative diseases. In animal models, a combination of both of these might therefore mimic the clinical pathology in humans. In rats, intrastriatal injections of ferric chloride, FeCl3, one week after a 60-minute oligemic episode, produced by bilateral clamping of the carotid arteries under pentobarbital anaesthesia (BCCA) impaired the animals' learning ability in a water maze task. Median adult rats, after intrastriatal 0.3 microg FeCl3, are impaired when challenged during the first three trial blocks, while after 0.06 microg FeCl3, an impairment is seen during the process of habituation to the challenge. Two-year-old animals do not show any learning effect at all after the combination of BCCA and intrastriatal FeCl3. Lazaroid U-74389G, a potent inhibitor of iron-induced lipid peroxidation, totally prevents the learning impairments in both median adult and aged animals, suggesting that iron-induced lipid peroxidation may be responsible for the late learning deficiencies. However, when U-74389G is applied one week after the oligemic episode but without the additional injection of iron, U-74389G on its own also impairs the animals' learning ability. The present animal model, when applied to clinical studies of lazaroids in humans, does seem able to give reliable information concerning the neuroprotective properties of such drugs.
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PMID:The effects of the 21-aminosteroid U-74389G on spatial orientation in rats after a cerebral oligemic episode and iron-induced oxidative stress. 1080 7

Hallervorden-Spatz disease (HSD) is a rare neurodegenerative disorder characterized by abnormally high deposits of iron in the brain. This report describes a child with HSD who presented with self-inflicted ulceration of the lip and tongue, which was initiated during periods of intense oro-facial spasms. Other findings included dental caries and trauma to the primary incisors. Comprehensive dental care was carried out under general anaesthesia. The self-mutilation of the oro-facial mucosa was eliminated by placement of upper and lower soft resin bite guards.
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PMID:Self-inflicted injury in a case of Hallervorden-Spatz disease. 1081 89

Anemia in a Jehovah's Witness can be a challenging situation for the general obstetrician and gynecologist. With today's multicultural society, this issue is not as uncommon as previously thought. The following article reviews the alternatives to heterologous blood transfusion available to those patients who will not accept blood. A review of perioperative management is discussed, including cell salvage systems, normovolemic hemodilution, and controlled hypotensive anesthesia. Strategies for pre- and postoperative management are also presented. These include iron, erythropoietin, and nutrition. There are many options available, so management can be tailored to each specific situation.
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PMID:Preparation for an elective surgical procedure in a Jehovah's Witness: a review of the treatments and alternatives for anemia. 1107 41


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