Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty eight elderly patients scheduled for urologic surgery were randomly assigned to receive in a double blind fashion subarachnoid hyperbaric bupivacaine 15 mg with the addition of 50 micrograms (group A, n = 7), 25 micrograms (group B, n = 7), 12.5 micrograms (group C, n = 7), of fentanyl or 1 ml of saline (group D, n = 7) for a total volume of 4 ml. The pattern of breathing and the ventilatory response to CO2 were studied before 90, 150, 480 minutes after the subarachnoid injection. In group A mild pruritus and sedation occurred in 5 patients, nausea, vomiting and periodic breathing occurred in 2 patients. In group B mild pruritus and sedation were observed in 4 patients, nausea, vomiting in 2 patients. No significant changes in VE, Vt/Ti and Ti/Ttot were observed between the groups. Patients receiving 50 micrograms of fentanyl showed a slope VE/PET CO2 significantly below baseline values at 90 and 150 minutes (p less than 0.05). In this group the baseline values were restored after 480 minutes. No side effects were observed in group C and D. 25 micrograms fo fentanyl is the only dose with a significant analgesic effect without any respiratory depression.
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PMID:[Post-operative analgesia with sub-arachnoid fentanyl: ventilatory effects in elderly patients]. 192 60

The major use of N-acetylcysteine in clinical toxicology is in the treatment of acetaminophen (paracetamol) overdosage. The hepatorenal toxicity of acetaminophen is mediated by a reactive metabolite normally detoxified by reduced glutathione. If glutathione is depleted, covalent binding to macromolecules and/or oxidation of thiol enzymes can lead to cell death. Oral or intravenous N-acetylcysteine or oral D,L-methionine mitigates acetaminophen-induced hepatorenal damage if given within 10 hours, but becomes less effective thereafter. In vivo, N-acetylcysteine forms L-cysteine, cystine, L-methionine, glutathione, and mixed disulfides; L-methionine also forms cysteine, thus giving rise to glutathione and other products. Oral therapy with N-acetylcysteine or methionine for acetaminophen poisoning is contraindicated in the presence of coma or vomiting, or if activated charcoal has been given by mouth. Nausea, vomiting, and diarrhea may also occur as a result of oral N-acetylcysteine administration. Anaphylactoid reactions including angioedema, bronchospasm, flushing, hypotension, nausea/vomiting, rash, tachycardia, and respiratory distress may occur 15-60 minutes into N-acetylcysteine infusion (20 hours intravenous regimen) in up to 10% of patients. Following accidental intravenous overdosage, the adverse reactions of N-acetylcysteine are similar but more severe; fatalities have occurred. A reduction in the loading dose of N-acetylcysteine may reduce the risk of adverse reactions while maintaining efficacy. Administration of N-acetylcysteine for a longer period might provide enhanced protection for patients in whom acetaminophen absorption or elimination is delayed. N-acetylcysteine may also have a role in the treatment of toxicity from carbon tetrachloride, chloroform, 1,2-dichloropropane, and other compounds. The possible use of N-acetylcysteine and other agents in the prevention of the neuropsychiatric sequelae of acute carbon monoxide poisoning is an important area for future research.
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PMID:Use of N-acetylcysteine in clinical toxicology. 192 4

Five patients presented to the emergency department (ED) following exposure in an enclosed space to methylene chloride (dichloromethane), used for removing paint. Two workers and three rescuers were involved. Two rescuers complained only of dizziness and mild nausea, and were subsequently discharged from the ED. One rescuer was asymptomatic. Worker no. 1 arrived in cardiac arrest and eventually died in the ED despite resuscitation efforts. Worker no. 2 also presented to the ED in cardiac arrest, and was successfully resuscitated to pulse and blood pressure. However, he never regained consciousness or spontaneous respirations, and died on the fourth day. Of interest is that worker no. 2's carboxyhemoglobin level increased from 2% to 8% over the 9 hours following admission, despite administration of 40% to 50% oxygen by endotracheal tube. Among the conclusions that can be drawn are (1) the cause of death in these patients was not carbon monoxide poisoning, but solvent-induced narcosis; (2) carboxyhemoglobin levels may continue to rise following cessation of exposure, despite administration of high flow oxygen; (3) rescuers can easily become victims if proper protective clothing and respirators are not worn.
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PMID:Methylene chloride: report of five exposures and two deaths. 222

