Acute cocaine intoxication in the conscious dog: studies on the mechanism of lethality.
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Animals↗
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Compared efficacy of diazepam or avizafone to prevent soman-induced electroencephalographic disturbances and neuropathology in primates: relationship to plasmatic benzodiazepine pharmacokinetics.
We performed an experiment to characterize the toxicity of soman in cynomolgus monkeys in which organophosphorus intoxication was followed by treatment with either the current three-drug therapy atropine/pralidoxime/diazepam or a combination of atropine/pralidoxime/avizafone, avizafone being the water soluble prodrug of diazepam. Clinical, electrophysiological, and histological approaches were combined. When benzodiazepines were injected at the similar molar dose of 0.7 micromol/kg, the protection against soman toxicity was better with the atropine/ pralidoxime/diazepam combination than with the atropine/pralidoxime/avizafone one. Pharmacokinetic studies demonstrated that this difference of efficacy could be explained by a lower plasmatic load of diazepam obtained after injection of avizafone at 0.7 micromol/kg, compared to the administration of diazepam at the same molar dose. Moreover, after injection of avizafone, plasmatic levels of diazepam were achieved faster and declined more rapidly than after administration of diazepam. Compared to diazepam given at a dose of 0.7 micromol/kg, injection of 1 micromol avizafone/kg gave a similar plasmatic load of benzodiazepine, but with a lower time to maximum plasma concentration (tmax) and a higher maximum plasma concentration (Cmax) for plasmatic diazepam. We therefore went on to demonstrate that administration of the atropine/pralidoxime/avizafone combination at a dose 1 micromol benzodiazepine/kg to intoxicated monkeys afforded electrophysiological and histological protection similar to that obtained after administration of atropine/pralidoxime/diazepam at a dose of 0.7 micromol diazepam/kg. Reflections on the possible incorporation of avizafone in three-drug emergency treatment are presented.
Animals↗
Acute ethanol intoxication after consumption of hairspray.
A 61-year-old woman with a history of alcohol dependence came to the emergency department with ethanol intoxication. Her serum ethanol concentration was 322 mg/dl. When questioned, she admitted to consuming a 14-oz bottle of hairspray mixed with water because of its denatured alcohol content. The woman had used nonbeverage sources of alcohol on a regular basis for a number of years after learning of the practice from fellow attendees of Alcoholics Anonymous meetings. Her primary reason for this behavior was to hide her continued alcohol abuse from her family. She consumed hairspray that contained 50% denatured alcohol by volume; the amount she ingested was equal to 7 fluid oz of ethanol, the equivalent of 14 1.25-oz shots of 80-proof liquor. Her serum ethanol concentration was consistent with that predicted by pharmacokinetic equations based on the consumption of one bottle of hairspray. The hairspray product contained specially denatured alcohol 40-B, which consists of ethanol and small quantities of t-butyl alcohol and denatonium benzoate. Ethanol is the substance of primary toxicologic concern. Clinicians need to be aware that numerous nonbeverage sources of alcohol exist and should be considered when a patient presents with acute intoxication. The source and its components should be identified as soon as possible in order to assess other potential toxicities.
Alcoholic Intoxication↗
[The immunocorrecting effect of vitamin E during ethanol intoxication].
Chronic alcohol intoxication of mice CBA and C57BL/6 strains decreased distinctly the content of T lymphocytes in peripheric blood and inhibited the immune response to sheep erythrocytes. Vitamin E, administered into mice at a dose of 5 IU and into guinea pigs--of 50 IU within 3 days, restored completely the immunity status of these animals. Besides, vitamin E decreased ethanol consumption in mice kept under conditions of alternative choice of water-ethanol within one week after its injection.
Alcoholic Intoxication↗
Chemistry and toxicology of molds isolated from water-damaged buildings.
