MODULATION OF NEURO-ENDOCRINE-IMMUNE RESPONSES IN SURGICAL STRESS

本研究的目的是如何调节手术应激中的神经内分泌免疫反应。结果如下：1。营养途径和谷氨酰胺补充：预先肠内营养和Ala-Gln富集的TPN均可增强局部、全身和远端器官对腹腔内细菌攻击的免疫反应。根据我们的发现，危重疾病只要肠内途径是可行的。当肠内营养不能耐受时，Ala-Gln富集TPN可能是增强宿主防御的一种选择。生长激素和胰岛素样生长因子1：生长激素和IGF-1通过适度增加血浆容量来支持这些活性，以及通过强烈的直接作用，增强PECs的吞噬和大肠杆菌杀灭活性。一氧化氮氧化酶抑制剂和NO供体：给予L-NAME可增加肺内中性粒细胞粘附，降低腹膜内中性粒细胞粘附。在这种腹膜炎模型中，由于中性粒细胞的隔离，NO抑制可能是有害的。一氧化氮给药可抑制肺内中性粒细胞粘附，降低腹腔内中性粒细胞粘附。

The purpose of this research was how to modulate neruo-endocrine-immune responses in surgical stress. The result is as follows :1. Nutritional routes and glutamine supplementation : Both antecedent enteral nutrition and Ala-Gln enriched TPN enhance local, systemic and remote organ immune responses to intraperitoneal bacterial chalenge. On the basis of our findings, critical illness whenever the enteral route is feasible. Ala-Gln enriched TPN may be an option for enhancing host defense when enteral nutrition can not be tolerated.2. Growth hormone and Insulin-like growth factor 1 : GH and IGF-1 enhance phagocytosis and the E.coli-killing activity of PECs, via a modestly increased plasma capacity to support these activities, as well as by a strong direct action.3. Nitric oxidase inhibitor and NO donor : Administration of L-NAME increased neutrophil adhesion in the lung, while decreasing that in the peritoneum. NO inhibition may be ditrimental, due to neutrophil sequestration, in this peritonitis model. NO donor administration prevented neutrophil adhesion in the lung, but decreased neutrophil adhesion in the peritoneal cavity.