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At least 163 records · Page 9Linked to original sources
PubMed1976

Comparisons of antidotal efficacy of chelating drugs upon acute toxicity of Ni(II) in rats.

Six chelating drugs were administered to rats by im injection at equimolar dosages in order to compare their relative effectiveness in prevention of death after a single parenteral injection of NiCl2. Triethylenetetramine and d-penicillamine were most effective antidotes for acute Ni (II)-toxicity. In order of decreasing antidotal effectiveness, diglycyl-L-histidine-N-methylamide, sodium diethyldithiocarbamate and calcium disodium versenate significantly reduced the acute mortality of rats following ip injection of Ni (II). Alpha-Lipoic acid was not effective as an antidote for acute Ni (II)-toxicity.

Animals↗
PubMedDate not supplied

Experimental studies on thallium toxicity in rats. II--The influence of several antidotal treatments on the tissue distribution and elimination of thallium, after subacute intoxication.

The influence of several antidotal treatments--e.g. Prussian Blue + Furosemide, Furosemide, activated Charcoal, Potassium Chloride and Potassium Iodide--on the tissue distribution and elimination of thallium after subacute intoxication is studied. From these experiments, the fate of electrolytes (Na+, K+, Cl-) may be evaluated. It was established that the efficacy of an antidotal treatment in thallium intoxication may be judged not only by the determination of its ability to interfere in the reabsorption and redistribution of thallium. Prussian Blue was the only antidotal that did not cause such a dangerous redistribution.

Animals↗
PubMed1985

Antidotes for gold (sodium bis[thiosulfato]gold[I]) intoxication in mice.

Eight compounds were examined to determine their relative efficacy as antidotes in acute gold intoxication in mice after the intraperitoneal injection of 200 mg/kg of Na3 [Au(S2O3)2] X 2H2O. Of the compounds examined, 2,3 dimercaptosuccinic acid was the most effective antidote. It was noted that with D-penicillamine those animals which did not survive died sooner (in a matter of hours) than the corresponding control animals which had received no antidote (about 3 days). In subsequent experiments in which Na3 [Au(S2O3)2] X 2H2O was administered at the lower level of 140 mg/kg, 2,3 dimercaptosuccinic acid showed itself to be capable of reducing kidney gold levels by a factor of about 5 and liver gold levels by a factor of approximately 2.

Animals↗
PubMed1984

[Antidotal treatment of acebutolol poisoning].

In rats, the intravenous infusion with acebutolol lead to a dose dependent decrease of arterial blood pressure, heart rate, cardiac output and total peripheral resistance, to sinus bradycardia, widening of the QRS complex, 1st and 2nd degree AV-block and intraventricular conductance disturbances. Nine possible antidotes were administered i.v. to rats which had been infused with 2 mg/kg X min acebutolol for 60 min. Isoprenaline proved the best antidote against acebutolol antagonizing the bradycardia by 88% and the hypotension completely. The activities of orciprenaline and prenalterol were lower than those of isoprenaline. Dopamine, epinephrine and norepinephrine antagonized acebutolol-induced hypotension, but did not influence considerably the bradycardia. Glucagon, on the other hand, antagonized the acebutolol-induced bradycardia by 47% but exerted only a small activity on the hypotension. Aminophyllin and calcium were nearly ineffective as antidotes against acebutolol. Isoprenaline and dopamine infused simultaneously restored heart rate, arterial blood pressure and cardiac output of acebutol-poisoned rats. The survival time of rats infused with 4 mg/kg X min acebutolol was doubled by the additional infusion of 0.2 mg/kg X min isoprenaline. The antagonistic activity of a treatment with isoprenaline and dopamine against the cardiovascular toxicity of acebutolol was confirmed in rabbits.

Acebutolol↗
PubMed1980

Physostigmine salicylate as an antidote.

Most poisonings with anticholinergics deal with simple cases without diagnostic or therapeutic difficulties; however, in difficult or unclarified cases a new method for diagnosis and treatment is the antidote physostigmine salicylate. Within 15 minutes after application of 2 mg of the antidote the central anticholinergic symptoms disappear, such as respiratory depression, coma, cramps and hallucinations as do the peripheral anticholinergic symptoms as cardiac rhythm disturbance, dry mouth and red dry skin. No fatal overdose with anticholinergic drugs occurs if the antidote is given in time.

Alcohol Withdrawal Delirium↗
PubMed1995

Antidotal effect of sodium thiosulfate in mice exposed to acrylonitrile.

