Somatostatin suppressed the activity of intestinal mucosal mast cells in rats with multiple organ failure
- VernacularTitle:生长抑素抑制多器官功能衰竭时肠黏膜肥大细胞活性
- Author:
Chengwei TANG
;
Cheng LAN
- Publication Type:Journal Article
- Keywords:
Somatostatin;
Intestinal mucosal mast cells;
Multiple organ failure.
- From:
Chinese Journal of Digestion
2001;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of somatostatin(SST) on the activity of intestinal mucosal mast cells(IMMC) and its pathological significance in the development of multiple organ failure(MOF). Methods The rat model of MOF was established by the peritoneal injection of zymosan. Thirty minutes after the injection of zymosan, SST at 2.300 ng?kg -1 ?h -1 or 0.023 ng?kg -1 ?h -1 was injected respectively through tail veins. The concentration of histamine and tumor necrosis factor-? (TNF-?) in plasma and intestinal tissue were measured. The pathological alterations of essential organ including intestine, liver, kidney, lung and heart were studied under light microscope. Their corresponding functions were reflected with alanine aminotransferase (ALT), cretinine (Cr) and oxygen pressure (PO 2). 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 (2.300 ng?kg -1 ?h -1 ) showed less serious inflammatory response under light microscope. ALT and Cr were decreased 53% and 60% respectively. However, the lung ventilation was improved and PO 2 was increased by 50%. The histamine level in the intestinal tissue from rats treated with SST remarkably increased( ( 8.60? 0.50 ) ng/g protein to ( 14.50? 1.08 ) ng/g protein), whilst the plasma histamine level did not show any significant changes. Exogeneous SST also resulted in lower level of TNF-? in intestine but no changes in plasma. Furthermore, degranulation of IMMC from the rats treated with SST was less obvious. Conclusion SST may prevent from or arrest the development of MOF through suppression of the release of inflammatory mediators, such as histamine and TNF-?.
