RESUMO
BACKGROUND: Inflammatory bowel disease (IBD) is associated with delay in gastric emptying, increase in ghrelin, and decrease in leptin. The aim was to investigate the correlation between gastroduodenal (GD) symptoms, gastric emptying, and serum levels of active ghrelin and leptin in IBD. Twenty-seven IBD patients and 26 healthy volunteers were asked to complete the Porto Alegre Dyspeptic Symptoms Questionnaire. A gastric emptying test for solids was performed using a C13 octanoic acid breath test. During this test, serum samples were collected for measuring active ghrelin and leptin concentrations by radioimmunoassay. SUMMARY: Patients with IBD demonstrated delayed gastric emptying compared with healthy volunteers. In patients with GD symptoms, the delay in gastric emptying was more pronounced, and there were significant correlations of satiety and vomiting with gastric emptying. Basal leptin, but not active ghrelin, increased in patients with GD symptoms compared with patients without these symptoms. There were negative correlations between basal active ghrelin with total Porto Alegre score and epigastric pain in IBD patients with GD symptoms. Key Messages: In IBD, satiety and vomiting were associated with delay in gastric emptying. Conversely, epigastric pain had a negative correlation with active ghrelin. Our results suggest that different pathophysiological mechanisms contribute to GD symptoms in IBD.
Assuntos
Duodeno/patologia , Duodeno/fisiopatologia , Esvaziamento Gástrico/fisiologia , Grelina/sangue , Doenças Inflamatórias Intestinais/sangue , Doenças Inflamatórias Intestinais/fisiopatologia , Estômago/patologia , Estômago/fisiopatologia , Adulto , Idoso , Testes Respiratórios , Caprilatos/análise , Isótopos de Carbono , Estudos de Casos e Controles , Feminino , Humanos , Leptina/sangue , Masculino , Pessoa de Meia-IdadeRESUMO
Several drugs have been employed for sedation during flexible fiberoptic bronchoscopy (FOB). Clonidine attenuates stress-induced sympathoadrenal responses and has sedative properties. We investigate the effects of clonidine premedication on hemodynamic and comfort parameters of patients submitted to FOB under airway topical anesthesia only. Patients received placebo (n = 22; men = 16; median age = 50.5 years) or intravenous clonidine (3 microg/kg; n = 20; men = 15; median age = 46.0 years) 15 min before FOB. Blood pressure (BP), heart rate (HR), plasma norepinephrine (nor) and cortisol levels were measured before, during, and 1 h after FOB. Comfort was assessed by the examiner and by the patients using a visual numerical scale (0-10). The placebo group showed significant increases in systolic BP, HR, and nor levels during FOB (SBP = 125 mmHg x 145 mmHg; HR = 74 bpm x 85 bpm; nor = 316.2 pg/dl x 483.1 pg/dl), whereas clonidine group did not display such changes. Clonidine group showed a lower frequency of cardiac arrhythmias than the placebo group during and after FOB (supraventricular = 39% x 50%; ventricular = 22% x 40%). Levels of comfort were high and comparable in both groups. We concluded that although clonidine led to a somewhat better hemodynamic profile, it did not contribute to better comfort in this setting.
Assuntos
Analgésicos , Broncoscopia/métodos , Clonidina , Medicação Pré-Anestésica/métodos , Simpatolíticos , Adulto , Idoso , Pressão Sanguínea/efeitos dos fármacos , Método Duplo-Cego , Feminino , Frequência Cardíaca/efeitos dos fármacos , Humanos , Hidrocortisona/sangue , Masculino , Pessoa de Meia-Idade , Dor/prevenção & controleRESUMO
We tested the hypothesis that the nitric oxide (NO) pathway in the central nervous system (CNS) plays a role in hypothermia, as well as in the febrile response during experimental septic shock, by regulating vasopressin (AVP) release. Experiments were performed on male Wistar rats treated with NG-nitro-L-arginine methyl ester (L-NAME), a non-selective NO synthase (NOS) inhibitor, injected intracerebroventricularly (250 microg/1 microl) 30 min before lipopolysaccharide (LPS) 1.5 mg/kg i.v. injection. One hour after LPS administration we observed a significant drop in body temperature (hypothermic response), followed by a temperature increase after the second hour (febrile response), which remained until the end of the experiment. Increased plasmatic AVP levels were concomitantly observed during hypothermia, nearly returning to basal levels during the febrile phase. When L-NAME was administered with LPS, plasmatic AVP concentrations remained high throughout the experiment, hypothermia was accentuated and the febrile response was abolished. Additionally, pre-treatment with beta-mercapto-beta,beta-cyclopentamethylenepropionyl1, O-Et-Tyr2, Val4, Arg8-vasopressin, an AVP V1 receptor blocker (10 microg/kg) administered i.v., reduced hypothermia and exacerbated the febrile response to endotoxin. In conclusion, our data indicate that the central NO pathway plays an inhibitory role in AVP release during experimental septic shock, which seems to be critical for the thermoregulation during this pathophysiological state.