There is increasing evidence of health risks associated with damp buildings and homes in which high levels of microbes are found. Although concerns have traditionally centered on microbial pathogens and allergenic effects, recent work has suggested that fungi pose the more serious risk. Evidence is accumulating that certain toxigenic molds are particularly a risk for human health through exposure, via inhalation, of fungal spores. Many of these fungi produce toxins (mycotoxins) some of which have been shown to cause animal and human intoxications, usually in an agricultural setting. The fungus, Stachybotrys chartarum (S. atra) is considered to be one of the more serious threats to people living and working in water-damaged buildings. This mold has a long history of being responsible for animal toxicoses, and in recent years, being associated with infant pulmonary hemosiderosis (bleeding in the lungs) of infants exposed to spores of this fungus in their homes. S. atra produces a variety of potent toxins and immunosuppressant agents, including a novel class of diterpenes (atranones) of unusual structure. More research is needed to determine the impact to health resulting from inhalation of toxigenic mold spores.
Animals↗
Cellular pathology of the nerve microenvironment in galactose intoxication.
The effect of chronic hyperglycemia and polyol pathway activation on the Schwann cell has not been resolved although injury to this cell has long been suspected in diabetic neuropathy. Hyperglycemia, resulting from galactose intoxication of four months duration, induces dose-dependent accumulations of endoneurial fluid sodium and chloride that are linked to polyol pathway activity and associated with dose-dependent increases in sciatic nerve water content, endoneurial fluid pressure and (Na+, K+)-ATPase activity. In order to understand the impact of these changes on the nerve microenvironment, cellular elements of the endoneurium were quantitatively and qualitatively assessed in rats receiving 0%, 10%, 20% or 40% galactose diets. After four months of galactose intoxication, dose-dependent changes in the size distribution of myelinated nerve fibers were apparent. A shift in size-frequency histograms of galactose-intoxicated animals towards smaller fibers was accompanied by a decrease in axon diameter and the volume fraction ratio of axon to myelinated nerve fibers. In the sciatic nerve of all 40% galactose-fed rats examined by electron microscopy, Schwann cells of myelinated fibers showed both reactive and degenerative changes. Demyelination was preceded by splitting at the intraperiod line. Remyelination was identified by axons with disproportionately thin myelin sheaths. Axonal dystrophy and degeneration were infrequently seen, but there was axonal regeneration. Dose-dependent increases in mast cell number were observed with degranulation apparent in rats receiving 20% and 40% galactose. Endothelial cell number and basal lamina thickness were increased in the endoneurial vessels of galactose-intoxicated rats. Increased cytoplasmic area and degenerative changes in pericytes were also noted. These observations indicate that significant morphologic changes accompany the hyperosmotic imbalance resulting from galactose intoxication of four months duration. Schwann cell injury and demyelination are present in a disorder linked to polyol metabolism since aldose reductase, the anabolic enzyme of the polyol pathway, is localized to this myelin-forming cell.
Animals↗
Acute ethanol intoxication decreases subsequent food intake and changes hepatic microsomal enzyme activities similarly to fasting.
The effect of intragastric ethanol, 7.8 g/kg, on the microsomal enzyme activities NADPH cytochrome c reductase, aminopyrine N-demethylase and aniline hydroxylase, were investigated in two sizes (150 g and 260 g) of mature male rats having free access to food and water for the 23 hours following ethanol administration. Controls received intragastric water and were given free access to food and water (fed controls) or only water (fasted controls). The ethanol group had a significantly lower food intake than the fed control group, and food intake in the large rats was more decreased by ethanol than that of the small rats, corresponding to slower recovery from intoxication. Ethanol and fasting increased aniline hydroxylation and decreased acetone enhancement of aniline hydroxylation to the same degree, whereas only fasting caused a significant decrease in aminopyrine N-demethylation. Some of the effects of acute ethanol intoxication on hepatic microsomal enzyme activities appear to be mediated via decreased food intake.
Alcoholic Intoxication↗
Effect of long term alcohol feeding on the pancreas in rat.
To elucidate the pathophysiological process of alcoholic pancreatitis, chronic alcohol intoxication was made in Wistar rats on balanced diet giving 20% ethanol freely for 60 weeks. The control rats received water. Histological picture of the pancreas, hormonal activity in the mucosa of upper digestive tract and the nature of pancreatic juice were examined in every 15th week. The results were as follows. 1) No histological changes were noted in the pancreas of control group. In the ethanol group, morphological abnormalities of the pancreas appeared after 30 weeks. Of the histological findings, the changes on the ductal system such as dilatation of pancreatic duct, plug formation in the ductal lumen and periductal fibrosis were significant. 2) The long term ethanol administration tended to decrease the amounts of gastrin, secretin and cholecystokinin contained in the gastrointestinal mucosa. 3) Regardless of the histological changes of the pancreas, almost no changes were noted in the bicarbonate and protein concentration during the experimental period of 60 weeks. From the above results, a mechanism obstructing pancreatic ductal system is considered to be important in the pancreatic lesions by alcohol rather than a mechanism of stimulating pancreatic exocrine secretion.
