Laboratory evaluation of WBA 8119 as a rodenticide for use against warfarin-resistant and non-resistant rats and mice. (1/71)

Feeding tests were carried out in the laboratory to evaluate WBA 8119 as a potential new rodenticide against wild common rats (Rattus norvegicus), ship rats (R. rattus) and house mice (Mus musculus). The results obtained are compared with data previously obtained for difenacoum, another member of the same series of 4-hydroxycoumarin anticoagulants. With warfarin-resistnat and non-resistant common rats, complete kills were obtained using a concentration of 0-0005% for 2 days, or 0-001% for 1 day: a 1-day test at 0-0005% killed 6 out of 10 and 17 out of 20 of the two types respectively. At 0-0005% complete kills of resistant ship rats were obtained after 2 days exposure and of resistant house mice after 1 day, but at 0-002% for 2 days there was some survival. Non-resistant ship rats and house mice were all killed after 2 days feeding on 0-002% bait. In 2-day palatability tests, R. norvegicus showed no significant aversion to the poison at 0-002% and 100% mortality was obtained. The poison was significantly unpalatable to R. rattus at 0-005% and to M. musculus at 0-005% and 0-002%, although with the last species these concentrations gave complete kills. It is concluded that WBA 8119 has greater activity than other known anticoagulants against the three commensal species examined. The laboratory results suggest that concentrations between 0-0005% and 0-002% would be suitable for field use against common rats, and between 0-002% and 0-005% for ship rats and house mice.  (+info)

Trials of the anticoagulant rodenticide WBA 8119 against confined colonies of warfarin-resistant house mice (Mus musculus L.). (2/71)

The efficacy of the newly developed anticoagulant rodenticide WBA 8119 was evaluated against the house mouse (Mus musculus L.) using individual and family groups of warfarin-resistant animals. WBA 8119 at 0-002%, 0-005% and 0-01% in pinhead oatmeal bait gave complete kills of mice in 'no-choice' feeding tests carried out in cages and small pens. In replicated 21-day treatments on families of mice confined in larger pens conditioned to feeding on plain foods, the overall mortalities obtained using the three formulated poison baits were 71/72, 62/63 and 57/57 respectively. The results of the WBA 8119 toxicity tests are considered in relation to previous findings on other anticoagulant rodenticides, particularly difenacoum. In equivalents tests, WBA 8119 performed better than difenacoum. The data thus suport the laboratory findings that WBA 8119 is the most active anticoagulant so far tested for the control of warfarin-resistant house mice.  (+info)

Methylation of 4-hydroxycoumarin with diazomethane. (3/71)

4-Hydroxycoumarin was methylated with diazomethane. A mixture of 4-methoxycoumarin and 2-methoxychromone was separated chromatographically.  (+info)

Determination of coumarin-type anticoagulants in human plasma by HPLC-electrospray ionization tandem mass spectrometry with an ion trap detector. (4/71)

BACKGROUND: Coumarin-type anticoagulants are used for the long-term treatment and prevention of thromboembolic disorders. The identification of these drugs is crucial in patients with an increased prothrombin time of unknown origin. The aim of this study was to develop a sensitive and specific method for the simultaneous determination of phenprocoumon, acenocoumarol, and warfarin in human plasma by HPLC-electrospray ionization tandem mass spectrometry. METHODS: After addition of the internal standard, p-chlorowarfarin, plasma samples were extracted using Oasis MCX solid-phase extraction cartridges. The compounds were separated on a Symmetry C18 column (Waters) with a mobile phase of acetonitrile-1 g/L formic acid (75:25 by volume) at a flow rate of 0.5 mL/min. RESULTS: Extraction and separation of the three drugs and the internal standard were accomplished in 9 min. The overall extraction efficiency was >89% for all three compounds. The limits of detection were 1 microg/L for phenprocoumon and warfarin and 10 microg/L for acenocoumarol. Regression analysis of the calibration data revealed good correlation (r(2) >or=0.995) for all compounds. Within-run accuracies for quality-control samples were +/- 1% to 7% of the target concentration, with CVs <9%. CONCLUSIONS: The proposed method enables the unambiguous identification and quantification of phenprocoumon, warfarin, and acenocoumarol in both clinical and forensic specimens. This method combines a new, rapid solid-phase extraction procedure with an extremely fast chromatographic analysis, which is especially advantageous for clinical laboratories.  (+info)

