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[PMID]:27951416
[Au] Autor:Hritcu L; Ionita R; Motei DE; Babii C; Stefan M; Mihasan M
[Ad] Endereço:Department of Biology, Alexandru Ioan Cuza University of Iasi, Bd. Carol I, No. 11, 700506, Romania. Electronic address: hritcu@uaic.ro.
[Ti] Título:Nicotine versus 6-hydroxy-l-nicotine against chlorisondamine induced memory impairment and oxidative stress in the rat hippocampus.
[So] Source:Biomed Pharmacother;86:102-108, 2017 Feb.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:6-Hydroxy-l-nicotine (6HLN), a nicotine derivative from nicotine degradation by Arthrobacter nicotinovorans pAO1 strain was found to improve behavioral deficits and to reverse oxidative stress in the rat hippocampus. Rats were given CHL (10mg/kg, i.p.) were used as an Alzheimer's disease-like model. The nicotine (0.3mg/kg) and 6HLN (0.3mg/kg) were administered alone or in combination in the CHL-treated rats. Memory-related behaviors were evaluated using Y-maze and radial arm-maze tests. The antioxidant enzymes activity and the levels of the biomarkers of oxidative stress were measured in the hippocampus. Statistical analyses were performed using two-way ANOVA and Tukey's post hoc test. F values for which p<0.05 were regarded as statistically significant. CHL-caused memory deficits and oxidative stress enhancing were observed. Both nicotine and 6HLN administration attenuated the cognitive deficits and recovered the antioxidant capacity in the rat hippocampus of the CHL rat model. Our results suggest that 6HLN versus nicotine confers anti-amnesic properties in the CHL-induced a rat model of memory impairment via reversing cholinergic function and decreasing brain oxidative stress, suggesting the use of this compound as an alternative agent in AD treatment.
[Mh] Termos MeSH primário: Clorisondamina/toxicidade
Hipocampo/efeitos dos fármacos
Transtornos da Memória/tratamento farmacológico
Nicotina/análogos & derivados
Nicotina/uso terapêutico
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antioxidantes/farmacologia
Antioxidantes/uso terapêutico
Hipocampo/metabolismo
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Aprendizagem em Labirinto/fisiologia
Transtornos da Memória/induzido quimicamente
Transtornos da Memória/metabolismo
Nicotina/farmacologia
Antagonistas Nicotínicos/toxicidade
Estresse Oxidativo/fisiologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (6-hydroxynicotine); 0 (Antioxidants); 0 (Nicotinic Antagonists); 6M3C89ZY6R (Nicotine); JD3M24F66I (Chlorisondamine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170209
[Lr] Data última revisão:
170209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


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[PMID]:27783305
[Au] Autor:Zabrodskii PF; Maslyakov VV; Gromov MS
[Ad] Endereço:Saratov Branch of the Samara Medical Institute REAVIZ, Saratov, Russia. pfzabrodsky@gmail.com.
[Ti] Título:Role of α7-Nicotinic Acetylcholine Receptors of B Cells in the Immunotoxic Effect of Organophosphorus Compounds.
[So] Source:Bull Exp Biol Med;161(6):779-781, 2016 Oct.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Experiments on white non-inbred rats demonstrated that treatment with organophosphorus compound dimethyl dichlorovinyl phosphate (DDVP) decreased T cell-independent antibody production by B cells and blood levels of IL-10 and IL-12; a similar effect was produced by GTS-21, a selective agonist of α7-nicotinic acetylcholine receptor. N-nicotinic receptor antagonist chlorisondamine in combination with DDVP partially prevented suppression of antibody production in comparison with the effect observed during intoxication with DDVP.
