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C. Timo-iaria - One of the best experts on this subject based on the ideXlab platform.

  • Effect of chemical stimulation of the dorsomedial hypothalamic nucleus on blood plasma glucose, triglycerides and free fatty acids in rats.
    Brain research bulletin, 1997
    Co-Authors: Cássia T. B. V. Zaia, Luis Carlos Jabur Gaziri, Dimas A. M. Zaia, Edson Delattre, Miriam Sterman Dolnikoff, C. Timo-iaria
    Abstract:

    The effects of chemical stimulation of the dorsomedial hypothalamic nucleus (DMH) on blood plasma concentration of glucose, triglycerides, insulin, and free fatty acids (FFA) were investigated in anesthetized adult Wistar rats. Microinjection of 12.5 nmol of norepinephrine into the DMH increased blood plasma concentration of glucose and FFA, decreased triglycerides, and did not change plasma insulin within 5 min; after 20 min, blood glucose and FFA reached control values. Microinjection of epinephrine (12.5 nmol) into the DMH also increased blood plasma glucose concentration and decreased triglycerides after 5 min. These effects are probably mediated by beta-Adrenergic mechanisms, because they were prevented by beta-Adrenergic Antagonist propranolol, but not by alpha-Adrenergic Antagonist prazosin. Microinjection into the DMH of glutamate, dopamine, or acetylcholine failed to cause any change in those metabolic parameters, corroborating the hypothesis that the DMH is part of a beta-Adrenergic pathway involved in short-term modulation of the availability of glucose and FFA.

Murray A Raskind - One of the best experts on this subject based on the ideXlab platform.

  • a pilot trial of the alpha 1 Adrenergic Antagonist prazosin for alcohol dependence
    Alcoholism: Clinical and Experimental Research, 2009
    Co-Authors: Tracy L Simpson, Andrew J Saxon, Carol A Malte, Charles W Meredith, Brittney Mcbride, Laura C Ferguson, Christopher Gross, Kim L Hart, Murray A Raskind
    Abstract:

    Background:  Current medications for alcohol dependence (AD) show only modest efficacy. None target brain norAdrenergic pathways. Theory and preclinical evidence suggest that norAdrenergic circuits may be involved in alcohol reinforcement and relapse. We therefore tested the α-1 Adrenergic receptor Antagonist, prazosin, as a pharmacotherapy for AD. Methods:  We randomized 24 participants with AD but without posttraumatic stress disorder to receive either prazosin or placebo in a 6-week, double-blind pilot study. Medication was titrated to a target dose of 4 mg QAM, 4 mg QPM, and 8 mg QHS by the end of week 2. Participants received 5 medical management treatment sessions. Participants were reminded 3 times each day via a text pager to take medications and to call a telephone monitoring system once daily to provide self-reports of alcohol consumption and craving, the primary outcome measures. Results were analyzed using mixed linear regression adjusted for drinking days per week at baseline and week number. Results:  Twenty of the 24 (83%) subjects completed. Among the completers, the prazosin group reported fewer drinking days per week than the placebo group during the final 3 weeks of the study. Since only 1 woman was randomized to placebo and only three women completed the trial, the following results focus on the 17 male completers. The prazosin group reported fewer drinking days per week and fewer drinks per week during the final 3 weeks of the study; average total number of drinking days for the placebo group 5.7 (SEM 1.9) versus 0.9 (SEM 0.5) for the prazosin group, and average total number of drinks 20.8 (SEM 6.5) for the placebo group versus 2.6 (SEM 1.3) for the prazosin group. Rates of adverse events were equivalent across conditions. Conclusions:  Prazosin holds promise as a pharmacologic treatment for AD and deserves further evaluation in a larger controlled trial.

