| Summary: | 碩士 === 輔仁大學 === 營養科學系碩士班 === 105 === Hemorrhagic shock is an emergent condition that usually caused by trauma, surgery, and parturition. When patients suffer from rapid blood loss, the hypovolemia may result in the decreases in energy and oxygen delivery which cause multiple organ failure (MOF). In clinical practice, patients are administered with resuscitation fluid rapidly to improve blood pressure and oxygen supply. However, resuscitation may elevate the production of reactive oxygen species (ROS) which induce inflammatory response and organ damages. Studies showed that fish oil have the anti-inflammatory activity. When fish oil concentration of the cell membrane is increased, the immune cells have decreased ability to produce pro-inflammatory cytokines. In addition, glutamine has been confirmed to be the main source of energy for immune cells and intestinal cells. Therefore, the aim of the present study was to investigate the effects of single or combination treatment of fish oil- and glutamine-supplemented resuscitation fluids on the THR-induced inflammatory responses and antioxidant activity. Male SD rats were divided into 6 groups, expect the control (NC group) and sham-operated (SM group) groups the other THR groups were suffered with 5 cm midline laparotomy and catheterization in the left carotid artery and right jugular vein. The blood was withdrawn from the left carotid artery to reach a mean arterial pressure 30 to 35 mmHg within 10 min for hemorrhagic shock induction. After 60 minutes of hypovolemia, rats were resuscitated with shed blood and equal volume of lactate Ringer’s solution without (TH group) or with L-alanyl-L-glutamine (GN group), fish oil (FA group) or L-alanyl-L-glutamine plus fish oil (GF group) within 10 minutes and followed by continuouslow infusion rate (~1.4 ml/h) of resuscitation fluids. After 42 h, rats were executed and we expect to demonstrate that glutamine- and fish oil-supplemented resuscitation fluids may attenuate THR-induced inflammatory response and target organ injury in rats. The results show that THR may decreased RBC count, hemoglobin and hematocrit, and the loss of blood albumin and the decrease of antioxidant capacity.Then THR model may lead to decrease plasma, pulmonary and intestinal MPO activity and the pulmonary content of interleukin (IL)-8, the content of IL-4 and IL-8 in the kidney were decreased.The utilization of protein in plasma and lipid peroxidation, SOD and GPx activities in RBC could be increased. THR rats were supplemented with L-alanyl-L-glutamine resuscitation fluid to reduce the plasma pro-inflammatory cytokines, liver protein carbonylation and RBC lipid peroxidation. However, THR rats were supplemented with fish oil resuscitation fluid may decrease the concentration of pro-inflammatory cytokines in plasma, liver, kidney and reduce the pulmonary adhesion factor secretion, but also reduce the lipid peroxidation of RBC. In addition, THR rats were supplemented with L-alanyl-L-glutamine and fish oil resuscitation fluids may significantly reduce the plasma, kidney and pro-inflammatory cytokine secretion and increase the anti-inflammatory in the kidney and jejunum, and may lead to enhance the plasma and RBC antioxidative capacity. In summary, our THR model in this study may reduce the systemic antioxidative capacity and enhance jejunum inflammation. THR rats were supplemented with L-alanyl-L-glutamine and fish oil resuscitation fluids may alleviate inflammatory response and increase the antioxidant effect to reduce the THR-induced inflammatory response and target organ injury.
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