Alcoholism↗
Caramiphen and scopolamine prevent soman-induced brain damage and cognitive dysfunction.
Exposure to soman, a toxic organophosphate nerve agent, causes severe adverse effects and long term changes in the peripheral and central nervous systems. The goal of this study was to evaluate the ability of prophylactic treatments to block the deleterious effects associated with soman poisoning. scopolamine, a classical anticholinergic agent, or caramiphen, an anticonvulsant anticholinergic drug with anti-glutamatergic properties, in conjunction with pyridostigmine, a reversible cholinesterase inhibitor, were administered prior to sbman (1 LD50). Both caramiphen and scopolamine dramatically attenuated the process of cell death as assessed by the binding of [3H]RoS-4864 to peripheral benzodiazepine receptors (omega3 sites) on microglia and astrocytes. In addition, caramiphen but not scopolamine, blocked the soman-evoked down-regulation of [3H]AMPA binding to forebrain membrane preparations. Moreover, cognitive tests utilizing the Morris water maze, examining learning and memory processes as well as reversal learning, demonstrated that caramiphen abolished the effects of soman intoxication on learning as early as the first trial day, while scopolamine exerted its effect commencing at the second day of training. Whereas the former drug completely prevented memory deficits, the latter exhibited partial protection. Both agents equally blocked the impairment of reversal learning. In addition, there is a significant correlation between behavioral parameters and [3H]RoS-4864 binding to forebrain membrane preparations of rats, which participated in these tests (r(21) = 0.66, P < 0.001; r(21) = 0.66, P < 0.001, -0.62, P < 0.002). These results demonstrate the beneficial use of drugs exhibiting both anti-cholinergic and anti-glutamatergic properties for the protection against changes in cognitive parameters caused by nerve agent poisoning. Moreover, agents such as caramiphen may eliminate the need for multiple drug therapy in organophosphate intoxications.
Animals↗
Comparison of urinary excretion characteristics of ethanol and ethyl glucuronide.
This study compared the urinary excretion characteristics of ethyl glucuronide (EtG) with that of ethanol, with focus on the effect of water-induced diuresis. Six healthy volunteers ingested an ethanol dose of 0.5 g/kg (range 25.0-41.5 g) as 5% (v/v) beer in 30 min and the same volume of water after 3 h. Urine collections were made before starting the experiment and at timed intervals over 31.5 h. The concentration of EtG was determined by an LC-MS method (LOQ = 0.1 mg/L). The urine samples collected immediately before starting drinking were all negative for ethanol and EtG, thus confirming that the participants had not recently ingested alcohol. Intake of beer resulted in a marked increase in excreted urine volume and a concomitant drop in creatinine concentration. The concentration of ethanol peaked at a mean value of 17 mmol/L in the 1.5-h urine collection. Except for one subject, EtG was first detectable (range 0.9-5.5 mg/L) at 1 h. Intake of water at 3 h produced another increase in urine volume and a drop in creatinine. The ethanol concentration curve was not influenced by the water diuresis, whereas this caused a distinct drop in the EtG concentration. When EtG was expressed relative to the creatinine value, this ratio was seemingly not affected by the intake of water. The ethanol concentration returned to zero at 6.5 h, whereas EtG was still detectable for up to 22.5-31.5 h, albeit at low levels in the end (< 1 mg/l). Only about 0.02% of the administered dose of ethanol (on a molar basis) was recovered in the urine as EtG. The results demonstrated that EtG remains detectable in the urine for many hours after the ethanol itself has been eliminated. Moreover, it was possible to lower the concentration of EtG by drinking large amounts of water prior to voiding, whereas this strategy did not influence the EtG/creatinine ratio or the concentration of ethanol.
Adult↗
Urea poisoning in suckler cows.