  • the α1 Adrenergic receptor Antagonist prazosin reduces alcohol drinking in alcohol preferring p rats
    Alcoholism: Clinical and Experimental Research, 2009
    Co-Authors: Dennis D Rasmussen, Murray A Raskind, Laura Alexander, Janice C Froehlich
    Abstract:

    Background Evidence supports a role for the norAdrenergic system in alcohol drinking in animals and humans. Our previous studies demonstrated the efficacy of prazosin, an α1-Adrenergic Antagonist, in decreasing alcohol drinking in rat models of alcohol dependence. Prazosin has also been shown to decrease alcohol drinking in treatment-seeking alcohol-dependent men. Clinically, the use of prazosin is limited by the requirement for multiple daily administrations, whereas doxazosin, a structurally similar α1-Adrenergic Antagonist, requires only once-daily dosing. In this study, we tested the hypothesis that doxazosin, like prazosin, would decrease alcohol drinking in rats selectively bred for alcohol preference (P line). Methods Adult male P rats were given 2 h/d scheduled access to a 2-bottle choice (15% v/v alcohol vs. water) session 5 d/wk (M–F), with food and water available ad libitum 24 h/d. Rats were injected with doxazosin (0 to 10 mg/kg, IP) 40 minutes prior to initiation of the alcohol access session in 3 trials (of 3, 5, and 5 consecutive days) each separated by 5 to 8 weeks. The third trial included 1 day without alcohol access (for locomotor testing), and 1 day of a single hour of alcohol access (for plasma alcohol determination). Results Doxazosin significantly reduced alcohol intake in all 3 trials. The 5 mg/kg dose consistently reduced alcohol intake, increased water drinking, did not affect locomotor activity, and resulted in lower plasma alcohol concentrations, suggesting that the doxazosin-induced reduction in alcohol drinking was not dependent on a motor impairment or an alteration in alcohol clearance. Conclusions Doxazosin decreases voluntary alcohol consumption by male alcohol-preferring (P) rats, supporting a role for the norAdrenergic system in alcohol drinking in P rats and suggesting that doxazosin could potentially be an effective once-daily pharmacotherapeutic agent for the treatment of alcohol use disorders.

  • the alpha1 Adrenergic Antagonist prazosin ameliorates combat trauma nightmares in veterans with posttraumatic stress disorder a report of 4 cases
    The Journal of Clinical Psychiatry, 2000
    Co-Authors: Murray A Raskind, Dorcas J Dobie, Evan D Kanter, Eric C Petrie, Charles E Thompson, Elaine R Peskind
    Abstract:

    BACKGROUND Central nervous system (CNS) Adrenergic hyperresponsiveness may be involved in the pathophysiology of posttraumatic stress disorder (PTSD). Two Vietnam combat veterans with PTSD prescribed the centrally active alpha1-Adrenergic Antagonist prazosin for symptoms of benign prostatic hypertrophy unexpectedly reported elimination of combat trauma nightmares. This observation prompted an open-label feasibility trial of prazosin for combat trauma nightmares in chronic combat-induced PTSD. METHOD Four consecutively identified combat veterans with chronic DSM-IV PTSD and severe intractable combat trauma nightmares participated in an 8-week open trial of escalating-dose prazosin. Nightmare severity response was rated using the nightmare item of the Clinician Administered PTSD Scale and the Clinical Global Impressions-Change scale. RESULTS The 2 patients who achieved a daily prazosin dose of at least 5 mg were markedly improved, with complete elimination of trauma nightmares and resumption of normal dreaming. The 2 subjects limited to 2 mg of prazosin to avoid excessive blood pressure reduction were moderately improved with at least 50% reduction in nightmare severity. CONCLUSION These clinical observations, together with neurobiological evidence for alpha1-Adrenergic regulation of CNS neurobiological systems relevant to PTSD, provide rationale for placebo-controlled trials of prazosin for PTSD combat trauma nightmares.

Cássia T. B. V. Zaia - One of the best experts on this subject based on the ideXlab platform.

  • Effect of chemical stimulation of the dorsomedial hypothalamic nucleus on blood plasma glucose, triglycerides and free fatty acids in rats.
    Brain research bulletin, 1997
    Co-Authors: Cássia T. B. V. Zaia, Luis Carlos Jabur Gaziri, Dimas A. M. Zaia, Edson Delattre, Miriam Sterman Dolnikoff, C. Timo-iaria
    Abstract:

