A comparison of dexmedetomidine, moxonidine and alpha-methyldopa effects on acute, lethal cocaine toxicity

Background: The treatment of cocaine toxicity is an important subject for emergency physicians. We investigated the effects of dexmedetomidine, moxonidine and alpha-methyldopa on acute cocaine toxicity in mice. Objectives: The aim of this study was to evaluate the effects of dexmedetomidine, moxonidine and alpha-methyldopa in a mouse model of acute cocaine toxicity. Materials and Methods: We performed an experiment consisting of four groups (n = 25 each). The first group received normal saline solution, the second group received 40 μg/kg of dexmedetomidine, the third group received 0.1 mg/kg of moxonidine and the fourth group received 200 mg/kg of alpha-methyldopa, all of which were intraperitoneally administered 10 minutes before cocaine hydrochloride (105 mg/kg). All animals were observed for seizures (popcorn jumping, tonic-clonic activity, or a loss of the righting reflex) and lethality over the 30 minutes following cocaine treatment. Results: The ratio of animals with convulsions was lower in all treated groups when compared to the control (P 0.05). In addition, the time to lethality was also longer in the same group (P < 0.001). Conclusions: The present study provides the first experimental evidence in support of dexmedetomidine treatment for cocaine-induced seizures. Premedication with dexmedetomidine reduces seizure activity in a mouse model of acute cocaine toxicity. In addition, while dexmedetomidine may be effective, moxonidine and alpha-methyldopa did not effectively prevent cocaine-induced lethality. © 2015, Iranian Red Crescent Medical Journal

Dismorfoloji ve Çoklu Anomaliler İKİ KARDEŞTE FEINGOLD SENDROMU

FEINGOLD SYNDROME IN TWO BROTHERS1E Bora,1B Uyanık,1TC ̧ ankaya,1D Erc ̧al,2K Atila,2SBora1Department of Medical Genetics, Dokuz Eylul UniversityFaculty of Medicine, Izmir, Turkey;2Department of General Sur-gery, Dokuz Eylul University Faculty of Medicine, Izmir, TurkeyFeingold syndrome (FS) is a dominantly inherited disease,combination of microcephaly with or without learning disabili-ties, extremity abnormalities, short palpebral fissures andesophageal/duodenal atresia. Approximately 60% of individu-als with FS have an affected parent and caused by mutation inthe MYCN gene, locus at 2p24.1. Our patient is 24-year-oldmale from unrelated parents and pictured microcephaly, up-slanting palpebral fissures, mild palpebral phimosis, small earlobules, micrognathia, 2nd and 5th fingers brachymesopha-langy, 5th finger clinodactyly, 2th-3th toes’ cutaneous syndac-tyly, clubbing fingernails, thenar and hypothenar atrophy,evanescenced dermatoglyphics on hand. According to theneuro-developmental examination; the patient showed mildmental retardation and learning disability. As a gastro-intesti-nal complaint, vomiting has been started at the age of five.Endoscopy and thorax CT showed the diameter was 2–3 mmin esophageal lumen and C2–C3 vertebral fusion defect. Hewas diagnosed as Feingold syndrome. The existence of similarclinical findings in his elder brother was also learned and con-sidered as the same entity. We described two brothers withFeingold syndrome according to the clinical findings and pre-sented since the syndrome is rare and they are the second andthird cases from Turkey. Further clinical and molecular inves-tigations are also planned.</p