Nalbuphine hydrochloride, an agonist-antagonist opioid, is reported to reverse the respiratory depression of moderate doses of fentanyl (20 micrograms.kg-1) and still provide good analgesia. We report four patients having abdominal aortic aneurysm repair in which we attempted to reverse the respiratory depression of large doses of fentanyl (50-75 micrograms.kg-1) with nalbuphine (0.3 mg.kg-1, 0.1 mg.kg-1 or 0.05 mg.kg-1). Nalbuphine reversed respiratory depression in all four patients and the respiratory rate increased from 10 to 23 breaths per minute, end-tidal CO2 decreased from 7.0 +/- 0.3 per cent to 5.6 +/- 0.7 per cent, and peak inspiratory pressure after 0.1 seconds increased from 4 +/- 1.4 to 13 +/- 2.6 mmHg. However, hypertension, increased heart rate, and significant increase in analogue pain scores accompanied reversal of respiratory depression. Agitation, nausea, vomiting, and cardiac dysrhythmias also were observed frequently. We do not recommend the use of nalbuphine to facilitate early extubation of the trachea after large doses of fentanyl for abdominal aortic surgery.
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PMID:Side effects of nalbuphine while reversing opioid-induced respiratory depression: report of four cases. 165

Diesel motors are employed to an increasing extent for occupational transport and fumes from diesel driven vehicles constitute an increasing problem as regards atmospheric pollution but, in particular, they constitute a considerable risk to health for the workers exposed to diesel exhaust fumes in their daily work. In the clinic for occupational medicine, The University Hospital, Copenhagen, 14 garage workers were examined. Eleven of these had been exposed to great quantities of diesel exhaust fumes for 2 to 29 years. All 11 presented acute symptoms due to diesel exhaust fumes in the form of headache, vertigo, fatigue, irritation of mucous membranes, nausea, abdominal discomfort or diarrhoea. Seven persons had been employed for more than five years as garage workers. Six complained of failure of memory, difficulty in concentration, irritability, increased sleep requirement, psychological changes or reduced libido. Neuropsychological examination was undertaken in these six persons and in five of them organic brain damage, mainly of slight extent, was demonstrated. Diesel exhaust fumes contain many toxic substances: carbon monoxide, nitrous gases, sulphur oxides, aldehydes and hydrocarbons. It is not possible to indicate a single compound which is responsible for possible brain damage and a combination effect may well be concerned. This is a casuistic material. Only few investigations have previously been available which illustrated a possible connection between the neurotoxic effects and, in particular, brain damage. It is now considered important to emphasize that this may constitute a problem on exposure to diesel exhaust fumes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Organic brain damage in garage workers after long-term exposure to diesel exhaust fumes]. 247 26

The side-effects of two opioid agonist-antagonists, nalbuphine and pentazocine, were assessed when used for patient-controlled postoperative analgesia. Forty ASA I or II patients scheduled for upper abdominal surgery were randomly allocated to two equal groups. The anaesthetic technique was the same for all the patients: premedication with atropine and diazepam, induction with thiopentone and suxamethonium and maintenance with fentanyl, pancuronium, nitrous oxide and halothane. Patient-controlled computer assisted analgesia (On-Demand Analgesia Computer) was started in the recovery room at least 2 h after the last administration of fentanyl. The parameters used were: a routine hourly dose (the half of that received during the previous hour), with on demand delivery of nalbuphine (15 micrograms.kg-1) or pentazocine (45 micrograms.kg-1) aliquots respectively, with a refractory period between two demands of 4 min and a total hourly maximum dose of 16 mg and 48 mg respectively. The following parameters were measured before the start of self-administration, and every hour afterwards for 24 h: systolic (Pasys) and diastolic blood pressures, heart rate, pressure-rate product (PRP), respiratory rate, end-tidal CO2 and pain (by way of a three point scale). Analgesia was assessed on a four-point scale every 6 h. The total doses of nalbuphine and pentazocine administered were 94 +/- 43 mg and 251 +/- 150 mg respectively. The only parameters significantly different between the two groups were Pasys and PRP, being higher in the pentazocine group. There were no significant differences in the side-effects (drowsiness, nausea, vomiting, headache, amnesia, logorrhoea and urine retention). All patients in both groups were satisfied with this technique.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of nalbuphine and pentazocine in the treatment of postoperative pain by self-administration]. 266 Jun 40

The effects of extradural sufentanil 50 micrograms were investigated in 10 normal volunteers. Eight of these were studied at a second session when adrenaline 1:200,000 was added to the sufentanil. Well-defined segmental analgesia developed rapidly after plain sufentanil and lasted approximately 3 h. Respiration was depressed for about the same period and was greatest in the first 2 h, as shown by a 15% increase in PECO2, while the slope and VE50 of the carbon dioxide response curve were depressed by 45% and 55%, respectively. Moderate drowsiness occurred in most subjects, while other side effects of itching, nausea and urinary retention occurred less frequently and were not severe. Addition of adrenaline 1:200,000 intensified segmental analgesia and prolonged duration to 5 h, while side effects were lessened. It is concluded that extradural sufentanil shows considerable promise for clinical use, and that the risk: benefit ratio is improved by adding adrenaline 1:200,000.
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PMID:Analgesic and respiratory effects of extradural sufentanil in volunteers and the influence of adrenaline as an adjuvant. 288 58

