| Background and AimsIschemia-reperfusion (I/R) injury is associated with hemorrhagic shock, intestinal transplantation, intestinal obstruction and severe trauma. Intestinal I/R is accompanied with decreased contractile activity, increased microvascular permeability and dysfunction of mucosal barrier. The injury can lead to bacterial translocation and progress into multiple organ dysfunction syndrome. The apoptosis of enteric neurons, smooth muscle cells and interstitial cells of Cajal (ICC) is involved in intestinal I/R injury, especially the injury of cholinergic neurons and the reduction of acetylcholine who is one of major excitatory transmitters. Although I/R injury is a leading cause of high morbidity and mortality in many patients, there is little drugs showing promising effect at the clinic. Hydrogen sulfide (H2S) is an endogenously gaseous mediator, regulating the process of many physiological functions in mammalian tissues. Recently, a great deal of evidence has demonstrated that H2S could protect from I/R injury in various organs, such as heart, lung, liver, kidney, and intestine. But the H2S was delivered prior to the onset of ischemia in most of these studies, there is little evidence to demonstrate whether H2S could protect intestinal contractile activity and enteric neurons from intestinal I/R injury when delivered it prior to the onset of reperfusion. This study aims at investigating the effect of H2S on contractile activity and enteric neurons and associated mechanisms when delivered it prior to the onset of reperfusion.MethodsA total of 24 Sprague-Dawley rats were randomly divided into four groups (n=6 for each group): the normal group (A), the sham-operated group (B), the I/R group (C), and the NaHS group. The rats of group C and group D were subjected to superior mesenteric artery (SMA) ischemia for 1h followed by a 4h of reperfusion period, and the solution of NaHS(10μmol/kg)was injected to the rats of group D intraperitoneal 20min prior to reperfusion. The sham-operated group was received the surgery without occlusion. Functional study was carried out through recording the spontaneous contraction of ileum and the responses to KCl (30mmol/L),ACh (10-5mol/L),electrical field stimulation (EFS;30V,10Hz,1.00ms,10s) in organ bath. Morphological study was designed to detect the change of Hu-positive and ChAT-positive enteric neurons in myenteric plexus. Results1. Compared with normal group, there is not significantly different from sham-operated group in frequency and area under curve (AUC) of spontaneous contraction, the responses to KCl, ACh and EFS, and the change of Hu-positive and ChAT-positive enteric neurons.2. Compared with sham-operated group, there is not significantly different from group C in frequency of spontaneous contraction, the responses to KCl and ACh. But there is significantly decrease in AUC of spontaneous contraction (p<0.05), the responses to EFS (p<0.05), and the change of Hu-positive and ChAT-positive enteric neurons (p<0.05).3. Compared with group C, there is not significantly different from group D in frequency of spontaneous contraction, the responses to KCl and ACh. But there is significantly increase in AUC of spontaneous contraction (p<0.05), the responses to EFS (p<0.05), and the change of Hu-positive and ChAT-positive enteric neurons (p<0.05).Conclusion1. Intestinal ischemia-reperfusion (I1h/R4h) does not lead to severe injury of ICC and smooth muscle cells. The reduction of spontaneous contractile activity of strips was mainly attributed to the impairment of the cholinergic neurons containing excitatory transmitter ACh.2. H2S could partial normalize spontaneous contractile activity by protecting enteric neurons especially excitatory neurons from intestinal I/R injury.
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