Although acute acrylonitrile (ACN) toxicity is very profound, the mechanism of its toxicity and immediate lethality is unclear. Many have suggested that ACN or its reactive metabolite acts directly at the target tissues, while others have implicated the release of CN ions from the parent compound as the toxic moiety. Since sodium thiosulfate (STS) is both an effective cyanide antidote and neutralizing agent capable of binding to reactive chemicals or metabolites, its antidotal role was investigated in mice exposed to 60 mg/kg intraperitoneal (IP) ACN injection. Treatment with an IP injection of 400 mg/kg of STS from 10 to 30 minutes before ACN administration protected animals from ACN-induced lethality. All mice appeared normal after prophylactic treatment with STS and showed no ill effects from ACN exposure. Similar data was observed when STS was administered 10 and 30 minutes after ACN administration. Non-protein sulfhydryl (NPSH) concentration was determined in the brain, kidneys, and liver of the mice exposed to a single or multiple doses of STS and ACN. The levels of NPSH were significantly lowered by ACN in the liver (45% of the control), and kidneys (51% of the control), whereas in the brain NPSH levels were least affected and decreased modestly (85% of the control) following either acute or chronic administration of acrylonitrile. The data indicate a marked protective effect of STS either before or after ACN exposure and this STS-induced antidotal response does not involve GSH in the brain.

Acrylonitrile↗
PubMedDate not supplied

[The selection of the indices of antidote efficacy].

The application of the following new indices of the efficacy of antidotes has been substantiated and discussed: the "antidotal potency" as a ratio of LD50 of a poison when an antidote used to LD99 in control intact animals, and the "index of solid protection" as a ratio of LD10 in the experiments to LD90 in controls. The two indices are true for changing the lethality curve slope, which makes it impossible to use the currently accepted "protection index" as a ratio of LD50 in experiments to LD50 in controls.

Animals↗
PubMedDate not supplied

[Effect of antidotes on the rate of absorption of 2,4-dinitrophenol from the digestive tract into the blood].

An investigation of the rate of the 2,4-dinitrophenol absorption from the digestive tract into the blood with the use of an antidote and its components (activated charcoal, tannin, magnesium oxide), stach water and paraffin oil demonstrated the activated charcoal and magnesium oxide to be the best antidotes among the ones studied. The antidote exerts a somewhat less marked, but still quite a strong action.

Animals↗
PubMed1993

Comparison of the hemodynamic effects of hydroxocobalamin and cobalt edetate at equipotent cyanide antidotal doses in conscious dogs.

OBJECTIVES: The hemodynamic effects of two cyanide antidotes, hydroxocobalamin and cobalt edetate were compared. DESIGN: This experimental study was performed in chronically instrumented conscious dogs and at equipotent cyanide antidotal doses (hydroxocobalamin 70 mg.kg-1; cobalt edetate 10.5 mg.kg-1). RESULTS: Peak plasma cobalt concentrations did not differ in the two groups (412 +/- 183 vs 400 +/- 160 mumol.l-1). Hydroxocobalamin induced a slight increase in mean arterial pressure (+17 +/- 9%, p < 0.05) and systemic resistance (+19 +/- 15%, p < 0.05). In contrast, cobalt edetate induced an increase in heart rate (+78 +/- 33%, p < 0.05), in cardiac output (+63 +/- 39%, p < 0.05), and in maximum rise of left ventricular pressure (+33 +/- 15%, p < 0.05), did not modify mean arterial pressure, and decreased systemic resistance (-36 +/- 15%, p < 0.05). These hemodynamic effects were associated with an increase in plasma catecholamine concentrations (epinephrine: 2524 +/- 3025 vs. 58 +/- 37 pg.ml-1, p < 0.05; norepinephrine: 1106 +/- 609 vs. 343 +/- 146 pg.ml-1, p < 0.05), which in contrast remained unchanged after hydroxocobalamin administration. Cobalt edetate also induced an increase in blood glucose concentrations (9.9 +/- 1.9 vs. 6.1 +/- 1.2 mmol.l-1, p < 0.05) and a moderate metabolic acidosis, whereas hydroxocobalamin did not. After adrenergic (alpha 1, beta) and cholinergic receptor blockade, cobalt edetate did not modify heart rate and various indices of cardiac function, suggesting that it has no direct cardiac effects. CONCLUSION: Considering its lack of hemodynamically relevant effects, these results indicate that hydroxocobalamin is potentially a safer cyanide antidote than cobalt edetate.

Animals↗
PubMed1988

CNS involvement in acute organophosphate poisoning: specific pattern of toxicity, clinical correlates and antidotal treatment.