Accidental urea intoxication resulted in the death of 17 of 29 suckler cows within six hours after the contamination of their drinking water with urea fertiliser. The other cows showed no lasting ill effects and neither their three-month-old calves nor the stock bull were affected. The urea concentration in the water was 86 mmol/litre, and the concentrations of ammonia nitrogen in the rumen fluid of two of the cows which were examined after death were 1825 and 957 mg/litre. The clinical signs and post mortem findings are described.
Animals↗
Morphometric analysis of brain lesions in rat fetuses prenatally exposed to low-level lead acetate: correlation with lipid peroxidation.
The effect of prenatal lead acetate exposure was studied microscopically together with the concentration of lead and lipid fluorescent products (LFP) in the brain of rat fetuses. Wistar rats were intoxicated with a lead solution containing either 160 or 320 ppm of lead acetate solution during 21 days through drinking water. The control group (ten rats) received deionized water for the same period. The rats were killed on gestation day 21 and fetuses were obtained; the placenta, umbilical cord and parietal cortex (Cx), striatum (St), thalamus (Th) and cerebellum (Ce) were collected for measuring tissue lead concentration, LFP as an index of lipid peroxidation and histopathologic examination. Lead contents were increased in placenta, umbilical cord, St, Th and Cx in both lead-exposed groups. Lead exposure increased (LFP) in placenta and umbilical cord, St, Th and Ce as compared to the control group. Histopathological examination showed severe vascular congestion in placenta, the Cx, St, Th and Ce with hyperchromatic and shrunken cells. Interstitial oedema was found in all regions studied of both lead exposed groups. The morphometric evaluation of the studied brain regions showed an absolute decrease in total cell number and increased number of damaged cells and interstitial oedema. Our results show that morphological changes in rat brain are correlated with increased lipid peroxidation, and the lead levels of the umbilical cord, however it is not clear whether oxidative stress is the cause or the consequence of these neurotoxic effects of lead.
Animals↗
Protective effect of melatonin on methylmercury-Induced mortality in mice.
Effect of melatonin on the mortality in methylmercury chloride (MMC)-intoxicated mice was evaluated. Mice were given MMC in the diet (40 mg Hg/g) with or without melatonin in drinking water (20 mg/ml) for 5 weeks. In the control group, given MMC alone, 4 of 10 mice began to show neurological signs (e.g., abnormal righting reflex, staggering gaitfallen and posture on its side) concomitant with loss of body weight 4-7 days before death. This group also showed 60% of survival rate on the 35th day. However, the treated group, concomitantly given melatonin, showed a 100% of survival rate on the 35th day, although 1 of 10 mice began to show the neurological signs on the 33rd day. The level of thiobarbituric acid reactive substance in the brain, as an indication of oxidative damage, showed a significant decrease in the treated group compared with the control group. Thus, the 100% survival rate in the treated group may be partly due to antioxidative effect of melatonin on the MMC induced neurotoxicity.
Animals↗
Alcohol intoxication and withdrawal.
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Acid-Base Equilibrium↗
Chronic amiodarone ingestion induces pulmonary toxicity in rats.
Patients who receive amiodarone may develop interstitial pulmonary disease. The objective of the present study was to develop an experimental model of interstitial pulmonary disease in rats based on the chronic oral administration of amiodarone diluted in water ad libitum. A total of 97 three-month old male Wistar rats weighing 133-167 g (control and intoxicated) were studied after daily administration of amiodarone (about 50 mg/kg) for 3 weeks and 3, 6, and 13 months. We carried out conventional histopathologic evaluation, morphometric studies of the alveolar wall, transmission electron microscopy, measurement of pulmonary volumes and forced expiratory flows, and computed respiratory system resistance and elastance during spontaneous breath cycles. Chronic ingestion of amiodarone by rats produced pulmonary disease that started as a phospholipidosis, as early as 3 weeks after the use of the drug. After 6, and mainly after 13 months, a focal inflammatory reaction with reactive alveolar epithelium was observed. Signals of a concomitant repair process were also present, but fibrosis was visible only by electron microscopy. The physiologic dysfunction could be identified after 13 months; expiratory flow (ml/sec) limitation and an increased respiratory system elastance (cmH2O/ml) were the main functional changes, respectively 10.8 (forced expiratory mean flow between 0-25% of forced vital capacity) and 5.36 in treated animals vs 13.3 and 3.65 in controls, reported as mean +/- SD for 6 animals in each group. A body of evidence suggests that amiodarone may cause changes in lung phospholipid metabolism that may be responsible for a part of the functional derangement observed in this study.
