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期刊论文
Somatostatin suppressed the activity of intestinal mucosal mast cells in rats with multiple organ failure
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[Abstract]: Multiple organ failure (MOF) is the most serious result followed by trauma and infection. Our previous study has shown that activated intestinal mucosal mast cells (IMMC) may play an important role in the development of MOF. Somatostatin (SST), one of gut peptides, is an important regulator in the neuro-endocrine-immune network. However, the effects of SST on IMMC especially in the case of MOF remain unclear. Objective: This study was aimed to investigate the effect of SST on the activity of IMMC in the development of MOF. Methods: The rat model of MOF was established by injection of zymosan. Thirty minutes after the injection of zymosan, SST at 2.3ng/Kg/h or 0.023ng/Kg/h was injected respectively through tail veins. The concentration of histamine and tumor necrosis factor-α (TNF-α) in plasma and intestine tissue were measured. The pathological alterations of essential organ including intestine, liver, kidney and lung were studied under light microscope. Their corresponding functions were reflected with alanine aminotransferase (ALT), cretinine (Cr) and oxygen pressure (PO2). In addition, the ultra structure of the IMMC was observed under a transmission electronic microscope. Results: Compared with the controlled rats, the rats injected with SST (2.3ng/Kg/h) showed less serious inflammatory response under light microscope. ALT and Cr were decreased 53% and 60% respectively. However, PO2 was increased 50%. The histamine level in the intestinal tissue from rats treated with SST remarkably increased (8.60±0.50 to 14.50±1.08 ng/g protein), while the plasma histamine level did not show any significant changes. Exdogeneous SST also resulted in lower level of TNF-α in intestine but no changes in plasma. Furthermore, degranulation of IMMC from the rats treated with SST was less obvious. Conclusions: SST may prevent from or arrest the development of MOF through suppression of inflammatory mediators releasing such as histamine and TNF-α.
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