OBJECTIVETo investigate the effects of acetamide at different doses on the expression of inhibitory amino acids (gamma-aminobutyric acid, GABA) and excitatory amino acid (glutamate, Glu) in the cerebral cortex of rats with acute tetramine (TET) poisoning.

METHODSEighty Sprague-Dawley rats (SPF) were randomly divided into five groups, with 16 rats in each group: saline control group, dimethyl sulfoxide (DMSO) control group, TET exposure group, high-dose (2.8 g/kg/d) acetamide treatment group, and super-high-dose (5.6 g/kg/d) acetamide treatment group. Rats in the exposure group and treatment groups were exposed to TET by intragastric administration after fasting, and were then intramuscularly injected with saline or different doses of acetamide in the following 5 days. The cortex of the temporal lobe was collected at 3 h, 12 h, 48 h, or 7 d after treatment. The expression levels of GABA and Glu in the cortex of the temporal lobe were determined by average optical density (OD) values in immunohistochemistry.

RESULTS1) Expression of GABA: The OD value of GABA in TET exposure group started to increase at 12 h after treatment, reached the peak at 48 h, and decreased to the normal level at 7 d. In the high-dose acetamide treatment group, the increase in OD at 12 h was not so significant as that in the TET exposure group, OD value decreased to the normal level at 48 h and was lower than that in the exposure group, and the changes were more like those in the control groups. In the super-high-dose acetamide treatment group, OD value began to increase significantly at 3 h and was significantly higher than that in the TET exposure group (P < 0.01), it reached the peak at 12 h, and was restored to the normal value at 48 h. 2) Expression of Glu: The OD value of Glu in TET exposure group at 3 h after treatment was significantly lower than those in the two control groups, it increased gradually from 12 h to 48 h, and recovered to the normal level at the 7th d. The changes in the high-dose acetamide treatment group were similar to those in the TET exposure group, but became more like those in the control groups after 48 h; the OD value in super-high-dose acetamide treatment group was significantly higher than that in the TET exposure group at 3 h after treatment (P < 0.01), while no significant difference was found at 12 h; it was significantly lower than those of all other groups at 48 h and 7 d (P < 0.01).

CONCLUSIONSTreatment with high dose of acetamide has some curative effect on TET poisoning-induced central nervous lesion, while the effect of super-high-dose acetamide on expression of neurotransmitters is too complex to evaluate.

Acetamides ; pharmacology ; Animals ; Bridged-Ring Compounds ; poisoning ; Cerebral Cortex ; drug effects ; metabolism ; Female ; Glutamic Acid ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; gamma-Aminobutyric Acid ; metabolism

OBJECTIVETo investigate the efficacy of hemoperfusion treatment in children with acute tetramine poisoning.

METHODSThirty-two children aged from 1 to 8 years ( mean 4.6+/-2.4 years) with acute tetramine poisoning received hemoperfusion treatment. Serum tetramine concentrations were measured by gas chromatography before hemoperfusion, 1 and 2 hrs after hemoperfusion initiation and 12 and 24 hrs by the end of hemoperfusion. The median time for full recovery of consciousness and the time to seizure control were observed.

RESULTSSeventeen children received hemoperfusion treatment for one time, 12 for twice, 2 for 4 times and 1 for 3 times. Twenty- seven (84%) cases recovered, 2 (7%) cases improved and 3 (9%) cases died of multi-organ failure. The serum tetramine concentrations 1 and 2 hrs after hrmoperfusion initiation were significantly lower than those before hemoperfusion (P<0.01). The serum tetramine concentrations 12 and 24 hrs by the end of hemoperfusion were also significantly lower than those before hemoperfusion (P<0.01). The median time for full recovery of consciousness and the time to seizure control were 5.4+/-4.2 and 10.1+/-7.3 hrs, respectively.

CONCLUSIONSHemoperfusion treatment is effective for acute tetramine poisoning in children.

