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| 2. |
- Jang, David H., et al.
(författare)
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Alterations in cerebral and cardiac mitochondrial function in a porcine model of acute carbon monoxide poisoning
- 2021
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Ingår i: Clinical Toxicology. - : Informa UK Limited. - 1556-3650 .- 1556-9519. ; 59:9, s. 801-809
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: The purpose of this study is the development of a porcine model of carbon monoxide (CO) poisoning to investigate alterations in brain and heart mitochondrial function. Design: Two group large animal model of CO poisoning. Setting: Laboratory. Subjects: Ten swine were divided into two groups: Control (n = 4) and CO (n = 6). Interventions: Administration of a low dose of CO at 200 ppm to the CO group over 90 min followed by 30 min of re-oxygenation at room air. The Control group received room air for 120 min. Measurements: Non-invasive optical monitoring was used to measure cerebral blood flow and oxygenation. Cerebral microdialysis was performed to obtain semi real time measurements of cerebral metabolic status. At the end of the exposure, both fresh brain (cortical and hippocampal tissue) and heart (apical tissue) were immediately harvested to measure mitochondrial respiration and reactive oxygen species (ROS) generation and blood was collected to assess plasma cytokine concentrations. Main results: Animals in the CO group showed significantly decreased Complex IV-linked mitochondrial respiration in hippocampal and apical heart tissue but not cortical tissue. There also was a significant increase in mitochondrial ROS generation across all measured tissue types. The CO group showed a significantly higher cerebral lactate-to-pyruvate ratio. Both IL-8 and TNFα were significantly increased in the CO group compared with the Control group obtained from plasma. While not significant there was a trend to an increase in optically measured cerebral blood flow and hemoglobin concentration in the CO group. Conclusions: Low-dose CO poisoning is associated with early mitochondrial disruption prior to an observable phenotype highlighting the important role of mitochondrial function in the pathology of CO poisoning. This may represent an important intervenable pathway for therapy and intervention.
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| 4. |
- Busardò, Francesco Paolo, et al.
(författare)
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Interpreting γ-hydroxybutyrate concentrations for clinical and forensic purposes
- 2019
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Ingår i: Clinical Toxicology. - : Taylor & Francis. - 1556-3650 .- 1556-9519. ; 57:3, s. 149-163
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Forskningsöversikt (refereegranskat)abstract
- ?-Hydroxybutyric acid is an endogenous substance, a therapeutic agent, and a recreational drug of abuse. This psychoactive substance acts as a depressant of the central nervous system and is commonly encountered in clinical and forensic practice, including impaired drivers, poisoned patients, and drug-related intoxication deaths.
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| 5. |
- Franzen, Lisa, et al.
(författare)
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Accuracy of on-site urine drug tests : an experimental study
- 2013
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Ingår i: Clinical Toxicology. - : Informa Healthcare. - 1556-3650 .- 1556-9519. ; 51:4, s. 348-349
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Objective: On-site drug tests (ODTs) are frequently used in hospitals to screen the urine of patients admitted for suspected poisoning. The purpose of this study is to evaluate the accuracy of such tests used in emergency departments in Sweden.Methods: Two brands, ColibriCheck™ and Concateno™, were tested for detecting amphetamine, benzodiazepines, opiates and tetrahydrocannabinol (THC) in urine. The results were compared with laboratory screening (CEDIA) and confirmation method (GC-MS). The study was conducted from December 2011 to March 2012 using samples from drug dependence clinics; 400 positive (100 in each drug group) and 200 negative (applied to all drug groups).Results: High specificity (Table 1) implies that most true negative samples are detected, but the risk of missing a true positive sample is high (6–26%). The incidence of false positive test results was low ( 1%). Limitations: inadequate blinding of the analysing procedure, emergency department samples were not included and GC-MS was performed on positive but not negative samples.Conclusion: The implications of this study are that positive ODTs are fairly reliable whereas negative ODTs neglect 6–26% of true drug presence. Consequently patients might be overlooked if treatment depended on the test result. ODTs’ intrinsic problems e.g. cross-reactivity and limited spectrum of analytes1, that are not addressed in our study, could further influence the reliability of test results.Reference1. Krasowski MD, Pizon AF, Siam MG, et al. Using molecular similarity to highlight the challenges of routine immunoassay-based drug of abuse/toxicology screening in emergency medicine. BMC Emerg Med 2009; 9:5.
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| 7. |
- Isbister, Geoffrey K, et al.
(författare)
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Human methyl parathion poisoning
- 2007
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Ingår i: Clinical Toxicology. - : Informa UK Limited. - 1556-3650 .- 1556-9519. ; 45:8, s. 956-960
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Tidskriftsartikel (refereegranskat)abstract
- Background. Methyl parathion is classed as an extremely hazardous pesticide with a rodent LD50 of 6 to 24 mg/kg. It has been banned in numerous countries, but there are few reports of acute methyl parathion poisoning. Methods. Plasma cholinesterase and acetylcholinesterase were measured in blood. Methyl parathion and the major metabolite 4-nitrophenol where measured in serum and urine. Based on the available concentration-time data, the pharmacokinetic parameters of methyl parathion were estimated for this patient. Case Report and Results. A 29-year-old male ingested 50 to 100mL (12 to 24 g) of methyl parathion causing delayed and prolonged suppression of acetylcholinesterase but almost no clinical effects. Absorption was predicted to last for 30 hours and the bioavailability appeared to be very low. Conclusions. Although it is feasible the patient ingested much less, a tenth of his alleged ingestion dose is more than the oral LD50 in rats. Methyl parathion appears to be less toxic in humans than parathion for similar amounts ingested, which is not consistent with the two pesticides having similar rodent LD50.
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| 8. |
- Knudsen, Kai, 1957, et al.
(författare)
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A case of life-threatening rectal administration of moist snuff.
- 2010
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Ingår i: Clinical toxicology (Philadelphia, Pa.). - : Informa UK Limited. - 1556-9519 .- 1556-3650. ; 48:6, s. 572-3
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Tidskriftsartikel (refereegranskat)abstract
- CASE REPORT: We report a case of self-administration of 75 sachets of moist snuff rectally in a previously healthy, 42-year-old man. He presented with symptoms of nausea, discomfort, and dizziness. He had dry and warm skin, a pulse rate of 53 bpm, a mean arterial blood pressure of 135 mmHg and fluctuations in consciousness. The patient was treated with mechanical ventilation because of respiratory insufficiency. No specific anti-nicotinergic treatment was given. Plasma levels of the nicotine metabolite cotinine were 8,691 μg/L 7 h after admittance and 9,814 μg/L after 12 h. Levels of cotinine in the urine were above >50,000 μg/L. The patient developed a mild pneumonia, but he was uneventfully extubated after 12 h of mechanical ventilation. All physiological parameters were restored and he was discharged from hospital after 36 h. CONCLUSION: Excessive rectal administration of moist snuff may be life threatening. Patients may require intensive care. Long-term sequelae were not seen in this case.
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| 9. |
- Larsson, Sonny, et al.
(författare)
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Poisoning with Cicuta virosa in Sweden
- 2015
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Ingår i: Clinical Toxicology. - 1556-3650 .- 1556-9519. ; 53:4, s. 345-345
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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