The present review was designed to integrate both experimental and clinical data and to focus on the problems of management of severe cases of acute organophosphate poisoning, which always show CNS involvement. AChE activity, in discrete regions of the human brain, was studied by quantitative histochemistry of 40 mu thick sections. The regional effects of AChE inhibition by organophosphates was examined in a comparative study of the brains of two victims and two control brains, matched for age and sex. The pattern of AChE inhibition was regionally selective. The most significant decreases were observed in the neocerebellum, thalamic nuclei and the cortex. This specific distribution of AChE inhibition may be correlated with some of the clinical characteristics of acute organophosphate poisoning. The diagnostic value of blood AChE levels was examined in a personal series of 53 patients, who needed artificial ventilation, intensive care monitoring and antidotal treatment. The effects and side-effects of the antidotal treatment were reassessed. Recommended regimen of therapy was outlined, based upon experience in this series and in recent animal studies. The logical therapy would be and almost always in the co-administration of an anticholinergic drug (usually atropine) and an AChE reactivator (oximes) in order to rapidly obtain the most beneficial effect in the critically ill patient. Seizures that do not respond to the specific antidotal therapy, should be treated with I.V. benzodiazepines. Artificial respiration and supportive measures are essential for patient' survival. They enable the patient to gain the necessary time for sufficient recovery of AChE activity.

Acetylcholinesterase↗
PubMedDate not supplied

Cyanide overdose: survival with fatal blood concentration without antidotal therapy.

Cyanide poisoning is an uncommon emergency department problem. It has a high mortality, and specific antidotal therapy can be lifesaving. We describe a 23-year-old man who ingested potassium cyanide and survived without antidotal therapy. His blood cyanide concentration was 4.65 mg/L, which is within the lethal range. The arterial venous oxygen saturation gradient was considered in the decision regarding antidote administration. Our experience underscores the importance of supportive care.

Adult↗
PubMed2004

Screening of functional antidotes of RNA aptamers against bovine thrombin.

A specific RNA aptamer (T705) against bovine thrombin had been obtained after seven rounds of SELEX (systematic evolution of ligands by exponential enrichment) selection from a random RNA library previously. In order to further investigate the relationship between the structure and function of this aptamer, three truncated RNA aptamers, T705a, T705b and T705c, were designed according to the secondary structure of T705 RNA. Our results showed that T705c keeping the precise stem-loop structure but lacking most of the stem region sequence of T705 could inhibit clot formation in vitro in the same way as its parental form. We also report here that single-stranded DNA (ssDNA) antisense oligonucleotides, c' and c'-22, which were complementary to different portions of T705c could act as efficient antidotes reversing the inhibitory activity of T705. It is demonstrated for the first time that ssDNA antisense oligonucleotides are potential antidotes of RNA aptamers and this may be an effective, rapid strategy to find antidotes of RNA aptamers which would be of important usefulness in basic research and drug screening.

Animals↗
PubMed2000

Tunneling through a coherent "Quantum antidot molecule"

We report experiments on resonant tunneling through a quantum antidot in the fractional quantum Hall regime. The envelope of the conductance peaks indicates tunneling via two resonant states, one of them bound on the lithographic antidot, the other on a hill of the disorder potential. Moreover, our analysis indicates that the coherent tunneling rate between the two states is an order of magnitude higher than the phase breaking rate, thus giving evidence for a coherently coupled "antidot molecule."

Journal Article↗
PubMed2002

Quantum antidot formation and correlation to optical shift of gold nanoparticles embedded in MgO.

Quantum antidots are subnanometer scale vacancy clusters, the localized electronic structure of which can significantly alter the properties of a nanomaterial. We use positron spectroscopy to study vacancy clusters generated during the formation of gold nanoparticles via ion implantation in an MgO matrix. We observed that quantum antidots are associated with the nanoparticle surfaces after annealing in an O2 atmosphere, but not after annealing in a H2 atmosphere. In the former case, the presence of quantum antidots bound to the gold nanoparticles correlates with the redshift of the gold surface plasmon resonance, thus allowing an explanation for the redshift based on the transfer of electrons away from the metal particles.

Journal Article↗
PubMed2002

Kondo effect in a quantum antidot.

We report Kondo-like behavior in a quantum antidot (a submicron depleted region in a two-dimensional electron gas) in the quantum-Hall regime. When both spins of the lowest Landau level are present all around the antidot, the resonances between extended edge states via antidot bound states show an abnormal feature in alternate Coulomb-blockaded regions. The feature becomes suppressed when the temperature or source-drain bias is raised as for Kondo resonances in quantum dots. Although the exact mechanism is unknown, Kondo-like correlated tunneling may arise from a Skyrmion-type edge reconstruction. This observation demonstrates the generality of the Kondo phenomenon.