Acute Disease ; Bridged-Ring Compounds ; blood ; poisoning ; Child ; Child, Preschool ; Female ; Hemoperfusion ; Humans ; Infant ; Male ; Time Factors

Animals ; Bridged-Ring Compounds ; poisoning ; Disease Models, Animal ; Female ; Male ; Mice ; Sodium Oxybate ; therapeutic use ; Unithiol ; therapeutic use

Acetamides ; pharmacology ; Animals ; Bridged-Ring Compounds ; poisoning ; Disease Models, Animal ; Female ; Male ; Rats ; Rats, Sprague-Dawley ; Troponin I ; blood

Expressions of GABA and GABA(A)R-alpha1 in the brain of rats poisoned by Tetramine were analyzed to explore the intoxication mechanism. Methods Sixty rats were randomly divided into control, sham poisoned, high-dose poisoned (1.0 mg/kg tetramine) and low-dose poisoned (0.1 mg/kg) groups. The expressions of GABA and GABA(A)R-alpha1 in the brain of the poisoned rats were detected and analyzed by immunohistochemistry and imaging analyzer. Results The expressions of both GABA and GABA(A)R-alpha1 were diffusely seen in the brains of the control and shame poisoned rat groups with a moderate expression level, whereas the expressions of both GABA and GABA(A)R-alpha1 were decreased in the brains of the high-dose poisoned group. In the low-dose poisoned rat group, the expression of GABA initially decreased and reached its lowest level 6 hours after poisoning, and then started to show an increase and reached the level of control groups at day 3. The expressions level reached its peak at days 5-7 after poisoning and remained above the level of control groups till 10 days after poisoning. Similarly, the expression of GABA(A)R-alpha1 in the brains of the low-dose poisoned group initially decreased and reached its lowest level 6-12 hrs after poisoning, and then started to increase and reached the level of control groups at days 7-10 after poisoning, respectively. Conclusion The expression of both GABA and GABA(A)R-alpha1 decreased in the brains of the high-dose poisoned rat group and these changes of GABA and GABA(A)R-alpha1 expressions may be associated with underlying mechanism of tetramine poisoning.
Animals ; Brain/pathology* ; Bridged-Ring Compounds/poisoning* ; Cerebral Cortex/pathology* ; Female ; Hippocampus/pathology* ; Immunohistochemistry ; Male ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-A/metabolism* ; Time Factors ; gamma-Aminobutyric Acid/metabolism*

To investigate the therapeutic effect of high-dosage gamma-aminobutyric acid (GABA) on acute tetramine (TET) poisoning, 50 Kunming mice were divided into 5 groups at random and the antidotal effects of GABA or sodium dimercaptopropane sulfonate (Na-DMPS) on poisoned mice in different groups were observed in order to compare the therapeutic effects of high-dosage GABA with those of Na-DMPS. Slices of brain tissue of the poisoned mice were made to examine pathological changes of cells. The survival analysis was employed. Our results showed that both high-dosage GABA and Na-DMPS could obviously prolong the survival time, delay onset of convulsion and muscular twitch, and ameliorate the symptoms after acute tetramine poisoning in the mice. Better effects could be achieved with earlier use of high dosage GABA or Na-DMPS. There was no significant difference in prolonging the survival time between high-dose GABA and Na-DMPS used immediately after poisioning. It is concluded that high-dosage GABA can effectively antagonize acute toxicity of teramine in mice. And it is suggested that high-dosage GABA may be used as an excellent antidote for acute TET poisoning in clinical practice. The indications and correct dosage for clinical use awaits to be further studied.
Acute Disease ; Antidotes/*administration & dosage ; Antidotes/therapeutic use ; Bridged Compounds/*poisoning ; Random Allocation ; Rodenticides/*poisoning ; Unithiol/therapeutic use ; gamma-Aminobutyric Acid/*administration & dosage ; gamma-Aminobutyric Acid/therapeutic use

Acute Disease ; Adult ; Autopsy ; Bridged-Ring Compounds ; poisoning ; Child ; Humans ; Male ; Poisoning ; pathology ; Rodenticides ; poisoning

OBJECTIVETo investigate the clinical significance of myocardial enzymes in patients with acute tetramine (TEM) poisoning.

