Effect of morphine and lacosamide on levels of dopamine and 5-HIAA in brain regions of rats with induced hypoglycemia.

The study aimed to determine the effect of morphine and lacosamide on levels of dopamine and 5-HIAA in a hypoglycemic model. Female Wistar rats (n = 30), mean weight of 180 g were treated as follow: Group 1 (control) received 0.9% NaCl, Group II; morphine (10 mg kg(-1)), Group III; lacosamide (10 mg kg(-1)), Group IV; insulin (10 U.I. per rat), Group V; morphine (10 mg kg(-1))+insulin, Group VI; lacosamide (10 mg kg(-1))+ insulin. All administrations were made intraperitoneally every 24 h, for 5 days. Animals were sacrificed after the last dose to measure the levels of glucose in blood; dopamine and 5-HIAA in cortex, hemispheres and cerebellum/medulla oblongata regions. Levels of glucose decreased significantly in animals treated with morphine, lacosamide and all groups that received insulin alone or combined with respect to control group. Levels of Dopamine diminished significantly in cortex and increased significantly in hemispheres of animals that received morphine. In cortex, 5-HIAA increase significantly in the groups treated with morphine, morphine+insulin and lacosamide+insulin, however a significant decrease of the same substance was witnessed in cerebellum and medulla oblongata of animals that received morphine or lacosamide plus insulin. GSH increased significantly in cortex and cerebellum/medulla oblongata of animals treated with morphine and lacosamide alone or combined with insulin. Lipid peroxidation decreased significantly in cortex and cerebellum/medulla oblongata of groups that received lacosamide alone or combined with insulin. These results indicate that hypoglycemia induced changes in cellular regulation while morphine and lacosamide are accompanied by biochemical responses.

Effect of nicotine on ATPase, catalase and calcium levels in the presence of oligoelements in brain regions of young rats.

UNLABELLED: The effect of nicotine on membrane alterations and fluidity changes in very young models remains unclear. The aim of this study was to evaluate the effect of nicotine on total ATPase, H(2)O(2) and calcium in brain of young rats in the presence of oligoelements. Male Wistar rats (weight 80 g) received intraperitoneally either a single dose or repeated doses for 4 days as follows: Group 1 (control) NaCl 0.9%; group 2 nicotine (1mg/kg); group 3 oligoelements (50 µl); and group 4 nicotine (1mg/kg) + oligoelements (50 µl). The brain regions (cortex, hemispheres and cerebellum + medulla oblongata) of each rat were then obtained to measure the concentrations of total ATPase, H(2)O(2) and calcium using spectrophotometric methods. RESULTS: Total ATPase increased significantly (p < 0.05) in groups treated with oligoelements in repeated doses in hemisphere region, and in groups that received oligoelements + nicotine in single or repeated doses in medulla oblongata. Catalase showed significant decreased in cerebellum/medulla oblongata. Results suggest that nicotine induces changes in membrane fluidity in brain of young rats, and that ATPase could be a biomarker of nicotine consumption in young subjects.

Reversibility of hepatic histological damage after surgical temporary obstruction of the common bile duct in a murine model.

The reversibility of hepatic histological damage after restoring bile flow in a murine model was assessed. 25 male Balb C mice (25-35 g, age 6 weeks) were divided into 5 groups and their common bile duct (CBD) fastened to obstruct the release of gall bladder and liver contents. Group I, CBD untied at day 10, group II at day 15, and groups III and IV at days 20 and 30, respectively. Hematoxilin-eosin stained liver slices were analysed 0, 5, 10 and 20 days after restoring bile flow. Group I showed slight histological lesions (second stage), as cholangiolar bile pigment concretion, pericholangiolar and portal collagen accumulation; group II, mild lesions (third stage), as cholangiolar hamartomatous proliferation and bile duct portal fibrosis; group III showed severe lesions (fourth stage), as loss of functional parenchyma, and also the second and first stage lesions. Group IV died before 30 days. First stage corresponds to absent lesions (control group). Group I recovered totally, group II recovered only from slight lesions and group III had irreversible damage. Severity of lesions increased gradually and accumulatively, irreversible hepatic damage was achieved at 20 days and is deadly at 30 days. Our model of temporary CBD obstruction was suitable to assess reversibility of hepatic histological damage.