[Mh] Termos MeSH primário: Linfócitos B/efeitos dos fármacos
Clorisondamina/farmacologia
Inibidores da Colinesterase/toxicidade
Diclorvós/toxicidade
Antagonistas Nicotínicos/farmacologia
Receptor Nicotínico de Acetilcolina alfa7/imunologia
[Mh] Termos MeSH secundário: Animais
Animais não Endogâmicos
Linfócitos B/citologia
Linfócitos B/imunologia
Compostos de Benzilideno/farmacologia
Inibidores da Colinesterase/imunologia
Diclorvós/antagonistas & inibidores
Diclorvós/imunologia
Feminino
Imunoglobulina M/biossíntese
Injeções Intramusculares
Interleucina-10/biossíntese
Interleucina-10/secreção
Interleucina-12/biossíntese
Interleucina-12/secreção
Masculino
Agonistas Nicotínicos/farmacologia
Piridinas/farmacologia
Ratos
Baço/citologia
Baço/efeitos dos fármacos
Baço/imunologia
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzylidene Compounds); 0 (Cholinesterase Inhibitors); 0 (Immunoglobulin M); 0 (Nicotinic Agonists); 0 (Nicotinic Antagonists); 0 (Pyridines); 0 (alpha7 Nicotinic Acetylcholine Receptor); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12); 7U370BPS14 (Dichlorvos); 8S399XDN2K (3-(2,4-dimethoxybenzylidene)anabaseine); JD3M24F66I (Chlorisondamine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161027
[St] Status:MEDLINE


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[PMID]:26947072
[Au] Autor:Kimura K; Tanida M; Nagata N; Inaba Y; Watanabe H; Nagashimada M; Ota T; Asahara S; Kido Y; Matsumoto M; Toshinai K; Nakazato M; Shibamoto T; Kaneko S; Kasuga M; Inoue H
[Ad] Endereço:Department of Physiology and Metabolism, Brain/Liver Interface Medicine Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8641, Japan.
[Ti] Título:Central Insulin Action Activates Kupffer Cells by Suppressing Hepatic Vagal Activation via the Nicotinic Alpha 7 Acetylcholine Receptor.
[So] Source:Cell Rep;14(10):2362-74, 2016 Mar 15.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Central insulin action activates hepatic IL-6/STAT3 signaling, which suppresses the gene expression of hepatic gluconeogenic enzymes. The vagus nerve plays an important role in this centrally mediated hepatic response; however, the precise mechanism underlying this brain-liver interaction is unclear. Here, we present our findings that the vagus nerve suppresses hepatic IL-6/STAT3 signaling via α7-nicotinic acetylcholine receptors (α7-nAchR) on Kupffer cells, and that central insulin action activates hepatic IL-6/STAT3 signaling by suppressing vagal activity. Indeed, central insulin-mediated hepatic IL-6/STAT3 activation and gluconeogenic gene suppression were impeded in mice with hepatic vagotomy, pharmacological cholinergic blockade, or α7-nAchR deficiency. In high-fat diet-induced obese and insulin-resistant mice, control of the vagus nerve by central insulin action was disturbed, inducing a persistent increase of inflammatory cytokines. These findings suggest that dysregulation of the α7-nAchR-mediated control of Kupffer cells by central insulin action may affect the pathogenesis of chronic hepatic inflammation in obesity.
[Mh] Termos MeSH primário: Insulina/farmacologia
Macrófagos do Fígado/metabolismo
Fígado/metabolismo
Nervo Vago/efeitos dos fármacos
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Mh] Termos MeSH secundário: Acetilcolina/metabolismo
Animais
Glicemia/análise
Células Cultivadas
Clorisondamina/farmacologia
Dieta Hiperlipídica
Interleucina-6/sangue
Interleucina-6/genética
Interleucina-6/metabolismo
Macrófagos do Fígado/citologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Nicotina/farmacologia
Obesidade/metabolismo
Obesidade/patologia
Fosforilação/efeitos dos fármacos
Ligação Proteica/efeitos dos fármacos
Receptores de Superfície Celular/genética
Receptores de Superfície Celular/metabolismo
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/efeitos dos fármacos
Nervo Vago/fisiologia
Receptor Nicotínico de Acetilcolina alfa7/deficiência
Receptor Nicotínico de Acetilcolina alfa7/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Emr1 protein, mouse); 0 (Insulin); 0 (Interleukin-6); 0 (Receptors, Cell Surface); 0 (STAT3 Transcription Factor); 0 (alpha7 Nicotinic Acetylcholine Receptor); 6M3C89ZY6R (Nicotine); JD3M24F66I (Chlorisondamine); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160308
[St] Status:MEDLINE


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[PMID]:26416846
[Au] Autor:Stocker SD; Lang SM; Simmonds SS; Wenner MM; Farquhar WB
[Ad] Endereço:From the Departments of Cellular and Molecular Physiology (S.D.S., S.M.L., S.S.S.) and Neural and Behavioral Sciences (S.D.S.), Pennsylvania State University College of Medicine, Hershey; and Department of Kinesiology and Applied Physiology (M.M.W., W.B.F.), University of Delaware, Newark. sstocker@
[Ti] Título:Cerebrospinal Fluid Hypernatremia Elevates Sympathetic Nerve Activity and Blood Pressure via the Rostral Ventrolateral Medulla.