    The effects of chemical stimulation of the dorsomedial hypothalamic nucleus (DMH) on blood plasma concentration of glucose, triglycerides, insulin, and free fatty acids (FFA) were investigated in anesthetized adult Wistar rats. Microinjection of 12.5 nmol of norepinephrine into the DMH increased blood plasma concentration of glucose and FFA, decreased triglycerides, and did not change plasma insulin within 5 min; after 20 min, blood glucose and FFA reached control values. Microinjection of epinephrine (12.5 nmol) into the DMH also increased blood plasma glucose concentration and decreased triglycerides after 5 min. These effects are probably mediated by beta-Adrenergic mechanisms, because they were prevented by beta-Adrenergic Antagonist propranolol, but not by alpha-Adrenergic Antagonist prazosin. Microinjection into the DMH of glutamate, dopamine, or acetylcholine failed to cause any change in those metabolic parameters, corroborating the hypothesis that the DMH is part of a beta-Adrenergic pathway involved in short-term modulation of the availability of glucose and FFA.

E F Collares - One of the best experts on this subject based on the ideXlab platform.

  • Effect of selective b-adrenoceptor blockade and surgical resection of the celiac-superior mesenteric ganglion complex on delayed liquid gastric emptying induced by dipyrone, 4-aminoantipyrine, and antipyrine in rats
    2020
    Co-Authors: A M Vinagre, E F Collares
    Abstract:

    Abstract There is evidence for participation of peripheral b-adrenoceptors in delayed liquid gastric emptying (GE) induced in rats by dipyrone (Dp), 4-aminoantipyrine (AA), and antipyrine (At). The present study aimed to determine whether b-adrenoceptors are involved in delayed GE induced by phenylpyrazole derivatives and the role of the prevertebral sympathetic nervous system in this condition. Male Wistar rats weighing 220-280 g were used in the study. In the first experiment rats were intravenously pretreated with vehicle (V), atenolol 30 mg/kg (ATE, b 1 -Adrenergic Antagonist), or butoxamine 25 mg/kg (BUT, b 2 -Adrenergic Antagonist). In the second experiment, rats were pretreated with V or SR59230A 2 mg/kg (SRA, b 3 -Adrenergic Antagonist). In the third experiment, rats were subjected to surgical resection of the celiac-superior mesenteric ganglion complex or to sham surgery. The groups were intravenously treated with saline (S), 240 mmol/kg Dp, AA, or At, 15 min after pretreatment with the Antagonists or V and nine days after surgery. GE was determined 10 min later by measuring the percentage of gastric retention (%GR) of saline labeled with phenol red 10 min after gavage. The %GR (means±SE, n=6) values indicated that BUT abolished the effect of Dp (BUT+Dp vs V+Dp: 35.0% ± 5.1% vs 56.4% ± 2.7%) and At (BUT+At vs V+At: 33.5% ± 4.7% vs 52.9% ±2.6%) on GE, and significantly reduced (Po0.05) the effect of AA (BUT+AA vs V+AA: 48.0%±5.0% vs 65.2%±3.8%). ATE, SRA, and sympathectomy did not modify the effects of treatments. These results suggest that b 2 -adrenoceptor activation occurred in delayed liquid gastric emptying induced by the phenylpyrazole derivatives dipyrone, 4-aminoantipyrine, and antipyrine. Additionally, the released neurotransmitter did not originate in the celiac-superior mesenteric ganglion complex

  • effect of selective β adrenoceptor blockade and surgical resection of the celiac superior mesenteric ganglion complex on delayed liquid gastric emptying induced by dipyrone 4 aminoantipyrine and antipyrine in rats
    Brazilian Journal of Medical and Biological Research, 2016
    Co-Authors: A M Vinagre, E F Collares
    Abstract:

