[Effects of carbachol injection in intestine on plasma levels of inflammatory medium in rats during gut ischemia/reperfusion].

OBJECTIVE: To investigate the effects of carbachol injection in intestine on plasma levels of tumor necrosis factor-alpha(TNF-alpha), interleukin-10 (IL-10) and cortisol in rats during gut ischemia/reperfusion. METHODS: Wistar rats were anaesthetized with soluble pentobarbitone, and subjected to superior mesenteric artery occlusion (SMAO) for 60 minutes, followed by reperfusion for 60 minutes. Animals were divided into three groups, pretreated group (carbachol injection in intestine at 30 minutes after SMAO; 0.1 mg/kg), treated group (carbachol injection at 30 minutes from onset of reperfusion), and controls (saline injection). Plasma TNF-alpha, IL-10 and cortisol levels were determined at 1.0, 2.5 and 6.0 hours after SMAO. RESULTS: The plasma levels of TNF-alpha significantly decreased in pretreated and treated groups than those in controls after carbachol injection (both P<0.01). However, the levels of IL-10 and cortisol didn't show significant differences among three groups. CONCLUSION: The RESULTS suggest that carbachol can reduce the proinflammatory cytokine release and have a less inhibitory effect on the anti-inflammatory cytokine. It is indicated that carbachol play a potential role in alleviating systemic inflammatory response during splanchnic ischemia/reperfusion injury.

[Carbachol alleviates inflammation in gut tissue during ischemia/reperfusion in rats].

OBJECTIVE: To investigate the effects of carbachol on local inflammation in gut tissue during ischemia/reperfusion (I/R). METHODS: A jejunal sac was formed in Wistar rats. The superior mesenteric artery was occluded (SMAO) for 60 minutes followed by reperfusion for another 60 minutes. Animals were divided into three groups, pretreatment group (carbachol was injected into the jejunal sac 30 minutes after SMAO, 0.1 mg/kg), treatment group (carbachol was injected in same dosage into the jejunal sac 30 minutes after reperfusion), and controls (saline injection). The contents of tumor necrosis factor-alpha(TNF-alpha) and activity of myeloperoxidase (MPO) in gut tissue were determined at 1 hours, 2.5 hours and 6 hours after SMAO. RESULTS: The contents of TNF-alpha and activity of MPO were significantly decreased in pretreatment and treatment groups compared with control group at 2.5 hours after SMAO (both P<0.05). There were no differences in both contents between pretreatment group and treatment group at any specified time. It was also found that there were less inflammatory pathological changes in the gut tissues in the two treated groups than that of control. CONCLUSION: The RESULTS suggest that carbachol could alleviate gut inflammatory response during gut ischemia/reperfusion injury by inhibiting proinflammatory cytokine release.

[Effects of carbachol on plasma levels of tumor necrosis factor-alpha and interleukin-10 in rats during gut ischemia-reperfusion].

OBJECTIVE: To investigate the effects of carbachol on the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10) and cortisol in plasma of rats during gut ischemia-reperfusion. METHODS: Wistar rats were anaesthetized with soluble pentobarbitone, and subjected to superior mesenteric artery occlusion (SMAO) for 60 minutes, followed by reperfusion for 60 minutes. Animals were divided into three groups, pretreated group (intramuscular injection carbachol at 30 minutes after SMAO, 0.1 mg/kg), treated group (intramuscular injection of carbachol at 30 minutes after reperfusion), and control group (saline injected). The levels of TNF-alpha, IL-10 and cortisol in plasma were determined at 0 hour, 1 hour, 2.5 hours and 6 hours after SMAO. RESULTS: The levels of TNF-alpha, IL-10 and cortisol significantly increased after SMAO (P<0.01 ). The levels of TNF-alpha significantly decreased in pretreated and treated groups than that in control after the intramuscular injection of carbachol (all P<0.01). However, the levels of IL-10 and cortisol did not show significant differences among three groups. It was also found that lower content of TNF-alpha in pretreated group than that in treated group, especially at 1 hour and 6 hours. CONCLUSION: The results suggest that carbachol reduce the proinflammatory cytokine releasing and has a less inhibiting effect on the anti-inflammatory cytokine. It is indicated that carbachol play a potential role in alleviating systemic inflammatory response during splanchnic ischemia-reperfusion injury.

[Effects of efferent vagus nerve excitation on inflammatory response in heart tissue in rats with endotoxemia].

OBJECTIVE: To study the effects of electrical stimulation of efferent vagus nerve on the inflammatory response in heart tissue in rats with endotoxemia. METHODS: Two hundred and ten Wistar rats were randomly divided into seven groups. Animals were subjected to bilateral cervical vagotomy, or a comparable sham surgical procedure in which the vagus nerves were isolated but not transected. The distal end of a vagus nerve trunk was placed across bipolar electrodes connected to a stimulation module and controlled by an acquisition system. Stimuli with constant voltage (5 V, 2 ms, 1 Hz) were applied to the nerve for 20 minutes immediately after administration of lipopolysaccharide (LPS, 10 mg/kg, E coli O111: B4, Sigma), and then were repeated 2 times after each of 10 minutes interval. Blood and tissue samples of these rats were collected at 1, 1.5 and 2 hours after LPS administration in all groups. Tumor necrosis factor-alpha (TNF-alpha) and myeloperoxidase (MPO) in heart tissue and serum MB isoenzyme of creatine kinase(CK-MB) were determined. RESULTS: The electrical stimulation of the efferent vagus nerve significantly decreased the contents of TNF-alpha and MPO in heart tissue and CK-MB in serum, and alleviated myocardial inflammation in heart tissue at all time points, especially at 1.5 hours after endotoxin challenge. CONCLUSION: The results suggested that excitation of the efferent vagus nerve can significantly alleviate the inflammatory response in the heart tissue, thus it might produce a potential protective effect on the heart during endotoxemia in rats.