[So] Source:Hypertension;66(6):1184-90, 2015 Dec.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevated NaCl concentrations of the cerebrospinal fluid increase sympathetic nerve activity (SNA) in salt-sensitive hypertension. Neurons of the rostral ventrolateral medulla (RVLM) play a pivotal role in the regulation of SNA and receive mono- or polysynaptic inputs from several hypothalamic structures responsive to hypernatremia. Therefore, the present study investigated the contribution of RVLM neurons to the SNA and pressor response to cerebrospinal fluid hypernatremia. Lateral ventricle infusion of 0.15 mol/L, 0.6 mol/L, and 1.0 mol/L NaCl (5 µL/10 minutes) produced concentration-dependent increases in lumbar SNA, adrenal SNA, and arterial blood pressure, despite no change in splanchnic SNA and a decrease in renal SNA. Ganglionic blockade with chlorisondamine or acute lesion of the lamina terminalis blocked or significantly attenuated these responses, respectively. RVLM microinjection of the gamma-aminobutyric acid (GABAA) agonist muscimol abolished the sympathoexcitatory response to intracerebroventricular infusion of 1 mol/L NaCl. Furthermore, blockade of ionotropic glutamate, but not angiotensin II type 1, receptors significantly attenuated the increase in lumbar SNA, adrenal SNA, and arterial blood pressure. Finally, single-unit recordings of spinally projecting RVLM neurons revealed 3 distinct populations based on discharge responses to intracerebroventricular infusion of 1 mol/L NaCl: type I excited (46%; 11/24), type II inhibited (37%; 9/24), and type III no change (17%; 4/24). All neurons with slow conduction velocities were type I cells. Collectively, these findings suggest that acute increases in cerebrospinal fluid NaCl concentrations selectively activate a discrete population of RVLM neurons through glutamate receptor activation to increase SNA and arterial blood pressure.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Hipernatremia/fisiopatologia
Bulbo/fisiopatologia
Sistema Nervoso Simpático/fisiopatologia
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/inervação
Análise de Variância
Animais
Pressão Sanguínea/efeitos dos fármacos
Clorisondamina/farmacologia
Relação Dose-Resposta a Droga
Antagonistas de Aminoácidos Excitatórios/farmacologia
Bloqueadores Ganglionares/farmacologia
Hipernatremia/líquido cefalorraquidiano
Hipotálamo/efeitos dos fármacos
Hipotálamo/fisiopatologia
Infusões Intraventriculares
Vértebras Lombares/inervação
Masculino
Muscimol/administração & dosagem
Muscimol/farmacologia
Neurônios/efeitos dos fármacos
Neurônios/fisiologia
Ratos Sprague-Dawley
Receptores de Glutamato/metabolismo
Cloreto de Sódio/administração & dosagem
Cloreto de Sódio/farmacologia
Sistema Nervoso Simpático/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (Ganglionic Blockers); 0 (Receptors, Glutamate); 2763-96-4 (Muscimol); 451W47IQ8X (Sodium Chloride); JD3M24F66I (Chlorisondamine)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150930
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.115.05936


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[PMID]:26235133
[Au] Autor:Pecaut MJ; Mehrotra S; Luo-Owen X; Bayeta EJ; Bellinger DL; Gridley DS
[Ad] Endereço:Department of Basic Sciences, Loma Linda University and Medical Center, Loma Linda, 92354 CA, United States; Division of Radiation Research, Loma Linda University and Medical Center, Loma Linda, 92354 CA, United States; Division of Biochemistry and Microbiology, Loma Linda University and Medical Cen
[Ti] Título:Chlorisondamine, a sympathetic ganglionic blocker, moderates the effects of whole-body irradiation (WBI) on early host defense to a live bacterial challenge.