    There is evidence for participation of peripheral β-adrenoceptors in delayed liquid gastric emptying (GE) induced in rats by dipyrone (Dp), 4-aminoantipyrine (AA), and antipyrine (At). The present study aimed to determine whether β-adrenoceptors are involved in delayed GE induced by phenylpyrazole derivatives and the role of the prevertebral sympathetic nervous system in this condition. Male Wistar rats weighing 220-280 g were used in the study. In the first experiment rats were intravenously pretreated with vehicle (V), atenolol 30 mg/kg (ATE, β1-Adrenergic Antagonist), or butoxamine 25 mg/kg (BUT, β2-Adrenergic Antagonist). In the second experiment, rats were pretreated with V or SR59230A 2 mg/kg (SRA, β3-Adrenergic Antagonist). In the third experiment, rats were subjected to surgical resection of the celiac-superior mesenteric ganglion complex or to sham surgery. The groups were intravenously treated with saline (S), 240 µmol/kg Dp, AA, or At, 15 min after pretreatment with the Antagonists or V and nine days after surgery. GE was determined 10 min later by measuring the percentage of gastric retention (%GR) of saline labeled with phenol red 10 min after gavage. The %GR (means±SE, n=6) values indicated that BUT abolished the effect of Dp (BUT+Dp vs V+Dp: 35.0%±5.1% vs 56.4%±2.7%) and At (BUT+At vs V+At: 33.5%±4.7% vs 52.9%±2.6%) on GE, and significantly reduced (P<0.05) the effect of AA (BUT+AA vs V+AA: 48.0%±5.0% vs 65.2%±3.8%). ATE, SRA, and sympathectomy did not modify the effects of treatments. These results suggest that β2-adrenoceptor activation occurred in delayed liquid gastric emptying induced by the phenylpyrazole derivatives dipyrone, 4-aminoantipyrine, and antipyrine. Additionally, the released neurotransmitter did not originate in the celiac-superior mesenteric ganglion complex.

Didier Lebrec - One of the best experts on this subject based on the ideXlab platform.

  • beta Adrenergic Antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices
    2010
    Co-Authors: Thierry Poynard, Paul Cales, Linda Pasta, G Ideo, J P Pascal, Luigi Pagliaro, Didier Lebrec
    Abstract:

    Abstract Background. The value of beta-Adrenergic—Antagonist drug therapy for the prevention of initial episodes of gastrointestinal bleeding in patients with cirrhosis and esophageal varices is uncertain, both positive and negative study results having been reported. Methods. In this study, we analyzed data on individual patients from four randomized, controlled trials to assess the efficacy of this treatment. Of the 589 patients studied, 286 received a beta-Adrenergic—Antagonist drug (propranolol in 203 and nadolol in 83) and 303 received placebo. Results. After two years, the mean (±SE) percentage of patients who had had no upper gastrointestinal bleeding was 78±3 percent in the beta-Adrenergic—Antagonist treatment group and 65±3 percent in the control group (P = 0.002). The percentage of patients without fatal bleeding was 90±2 percent in the treatment group and 82±3 percent in the control group (P = 0.01). The percentage of patients surviving after two years was 71 ±3 percent in the treatment group a...

  • hemodynamic effects of nipradilol a new β Adrenergic Antagonist combined with a nitroxy base in rats with intra or extra hepatic portal hypertension
    Journal of Hepatology, 1993
    Co-Authors: Masaru Ohsuga, Stephane Cailmail, Didier Lebrec
    Abstract:

    It has been demonstrated that β -Adrenergic Antagonists and nitrovasodilators reduce portal pressure in patients with portal hypertension. Thus, the hemodynamic effects of nipradilol, a new β -Adrenergic Antagonist combined with a nitroxy base, was studied in conscious and unrestrained rats in two models of portal hypertension. The hemodynamic effects were compared to those obtained after propranolol administration. Both nipradilol (20 mg/kg) and propranolol (20 mg/kg) significantly decreased portal pressure in both groups of portal hypertensive rats. In cirrhotic rats, nipradilol decreased portal pressure (−24 ± 2%) more than propranolol (−9 ± 2%). Both nipradilol and propranolol significantly decreased portal tributary blood flow and cardiac index in both groups. Changes in portal tributary blood flow and cardiac index were not significantly different between nipradilol and propranolol. Propranolol, but not nipradilol significantly increased hepatocollateral resistance in cirrhotic rats but not in portal vein stenosed rats. Thus, the marked reduction of portal pressure after nipradilol administration depends in part on a limited increase in hepatocollateral resistance. Nipradilol significantly decreased mean arterial pressure, while propranolol did not change this value in either groups. In conclusion, nipradilol markedly decreased portal pressure in rats with portal hypertension. This beneficial effect suggests that nipradilol should be tested in the patients with portal hypertension.