Acquired coagulopathy due to anticoagulant rodenticide poisoning. (5/71)

A 35-year-old woman was admitted to hospital because of epistaxis, hematomas, and metrorrhagia. Laboratory data indicated severe coagulopathy with prolonged prothrombin time and decreased serum concentrations of vitamin K-dependent clotting factors II, VII, IX, and X. The patient denied taking any oral anticoagulants. She was given transfusions of red blood cells, fresh frozen plasma (1,180 mL) and phytomenadione daily for 6 weeks (total dose 550 mg), which normalized the coagulation factors concentration. After all other possible causes of acquired coagulopathy had been excluded, rodenticide poisoning was suspected on the basis of her epidemiologic history. The patient was a war refugee from Bosnia and Herzegovina. During her absence, the troops of United Nations Protection Force performed rodent extermination in and around her house. History data and therapeutic effects suggested that the coagulopathy had been caused by prolonged exposure to long-acting anticoagulant rodenticide. This could also explain the need for protracted phytomenadione therapy.  (+info)

Brodifacoum toxicosis in two neonatal puppies. (6/71)

Eight out of a litter of 13 puppies were either born dead or died within 48 hours of birth. Three puppies that died shortly after birth were necropsied. Two puppies had hemorrhage in the thoracic and peritoneal cavities, intestinal serosa, and meninges. The third puppy was smaller than the other two puppies but did not have detectable hemorrhage. Brodifacoum, a second-generation coumarin anticoagulant, was detected in livers from the two puppies with hemorrhage. The dam did not have clinical signs of coagulopathy before or subsequent to whelping. The owners were confident that the dog had not been exposed to rodenticide for at least 4 weeks before whelping. A presumptive diagnosis of in utero brodifacoum toxicity was made. To the authors' knowledge this is the first time a second-generation coumarin anticoagulant has been detected in the liver of a newborn animal. This case is also unique because the dam was unaffected, suggesting that fetuses are more susceptible to brodifacoum toxicity than adult animals.  (+info)

Electrooxidation of iodide in the presence of 4-hydroxycoumarin: application to a simple coulometric titration of 4-hydroxycoumarin. (7/71)

The electrochemical oxidation of iodide ion in the presence of 4-hydroxycoumarin (1) was studied using cyclic voltammetry and controlled-potential coulometry. The result indicates that the resulting iodine takes part in a halogenation reaction and reacts with 4-hydroxycoumarin (1). According to the obtained results, a new and simple coulometric titration method with potentiometric end-point detection for the determination of 4-hydroxycoumarin (1) is presented. In the presented method, 2-200 micromol of 4-hydroxycoumarin (1) was successfully determined.  (+info)

A 44-year-old woman with hematemesis and cutaneous hemorrhages as a result of superwarfarin poisoning. (8/71)

The authors present the case of a 44-year-old American Indian woman with hematemesis, spontaneous cutaneous hemorrhages, and multiple ecchymoses. Coagulation factor analyses demonstrated both prolonged prothrombin time (PT, >40 s) and prolonged partial thromboplastin time (PTT, >120 s). Measurement of the serum level of brodifacoum (37 ng/mL), one of the superwarfarin agents commonly used in rodenticides, confirmed poisoning as the cause of the patient's symptoms. Substantial amounts of fresh frozen plasma and vitamin K were required to obtain normal coagulation parameters and maintain these parameters over a 3-week inhospital period. Oral administration of vitamin K (100 mg daily) maintained normal PT (14.1 s), PTT (33.0 s), and international normalized ratio (INR, 1.48) at 2 weeks after the patient was discharged from the hospital. By 2 months postdischarge, PT, PTT, and INR returned to elevated levels because of patient noncompliance with the prescribed tapering vitamin K regimen.  (+info)

• 1
• 2
• 3
• 4
• 5
• 6
• 7
• 8
• 9