[So] Source:Immunol Lett;167(2):103-15, 2015 Oct.
[Is] ISSN:1879-0542
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:There is a growing consensus that long-term deficits in the brain are due to dynamic interactions between multiple neural and immune cell types. Specifically, radiation induces an inflammatory response, including changes in neuromodulatory pro- and anti-inflammatory cytokine secretion. The purpose of this study was to establish that there is sympathetic involvement in radiation-induced decrements early in in vivo immune function host defense. Female, 8-9 week-old C57BL/6J mice were exposed to whole-body irradiation (WBI). There were 8 groups with radiation (0 vs. 3 Gy protons), immune challenge (Escherichia coli) and exposure to the sympathetic ganglionic blocker, chlorisondamine (1 mg/kg weight, i.p.), as independent variables. Ten days post-irradiation, mice were inoculated with E. coli intraperitoneally and sacrificed 90-120 min later. The data suggest that radiation-induced changes in immune function may in part be mediated by the sympathetic nervous system. Briefly, we found that radiation augments the bacteria-induced inflammatory cytokine response, particularly those cytokines involved in innate immunity. However, this augmentation can be reduced by the ganglionic blockade.
[Mh] Termos MeSH primário: Bactérias/imunologia
Infecções Bacterianas/imunologia
Clorisondamina/farmacologia
Bloqueadores Ganglionares/farmacologia
Interações Hospedeiro-Patógeno/efeitos dos fármacos
Interações Hospedeiro-Patógeno/imunologia
Irradiação Corporal Total
[Mh] Termos MeSH secundário: Animais
Infecções Bacterianas/metabolismo
Plaquetas/efeitos dos fármacos
Peso Corporal/efeitos dos fármacos
Catecolaminas/sangue
Citocinas/metabolismo
Eritrócitos/efeitos dos fármacos
Escherichia coli/imunologia
Feminino
Leucócitos/efeitos dos fármacos
Leucócitos/imunologia
Leucócitos/metabolismo
Subpopulações de Linfócitos/imunologia
Subpopulações de Linfócitos/metabolismo
Camundongos
Tamanho do Órgão/efeitos dos fármacos
Fagocitose/imunologia
Espécies Reativas de Oxigênio/metabolismo
Explosão Respiratória/imunologia
Baço/citologia
Baço/efeitos dos fármacos
Baço/imunologia
Baço/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Catecholamines); 0 (Cytokines); 0 (Ganglionic Blockers); 0 (Reactive Oxygen Species); JD3M24F66I (Chlorisondamine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:150921
[Lr] Data última revisão:
150921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150804
[St] Status:MEDLINE


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[PMID]:25659615
[Au] Autor:Liu D; Zhang HG; Chang MT; Li Y; Zhang LY
[Ad] Endereço:Trauma Center, State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
[Ti] Título:Melanocortin-4 receptor agonists alleviate intestinal dysfunction in secondary intra-abdominal hypertension rat model.