Journal Article↗
PubMed1985

Vinca alkaloid skin toxicity: antidote and drug disposition studies in the mouse.

A murine (BALB/c) skin toxicity model was used to evaluate various possible antagonists to vinca alkaloid-induced skin ulceration. Reproducible dose-response relationships were developed for vinblastine (VBL) and vindesine (VDS). With vincristine (VCR) only about 70% of mice developed dose-dependent ulceration. On an equal weight basis, VCR proved to be significantly more toxic than either VBL or VDS (P less than .05 by Student's t-test). Effective local intradermal antidotes to VBL, VDS, and VCR included hyaluronidase, normal saline, and calcium leucovorin (P less than .05 by the Student's Newman-Keuls multiple range test). Mild, topical skin heating significantly reduced VCR ulceration. In contrast, diphenhydramine and sodium bicarbonate were ineffective as local antidotes. Topical skin cooling, however, significantly increased vinca-induced skin ulcers for VBL, VDS, and VCR (P less than .05). Hydrocortisone, vitamin A topical cream, and isoproterenol increased skin toxicity. [3H]VBL was given intradermally to follow the drug's pharmacokinetic disposition from the skin and adherent panniculus carnosus muscle. [3H]VBL exhibited two phases of elimination: a rapid early phase [half-life (t 1/2) of approximately equal to 30 min] and a prolonged terminal phase (t 1/2 of approximately equal to 17 hr). The application of heat increased the distributive, early phase by 0.5-2.5 hours and did not enhance the terminal elimination of the drug from skin. Intradermal hyaluronidase significantly reduced the area under the ulceration multiplied by the time curve to one-seventh the control value, the peak [3H]VBL skin concentration to one-half the control value and the terminal [3H]VBL t 1/2 in skin to one-third the control level (P less than .05 by Student's t-test). These results show hyaluronidase to be an effective antidote for vinca-induced skin ulceration. Local glucocorticosteroids and topical cooling are definitely contraindicated in the management of inadvertent vinca alkaloid extravasations.

Administration, Topical↗
PubMed1983

Optical isomers of 2,3-dimercapto-1-propanesulfonate: antidotal activity, in vitro and in vivo, against sodium arsenite.

DMPS (2,3-dimercapto-1-propanesulfonate, Na salt) is an important water soluble analog of dimercaprol. All investigations of this antidote for heavy metal intoxication have dealt only with the racemic mixture. In the present report, the optical isomers of DMPS have been separated and the arsenic-antidote activity of the levo-rotatory (-)-isomer, the dextro-rotatory (+)-isomer and the racemic mixture of DMPS have been investigated in vivo and in vitro. The individual optical isomers and the racemic mixture of DMPS are effective equally, in vitro, in preventing the inhibition by sodium arsenite of the activity of mouse kidney pyruvate dehydrogenase complex. In addition, when pyruvate dehydrogenase is inhibited, in vitro, by sodium arsenite, any of the three DMPS preparations will reverse the inhibition equally well. The in vitro evidence suggests that two molecules of DMPS are required to prevent the effects of one molecule of sodium arsenite. Neither the LD50 nor the ED50 values of each of the three forms of DMPS differ significantly when measured i.p. in mice. In addition, there is no striking difference between the effectiveness of the levo- or dextro-rotatory DMPS when given orally to mice challenged with sodium arsenite. Thus, the use of the individual optical isomers of DMPS does not appear to have any advantage over the racemic mixture as an arsenic antidote under these conditions.

Administration, Oral↗
PubMedDate not supplied

Efficacy of pralidoxime iodide and obidoxime dichloride as antidotes in diazinon-poisoned goslings.

The antidotal efficacy of pralidoxime iodide and obidoxime dichloride was investigated in goslings poisoned by a supralethal dose of the organophosphorus insecticide diazinon. Various doses of both drugs were administered by intramuscular injection when the poisoned birds were unable to walk. Pralidoxime at 100 mg/kg brought about a complete and speedy clinical recovery. Fifty mg/kg induced recovery in 4 of 6 poisoned goslings, and 25 mg/kg successfully trated only 1 of 6 birds. Obidoxime at 25 mg/kg showed no therapeutic properties whereas 50 and 100 mg/kg delayed the death of some birds by several hours. At 100 mg/kg, all goslings had transient signs of intoxication, which precluded the use of this compound as an antidote at higher doses. The mode of action of these antidotes in diazinon-poisoned goslings is discussed.

Animals↗