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The research purposes intestinal ischemia-reperfusion (ischemia-reperfusion, I / R) injury occurs during hemorrhagic shock, small bowel transplantation, mechanical obstruction and severe trauma, can cause intestinal contractile activity was reduced, increased microvascular permeability and decreased intestinal mucosal barrier function, and can lead to bacterial translocation leading to multiple organ dysfunction syndrome. Intestinal ischemia-reperfusion can cause intestinal neurons, smooth muscle cells, and apoptosis of interstitial cells of Cajal (interstitial cells of Cajal, ICC) caused by small intestinal motility dysfunction, especially enteric nervous system (enteric nervous system, ENS) cholinergic intestinal nerve damage reduction is the most important one of the reasons causing the excitatory neurotransmitter acetylcholine (acetylcholine, ACh). Intestinal ischemia reperfusion in clinical practice is more common and can cause serious complications and mortality, but still lack of effective treatment. Hydrogen sulfide (hydrogen sulfide, H2S) is an endogenous gas signaling molecules that play many important physiological functions in mammals. Recently, many scholars have confirmed in a variety of organs such as the heart, lung, liver, kidney, intestinal ischemia-reperfusion model play a protective role. Most of these experiments are before ischemia preventive give hydrogen sulfide, experiments have not yet confirmed that hydrogen sulfide can play the protective enteric nervous and intestinal motor function after ischemia. The purpose of this project is to study given before reperfusion after ischemia the hydrogen sulfide whether the role and mechanism of protection intestinal contractile activity and intestinal neurons. Research Methods 24 male Sprague-Dawley rats were randomly divided into four groups (n = 6): normal group (A), sham group (B), intestinal ischemia reperfusion group (C), intestinal ischemia reperfusion plus sulfide hydrogen intervention group (D). Release group C and D rats by occlusion of the superior mesenteric artery 1h the vascular clips reperfusion 4h to create intestinal ischemia-reperfusion model; hydrogen sulfide donor NaHS (10μmol/kg) at reperfusion 20min before intraperitoneal injection ; B rats underwent open only flip the gut without clipping artery. Functional experiments ileal muscle strips isolated from the body organs of a thermostatic bath the 'Free perfusion technology records spontaneous contraction and of potassium chloride (KCl; 30 mmol / L), acetylcholine (ACh; 10-5mol / L), electrical field stimulation (electrical field stimulation , EFS; 30V, 10Hz, 1.00ms, 10s) reaction. Morphological experiments by immunofluorescence detection myenteric plexus (myenteric plexus, MP) Hu protein, choline acetyl transferase (cholineacetyltransferase, ChAT) receptor-positive neurons expression changes. 1, compared with the normal group, sham group isolated muscle strips spontaneous contraction frequency, the area under the curve, the reaction of KCl, ACh and EFS Hu protein and ChAT receptor-positive neurons expression did not change significantly. 2, compared with the sham group, ischemia reperfusion rats spontaneous contraction frequency of isolated muscle strips, no significant changes in response to KCl and ACh; spontaneous contraction of isolated muscle strips of the area under the curve to reduce (p lt; 0.05) response to EFS was significantly decreased (p lt; 0.05); immunofluorescence Hu protein, ChAT receptor-positive neurons in expression were significantly lower (p lt; 0.05). 3, compared with ischemia-reperfusion group, hydrogen sulfide intervention rats spontaneous contraction frequency of isolated muscle strips, no significant change in response to KCl and ACh; spontaneous contraction of isolated muscle strips in the area under the curve increased (p lt; 0.05), the reaction of EFS increased (p lt; 0.05); immunofluorescence Hu protein, ChAT receptor-positive neurons in expression were significantly increased (p lt; 0.05). Conclusions intestinal ischemia reperfusion (I1h/R4h) did not cause significant damage to the ICC and smooth muscle cells, mainly cause excitatory neurotransmitter ACh-containing choline intestinal nerve damage causes muscle strips in vitro spontaneous contractions vitality decline. , Hydrogen sulfide by protecting intestinal neuronal excitatory neurons partially protects the contractile function of isolated muscle strips.
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