[So] Source:J Surg Res;195(1):263-70, 2015 May 01.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Intra-abdominal hypertension (IAH) is a potentially life-threatening disease. Melanocortin-4 (MC4) receptor activation exhibits life-saving properties. The aim of the present study was to examine whether treatment with the MC4 receptor agonist RO27-3225 ameliorates intestinal injury in IAH rats. METHODS: A total of 72 male Sprague-Dawley rats were randomized into six groups. Group 1 was the sham group. Group 2, the sham + RO group, received RO27-3225 (180 µg/kg, intraperitoneally). IAH was induced in group 3, the IAH group, by blood draw (mean arterial pressure = 30 mm Hg for 90 min) followed by shed blood and/or Ringer solution reinfusion. Intra-abdominal pressure was increased to 20 mm Hg by injecting air into the peritoneal cavity. Group 4, the RO group, was administered RO27-3225 at 5 min after blood draw. Groups 5 and 6 were the chlorisondamine (Chl) and HS024 groups, in which the rats were pretreated with the nicotinic acetylcholine receptor antagonist Chl or selective MC4 receptor antagonist (HS024), respectively, at 2 min before RO27-3225 was administered. RESULTS: RO27-3225 restored mean arterial pressure, reduced tumor necrosis factor-α, and interleukin-1ß messenger RNA expression increased by IAH, alleviated histologic damage, and improved superoxide dismutase activity in the intestine. Compared with the IAH group, the levels of intestinal fatty acid-binding protein, intestinal edema and intestinal permeability were lower in the RO group. Furthermore, the RO27-3225 treatment increased the expression of Rho-associated coiled-coil-containing protein kinase 1 and phosphorylated myosin light chain. Chl and HS024 abrogated the protective effects of RO27-3225. CONCLUSIONS: These data indicate that the MC4 receptor agonist counteracts the intestinal inflammatory response, ameliorating intestinal injury in experimental secondary IAH by MC4 receptor-triggered activation of the cholinergic anti-inflammatory pathway. It may represent a promising strategy for the treatment of IAH in the future.
[Mh] Termos MeSH primário: Hipertensão Intra-Abdominal/tratamento farmacológico
Peptídeos/uso terapêutico
Receptor Tipo 4 de Melanocortina/agonistas
[Mh] Termos MeSH secundário: Animais
Clorisondamina
Modelos Animais de Doenças
Avaliação Pré-Clínica de Medicamentos
Proteínas de Ligação a Ácido Graxo/metabolismo
Hemodinâmica/efeitos dos fármacos
Interleucina-1beta/metabolismo
Mucosa Intestinal/efeitos dos fármacos
Intestinos/metabolismo
Intestinos/patologia
Masculino
Cadeias Leves de Miosina/metabolismo
Peptídeos/farmacologia
Peptídeos Cíclicos
Distribuição Aleatória
Ratos Sprague-Dawley
Receptor Tipo 4 de Melanocortina/antagonistas & inibidores
Superóxido Dismutase/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Quinases Associadas a rho/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acid-Binding Proteins); 0 (HS 024); 0 (Interleukin-1beta); 0 (Myosin Light Chains); 0 (Peptides); 0 (Peptides, Cyclic); 0 (Receptor, Melanocortin, Type 4); 0 (Tumor Necrosis Factor-alpha); 0 (butir-His-Phe-Arg-Trp-Sar-NH2); EC 1.15.1.1 (Superoxide Dismutase); EC 2.7.11.1 (ROCK1 protein, rat); EC 2.7.11.1 (rho-Associated Kinases); JD3M24F66I (Chlorisondamine)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150404
[Lr] Data última revisão:
150404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150210
[St] Status:MEDLINE


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[PMID]:24105450
[Au] Autor:de Haan JJ; Windsant IV; Lubbers T; Hanssen SJ; Hadfoune M; Prinzen FW; Greve JW; Buurman WA
[Ad] Endereço:1Department of Surgery, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre+, Maastricht, The Netherlands. 2Department of Internal Medicine, Medisch Spectrum Twente, Enschede, The Netherlands. 3Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre+, Maastricht, The Netherlands. 4Department of Surgery, Atrium Medical Center, Heerlen, The Netherlands.
[Ti] Título:Prevention of hemolysis-induced organ damage by nutritional activation of the vagal anti-inflammatory reflex*.