Amiodarone↗
[The relationship between the course of bismuth encephalopathy and the amount of bismuth in blood and urine].
Study of the course of bismuth encephalopathy following the ingestion of a bismuth salt in relation to blood and urinary bismuth levels indicates a close parallel between the improvement in the clinical picture and the decrease in the degree of toxic impregnation of the body. This confirms the direct responsibility of bismuth for the disorder. Regression of myocolonic movements goes with the fall in blood bismuth levels, whilst improvement in the confusional syndrome is aomewhat delayed. There is a significant correlation between bismuth levels in the blood and urine. The excretion of bismuth is slow, and the persistence of blood and urinary bismuth levels higher than normal for several weeks after the acute phases and the interruption of the ingestion of bismuth salts reflects the existence of stable bonds between the metal and cellular constituents. The authors have observed a non-negligeable solubility of bismuth sub-nitrate in certain drinking waters, which brings up the hypothesis of a possible role of the hydrosobulity of bismuth in the pathogenesis of the intoxication.
Adult↗
Marijuana intoxication and brain activation in marijuana smokers.
OBJECTIVE AND METHOD: The acute effects of delta9 tetrahydrocannabinol (THC) on cerebral blood flow (CBF) were studied in human subjects. Regional CBF was measured with 15O-water and Positron Emission Tomography (PET) in 32 volunteers with a history of exposure to marijuana. Scans were performed before and after intravenous (I.V.) infusion of either of two doses of THC or a placebo, given under double blind conditions. RESULTS: THC but not placebo increased CBF especially in the frontal regions bilaterally, insula and cingulate gyrus and sub-cortical regions with somewhat greater effects in the right hemisphere. While most regions showed significant change at 60 minutes for the lower dose group, the higher dose group had significant change at 30 and 60 minutes. There was a highly significant change in the anterior/posterior ratio for the two THC groups reflecting minimal change in occipital flow but significant increases in frontal flow. Self ratings of THC intoxication showed significant effects, and regression analysis indicated it correlated most markedly with the right frontal region. CONCLUSION: Behavioral manifestations of marijuana intoxication may be associated with increased functional activity of the brain especially the frontal cortex, insula and cingulate gyrus.
Adult↗
On-line, simultaneous quantification of ethanol, some metabolites and water vapour in breath following the ingestion of alcohol.
Selected ion flow tube mass spectrometry, SIFT-MS, has been used to measure simultaneously the concentrations in exhaled breath of ethanol, acetaldehyde, ammonia, acetone and, routinely, water vapour, following the ingestion of various amounts of ethanol in 500 ml of water. These breath analyses were obtained from only single exhalations, the results being available immediately in real time. The breath ethanol reaches concentrations that are only approximately consistent with its dilution in blood and body water. For moderate ethanol doses the decay quickly exhibits first-order kinetics (a single exponential decay) whereas for relatively large ethanol doses, the initial decay of ethanol from the breath is slow, indicating saturation kinetics. For smaller doses, and following a meal, the breath ethanol increases only slightly indicating that it is largely metabolized in the stomach. We suggest that the time delay (following ethanol ingestion) before the breath ethanol begins to increase is an indicator of the gastric emptying rate. Then the rate of decay of ethanol from the breath/blood is related to its rate of metabolism subsequent to its dispersal into the body water. The much lower breath acetaldehyde levels correlate well with the ethanol levels indicating that it is mostly formed from the metabolism of the ethanol. The breath ammonia is seen to 'dip' following the water/alcohol drink and this is consistent with previous work in which this same phenomenon was observed following the ingestion of comparable volumes of liquid meals. The simultaneous breath acetone concentrations increase somewhat with time as is expected during the fasting state. The water vapour measurements are indicators of the precision and accuracy of the breath analyses, these being sufficient to show the differences between the breath (body) temperatures of the individuals of less than 1 degrees C. This study demonstrates the potential of SIFT-MS for non-invasive physiological measurement.
Acetaldehyde↗