RESUMO
Ghrelin, an endogenous ligand for growth hormone secretagogue receptor (GHS-R), has been identified in the rat and human gastrointestinal tract. Ghrelin has been proposed to play a role in gastric acid secretion. Nitric oxide (NO) was shown as a mediator in the mechanism of ghrelin action on gastric acid secretory function. However, there is a little knowledge about this topic. We have investigated the role of ghrelin in gastric acid secretion and the role of NO as a mediator. Wistar albino rats were used in this study. The pyloric sphincter was ligated through a small midline incision. By the time, saline (0.5 ml, iv) was injected to the control group, ghrelin (20 microg/kg, iv) was injected to the first experimental group, ghrelin (20 microg/kg, iv) + L-NAME (70 mg/kg, sc) was injected to the second group and L-NAME (70 mg/kg, sc) was administered to the third group. The rats were killed 3 h after pylorus ligation; gastric acid secretion, mucus content and plasma nitrite levels were measured. Exogenous ghrelin administration increased gastric acid output, mucus content and total plasma nitrite levels, while these effects of ghrelin were inhibited by applying L-NAME. We can conclude that ghrelin participates in the regulation of gastric acid secretion through NO as a mediator.
Assuntos
Ácido Gástrico/metabolismo , Grelina/farmacologia , Óxido Nítrico/fisiologia , Animais , Inibidores Enzimáticos/farmacologia , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/fisiologia , Masculino , Muco/metabolismo , NG-Nitroarginina Metil Éster/farmacologia , Óxido Nítrico Sintase/antagonistas & inibidores , Nitritos/sangue , Ratos , Ratos WistarRESUMO
In this experimental study, consist of 54 Sprague-Dawley rats, we tried to observe the effectiveness of haemopoietic growth factors such as G-CSF and GM-CSF in treatment of sepsis and see if they have any effects on phagocytic activity of macrophages when are administered after establishment of sepsis. In first phase of this study, twenty one rats were randomly divided into three groups of 7 animals each. Cecal ligation and perforation were carried out in each rat and sepsis made up. The Control group received 2 x 0.2 cc %5 dextrose injection subcutaneous (s.c.).. The G-CSF group received 2 x 1 g G-CSF with 0.2 cc %5 dextrose s.c. The GM-CSF received 1 x 2 g GM-CSF with 0.2 cc %5 dextrose s.c. Seventh day survival was considered as criterion in the three groups. In second phase of this study, thirty three rats were randomly divided into three groups of 11 animals each. The same procedures were carried out also in these groups. Leukocyte counts and peripheric spread were analyzed in postoperative 24th and 72th hours, alveolar and peritoneal macrophages were Investigated in postoperative 72nd hour. There was significantly neutrophilic leukocytosis in the G-CSF group according to the control group. Nevertheless, there was no change in the phagocytic activity of alveolar and peritoneal macrophages. GM-CSF brought about positive effect of phagocytic activity of macrophages without change of leucocyte count in the sepsis, but it caused neutrophilic, monocytosis and lymphocytopenia. The seventh day survival rates in control, G-CSF, GM-CSF groups were as; 42.8%, 71.4%, 28.5% respectively. As a result, we saw that G-CSF has no effect on the phagocytic activity of macrophages, while increases the survival by enhancing the count and probably the function of neutrophils. GM-CSF fails to increase survival while effects the phagocytic activities of macrophages positively and enhances the peripheral neutrophil and monosit counts without changing the total number of leukocytes.