[So] Source:Crit Care Med;41(11):e361-7, 2013 Nov.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Acute hemolysis is associated with organ damage, inflammation, and impaired vascular function. Stimulation of the cholecystokinin-1 receptor-dependent vagal anti-inflammatory reflex with lipid-rich enteral nutrition was demonstrated to prevent tissue damage and attenuate inflammation. This study investigates the effects of nutritional activation of the vagal anti-inflammatory reflex on organ integrity, systemic inflammation, and microcirculation during hemolysis. DESIGN: Prospective randomized controlled study. SETTING: University research unit. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Intravascular hemolysis was simulated by infusion of prelysed erythrocytes. Animals were fasted or received lipid-rich enteral nutrition. Pegylated (PEG)-CCK9A, A70104 (a cholecystokinin-1 receptor antagonist), and chlorisondamine (a nicotinic acetylcholine receptor antagonist) were applied to investigate involvement of the vagal reflex. MEASUREMENTS AND MAIN RESULTS: Nutritional intervention reduced hemolysis-related renal tubular cell damage, hepatocyte damage, ileal leakage of horseradish peroxidase, and bacterial translocation compared with food deprivation (all p < 0.05). Also circulating interleukin (IL)-6 levels were decreased by enteral nutrition (p < 0.05). Blockage of the cholecystokinin-1 receptor or the nicotinic acetylcholine receptor reversed the protective nutritional effects compared with vehicle (p < 0.05), whereas PEG-CCK9 mimicked the impact of enteral feeding in fasted animals (p < 0.05). Furthermore, nutritional intervention increased renal, hepatic, and intestinal blood flow compared with fasting (all p < 0.05), as evaluated using fluorescent microspheres. CONCLUSIONS: Nutritional activation of the vagal anti-inflammatory reflex preserves tissue integrity and attenuates systemic inflammation in a rodent model of acute hemolysis. In addition, lipid-rich nutrition improves renal, hepatic, and intestinal microcirculation. These findings implicate stimulation of the autonomic nervous system by nutritional means as a potential therapy to prevent complications of acute hemolysis. (Crit Care Med 2013; 41:e361-e367).
[Mh] Termos MeSH primário: Sistema Digestório/fisiopatologia
Alimentos
Hemólise/fisiologia
Inflamação/prevenção & controle
Quinolinas/farmacologia
Receptores da Colecistocinina/antagonistas & inibidores
Nervo Vago/fisiologia
[Mh] Termos MeSH secundário: Animais
Clorisondamina/farmacologia
Gorduras na Dieta
Mediadores da Inflamação/metabolismo
Masculino
Microcirculação
Antagonistas Nicotínicos/farmacologia
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dietary Fats); 0 (Inflammation Mediators); 0 (Nicotinic Antagonists); 0 (Quinolines); 0 (Receptors, Cholecystokinin); 119295-94-2 (A 65186); JD3M24F66I (Chlorisondamine)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:131028
[Lr] Data última revisão:
131028
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:131010
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0b013e31828e9262


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[PMID]:21947406
[Au] Autor:Tang X; Hu T
[Ad] Endereço:Department of Neural and Behavioral Sciences, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. xxt2@psu.edu
[Ti] Título:Neural control of arterial pressure variability in the neuromuscularly blocked rat.
[So] Source:Eur J Appl Physiol;112(6):2013-24, 2012 Jun.
[Is] ISSN:1439-6327
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The baroreflexes stabilize moment-to-moment arterial pressure. Sinoaortic denervation (SAD) of the baroreflexes results in a large increase in arterial pressure variability (APV) across various species. Due to an incomplete understanding of the nonlinear interactions between central and peripheral systems, the major source of APV remains controversial. While some studies suggested that the variability is endogenous to the central nervous system (CNS), others argued that peripheral influences may be the main source. For decades, abnormal cardiovascular variability has been associated with a number of cardiovascular diseases including hypertension, heart failure, and stroke. Delineating mechanisms of the APV is critical for the improvement of current strategies that use APV as a clinical tool for the diagnosis and prognosis of cardiovascular diseases. In this study, with a unique chronic neuromuscularly blocked (NMB) rat preparation that largely constrains peripheral influences, we determined the CNS contribution to the post-SAD APV. First, we confirmed that SAD significantly increased APV in the NMB rat, then demonstrated that post-SAD ganglionic blockade substantially reduced APV, and subsequent intravenous infusions of phenylephrine and epinephrine (in presence of ganglionic blockade) only slightly increased APV. These data suggest that the CNS is an important source, and skeletal activity, thermal challenges or other forms of peripherally generated cardiovascular stress are not required for the post-SAD APV. In addition, we showed that bilateral aortic denervation produced a larger increase in APV than bilateral carotid sinus denervation, suggesting that the aortic baroreflex plays a more dominant role in the control of APV than the carotid sinus.
