Abstract

Previous studies have shown that delayed apoptotic polymorphonuclear neutrophils (PMNs) might play an important role in the development of multiple organ dysfunction syndromes (MODS). Somatostatin (SST) may improve the histopathological lesions as well as functions of vital organs in rats with MODS. This study was to investigate the association of SST levels in plasma or jejunum tissue and PMN life in macaques following intestinal ischemia reperfusion. SST levels in macaque plasma or jejunum tissue were significantly decreased after intestinal ischemia reperfusion (IR) injury. The apoptotic rate of PMNs was obviously reduced (15.4±1.41 to 3.5±0.53%, P<0.05). However, the number of peritoneal apoptotic macrophages was clearly increased. The apoptotic rate of PMNs was significantly increased (20.0±2.24 to 50.2±1.81%, P<0.01) after incubated with SST in vitro. Specific DNA ladder bends from PMNs were visualized with agarose electrophoresis. Specific bindings between PMNs and the antibodies for SSTR1 (547.9±19.98 RU/ml) or SSTR2 (27.6±20.56 RU/ml) were detected. The results showed physiological apoptosis of PMNs in macaques could be induced by SST through SSTRs on PMNs. The decreased SST levels in macaque plasma or jejunum tissue following intestinal ischemia-reperfusion might extend PMN life and promote the occurrence of MODS.

Key words: Polymorphonuclear neutrophils (PMNs), macrophage, apoptosis, somatostatin, macaque, multiple organ dysfunction syndromes (MODS).