Acute administration of mecamylamine, a centrally active nicotinic cholinergic agonist, has been shown to increase amount of smoking as indicated by smoking topography (e.g., puff rate, puff duration), expired carbon monoxide changes, and other inferential measures. In the present study, subjects showed significantly greater increases in plasma nicotine following smoking of two high-nicotine research cigarettes when pretreated with mecamylamine than when pretreated with placebo, even though no significant differences in puff volume or puff number were detected. Interestingly, none of our subjects reported nausea, although some achieved plasma nicotine levels at which nausea would typically be expected. We attribute the observed increases in nicotine intake to compensatory behavior designed to overcome mecamylamine's blocking effects.
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PMID:Mecamylamine pretreatment increases subsequent nicotine self-administration as indicated by changes in plasma nicotine level. 310 64

The plasma concentration of arginine vasopressin (AVP) is increased in diabetic ketoacidosis (DKA) in man and the rat. Although haemodynamic changes and nausea/emesis may account for the increased secretion of AVP in severe human DKA, they appear not to be responsible in moderate DKA. Streptozotocin-treated rats were studied to investigate other factors possibly involved in the secretion of AVP in DKA. Wistar rats were injected i.p. with streptozotocin (150 mg/kg body weight). Diabetic rats were maintained on 3-4 units protamine-zinc insulin (PZI)/day for 11 days, after which PZI was withdrawn for 3 days in half the rats. The plasma concentration of AVP was greater in rats with DKA than in normal controls (mean 11.4 pmol/l compared with 1.6 pmol/l; P less than 0.05). Rats with DKA had higher plasma osmolality and concentrations of blood glucose, beta-hydroxybutyrate and acetoacetate, but lower plasma carbon dioxide content than diabetic and normal controls (P less than 0.05). There were no differences in plasma levels of sodium, urea or haematocrit between rats with DKA and controls. In a separate study involving the same procedures, daily systolic blood pressure was measured using a tail cuff to occlude arterial inflow to the tail, and subsequent detection of the cuff pressure at which the first arterial pulsation appeared. No significant differences were detected between normal and diabetic rats and rats with DKA. Exponential relationships between plasma osmolality and plasma AVP (correlation coefficient, r = + 0.75; P less than 0.01), and plasma ketone bodies and plasma AVP (r = +0.60; P less than 0.05) were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible mechanisms responsible for the rise in plasma vasopressin associated with diabetic ketoacidosis in the rat. 312 19

"Environmental tobacco smoke" (ETS) is the term used to characterize tobacco combustion products inhaled by nonsmokers in the proximity of burning tobacco. Over 3800 compounds are in tobacco smoke, many of which are known carcinogens. Most ETS exposure is from sidestream smoke emitted from the burning tip of the cigarette. Sidestream smoke is hazardous because it contains high concentrations of ammonia, benzene, nicotine, carbon monoxide, and many carcinogens. Nonsmokers chronically exposed to ETS are believed to assume health risks similar to those of a light smoker. Children of parents who smoke have more respiratory infections, more hospitalizations for bronchitis and pneumonia, and a smaller rate of increase in lung function compared to children of parents who do not smoke, particularly during the first year of life. Among adults with preexisting health conditions such as allergies, chronic lung conditions, and angina, the symptoms of these conditions are exacerbated by exposure to ETS. The acute health effects among healthy adults include headaches, nausea, and irritation of the eyes and nasal mucous membranes. The evidence for a relationship between ETS and cancer at sites other than lung is insufficient to draw any positive conclusions. For lung cancer, studies have consistently shown an excess risk between 10% and 300%, with a summary relative risk of 1.3 (95% confidence interval = 1.1-1.5). A dose-response relation is suggested but difficult to assess completely. Histologic types of lung cancer are generally similar to those most closely associated with active smoking, although other histologic types have also been found. Both excess relative risks and the dose responses are underestimates of the true excess risk and of the range of dose-response effect. Although the temporal relationship between exposure and disease occurrence is established, many questions are unanswered. The findings are consistent with many known biologic effects of active smoking and are partially analogous to the biologic effects of direct smoke inhalation. As many as 5000 nonsmokers are estimated to die annually from lung cancer as a result of exposure to ETS. There is great potential for prevention of these premature deaths. The two major preventive actions are (a) eliminating the source by reducing the amount of direct smoking and (b) limiting the level of exposure by restricting where tobacco can be smoked. Specific preventive actions include smoking cessation, smoking prevention, restriction of advertising, increased taxation on tobacco, and adoption of stringent nonsmoking policies in the workplace, schools, and public places.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Health hazards of passive smoking. 328 40


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