[Mh] Termos MeSH primário: Pressão Arterial/fisiologia
Sistema Nervoso Central/fisiologia
Músculo Esquelético/fisiologia
Sistema Nervoso Periférico/fisiologia
Nó Sinoatrial/fisiologia
[Mh] Termos MeSH secundário: Animais
Aorta/inervação
Aorta/fisiologia
Barorreflexo/fisiologia
Doenças Cardiovasculares/fisiopatologia
Seio Carotídeo/fisiologia
Clorisondamina/farmacologia
Denervação/métodos
Epinefrina/farmacologia
Feminino
Fenômenos Fisiológicos do Sistema Nervoso
Bloqueio Neuromuscular/métodos
Fenilefrina/farmacologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
1WS297W6MV (Phenylephrine); JD3M24F66I (Chlorisondamine); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1212
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110928
[St] Status:MEDLINE
[do] DOI:10.1007/s00421-011-2160-4


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[PMID]:21107310
[Au] Autor:Khokhar JY; Tyndale RF
[Ad] Endereço:Centre for Addiction and Mental Health (CAMH), University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:Drug metabolism within the brain changes drug response: selective manipulation of brain CYP2B alters propofol effects.
[So] Source:Neuropsychopharmacology;36(3):692-700, 2011 Feb.
[Is] ISSN:1740-634X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Drug-metabolizing cytochrome P450 (CYPs) enzymes are expressed in the liver, as well as in extrahepatic tissues such as the brain. Here we show for the first time that drug metabolism by a CYP within the brain, illustrated using CYP2B and the anesthetic propofol (2, 6-diisopropylphenol, Diprivan), can meaningfully alter the pharmacological response to a CNS acting drug. CYP2B is expressed in the brains of animals and humans, and this CYP isoform is able to metabolize centrally acting substrates such as propofol, ecstasy, and serotonin. Rats were given intracerebroventricularly (i.c.v.) injections of vehicle, C8-xanthate, or 8-methoxypsoralen (CYP2B mechanism-based inhibitors) and then tested for sleep time following propofol (80 mg/kg intraperitoneally). Both inhibitors significantly increased sleep-time (1.8- to 2-fold) and brain propofol levels, while having no effect on plasma propofol levels. Seven days of nicotine treatment can induce the expression of brain, but not hepatic, CYP2B, and this induction reduced propofol sleep times by 2.5-fold. This reduction was reversed in a dose-dependent manner by i.c.v. injections of inhibitor. Sleep times correlated with brain (r=0.76, P=0.0009), but not plasma (r=0.24, P=0.39) propofol concentrations. Inhibitor treatments increased brain, but not plasma, propofol levels, and had no effect on hepatic enzyme activity. These data indicate that brain CYP2B can metabolize neuroactive substrates (eg, propofol) and can alter their pharmacological response. This has wider implications for localized CYP-mediated metabolism of drugs, neurotransmitters, and neurotoxins within the brain by this highly variable enzyme family and other CYP subfamilies expressed in the brain.
[Mh] Termos MeSH primário: Anestésicos Intravenosos/farmacologia
Encéfalo/efeitos dos fármacos
Citocromo P-450 CYP2B1/metabolismo
Inativação Metabólica/fisiologia
Propofol/farmacologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Clorisondamina/farmacologia
Relação Dose-Resposta a Droga
Interações Medicamentosas
Inibidores Enzimáticos/farmacologia
Injeções Intraventriculares
Masculino
Metoxaleno/farmacocinética
Nicotina/metabolismo
Nicotina/farmacologia
Agonistas Nicotínicos/farmacologia
Antagonistas Nicotínicos/farmacologia
Propofol/metabolismo
Ratos
Ratos Wistar
Sono/efeitos dos fármacos
Fatores de Tempo
Trítio/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anesthetics, Intravenous); 0 (Enzyme Inhibitors); 0 (Nicotinic Agonists); 0 (Nicotinic Antagonists); 10028-17-8 (Tritium); 6M3C89ZY6R (Nicotine); EC 1.14.14.1 (Cytochrome P-450 CYP2B1); JD3M24F66I (Chlorisondamine); U4VJ29L7BQ (Methoxsalen); YI7VU623SF (Propofol)
[Em] Mês de entrada:1105
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:101126
[St] Status:MEDLINE
[do] DOI:10.1038/npp.2010.202


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[PMID]:20639744
[Au] Autor:Lubbers T; De Haan JJ; Hadfoune M; Zhang Y; Luyer MD; Grundy D; Buurman WA; Greve JW
[Ad] Endereço:Department of Surgery, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre, Maastricht, The Netherlands.