METHODSThe dynamic changes of the activity of myocardial enzymes and ECG were observed in 67 patients with acute TEM poisoning as well as in 67 healthy people for medical checkup at outpatient department as the control group.

RESULTSMyocardial enzymes of the patients with acute TEM poisoning were increased to different extents on the first day. There was significant difference in the activity of aspartate aminotransferase (AST), creatine phosphokinase (CPK), lactic dehydrogenase (LDH), alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) and CPK isoenzyme MB (CK-MB) between the patients and the healthy people in the control group (P < 0.01). There was significant difference in the myocardial enzymes at different time points among the patients with mild, middle and severe poisoning (P < 0.01). The severer the TEM poisoning was, the higher the activity of myocardial enzymes and the abnormal rate of ECG were. The activity of CPK was the earliest to rise with the highest aptitude of fluctuation and the longest time of elevation. The change of the myocardial enzymes was earlier than that of ECG. The abnormal rate of AST, CPK, CK-MB, LDH, alpha-HBDH was 86.57%, 98.51%, 94.03%, 89.55% and 79.10% respectively. The abnormal rate of ECG was 49.3% on the third day of poisoning. Measurement of myocardial enzymes was better than ECG in sensitivity.

CONCLUSIONAcute tetramine poisoning can damage myocardium, which is reversible. CPK is a typical marker for the damage and can serve as one of the important clinical monitoring indices.

Acute Disease ; Adolescent ; Adult ; Aspartate Aminotransferases ; metabolism ; Bridged-Ring Compounds ; poisoning ; Child ; Child, Preschool ; Creatine Kinase ; metabolism ; Creatine Kinase, MB Form ; metabolism ; Electrocardiography ; Female ; Humans ; Hydroxybutyrate Dehydrogenase ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Male ; Middle Aged ; Myocardium ; enzymology

Acute Disease ; Adolescent ; Adult ; Aged ; Bridged-Ring Compounds ; poisoning ; Child ; Child, Preschool ; Emergencies ; Female ; Humans ; Infant ; Male ; Middle Aged ; Poisoning ; therapy

OBJECTIVE: To find whether Bcl-2 and Caspase-3 take part in the pathophysiological mechanism of tetramine toxification. METHODS: Sixty Sprague-Dawley rats were divided into normal control group, the sham poisoned group, high dose poisoned group, low dose poisoned group. High dose poisoned group were administered 1.0 mg/kg weight body tetramine by mouth, however low dose poisoned group was administered tetramine 0.1 mg/kg weight body by mouth. The rats of the sham poisoned group were administered water, and rats of normal control group were given nothing. Bcl-2 and Caspase-3 were detected by immunohistochemistry staining and the results were assessed by image analysis system. RESULTS: The expressions of Bcl-2 and Caspase-3 in all organs were similar, ie, Bcl-2 and Caspase-3 expressed obviously in all organs of high dose poisoned group; in all organs of low dose poisoned group, they were hardly detected at 30 min after administration, however, at 3 h after administration, they could be detected obviously; Bcl-2 got to peak at 6 h-3 d after administration and Caspase-3 got to peak at 24 h-3 d after administration. CONCLUSION Bcl-2 and Caspase-3 take part in the pathophysiological procedure of tetramine poisoned rats.
Animals ; Bridged-Ring Compounds/poisoning* ; Caspase 3/metabolism* ; Dose-Response Relationship, Drug ; Immunohistochemistry ; Kidney/pathology* ; Liver/pathology* ; Lung/pathology* ; Male ; Myocardium/pathology* ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Spleen/pathology* ; Time Factors