[Ti] Título:Lipid-enriched enteral nutrition controls the inflammatory response in murine Gram-negative sepsis.
[So] Source:Crit Care Med;38(10):1996-2002, 2010 Oct.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Controlling the inflammatory cascade during sepsis remains a major clinical challenge. Recently, it has become evident that the autonomic nervous system reduces inflammation through the vagus nerve. The current study investigates whether nutritional stimulation of the autonomic nervous system effectively attenuates the inflammatory response in murine Gram-negative sepsis. DESIGN: Controlled in vivo and ex vivo experimental study. SETTINGS: Research laboratory of a university hospital. SUBJECTS: Male C57bl6 mice. INTERVENTIONS: Mice were intraperitoneally challenged with lipopolysaccharide derived from Escherichia coli. Before lipopolysaccharide administration, mice were fasted or enterally fed either lipid-rich nutrition or low-lipid nutrition. Antagonists to cholecystokinin receptors or nicotinic receptors were administered before lipopolysaccharide administration. Blood and tissue samples were collected at 90 mins. Mesenteric afferent discharge was determined in ex vivo preparations in response to both nutritional compositions. MEASUREMENTS AND MAIN RESULTS: Both lipid-rich and low-lipid nutrition dose-dependently reduced lipopolysaccharide-induced tumor necrosis factor-α release (high dose: both 1.4 ± 0.4 ng/mL) compared with fasted mice (3.7 ± 0.8 ng/mL; p < .01). The anti-inflammatory effect of both nutritional compositions was mediated through cholecystokinin receptors (p < .01), activation of mesenteric vagal afferents (p < .05), and peripheral nicotinic receptors (p < .05). Lipid-rich nutrition attenuated the inflammatory response at lower dosages than low-lipid nutrition, indicating that enrichment of enteral nutrition with lipid augments the anti-inflammatory potential. Administration of lipid-rich nutrition prevented endotoxin-induced small intestinal epithelium damage and reduced inflammation in the liver and spleen compared with fasted (all p < .01) and low-lipid nutrition controls (all p < .05). CONCLUSIONS: The current study demonstrates that lipid-rich nutrition attenuates intestinal damage and systemic as well as organ-specific inflammation in murine Gram-negative sepsis through the nutritional vagal anti-inflammatory pathway. These findings implicate enteral administration of lipid-enriched nutrition as a promising intervention to modulate the inflammatory response during septic conditions.
[Mh] Termos MeSH primário: Nutrição Enteral
Inflamação/prevenção & controle
Lipídeos/administração & dosagem
Sepse/terapia
[Mh] Termos MeSH secundário: Animais
Benzodiazepinonas/farmacologia
Clorisondamina/farmacologia
Devazepida/farmacologia
Modelos Animais de Doenças
Endotoxemia/imunologia
Endotoxemia/prevenção & controle
Nutrição Enteral/métodos
Inflamação/imunologia
Inflamação/microbiologia
Lipídeos/uso terapêutico
Lipopolissacarídeos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Compostos de Fenilureia/farmacologia
Receptores da Colecistocinina/antagonistas & inibidores
Sepse/complicações
Sepse/imunologia
Fator de Necrose Tumoral alfa/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzodiazepinones); 0 (Lipids); 0 (Lipopolysaccharides); 0 (Phenylurea Compounds); 0 (Receptors, Cholecystokinin); 0 (Tumor Necrosis Factor-alpha); 0 (lipopolysaccharide, E coli O55-B5); 370JHF4586 (L 365260); JD3M24F66I (Chlorisondamine); JE6P7QY7NH (Devazepide)
[Em] Mês de entrada:1010
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:100720
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0b013e3181eb90d7



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