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The Influence of Therapeutic Mild Hypothermia on Immune Function of Rats with Hemorrhagic Shock Induced by Severe Injury

Author: YangJun
Tutor: ZhangLianYang
School: Third Military Medical University
Course: Surgery
Keywords: Trauma Hemorrhagic shock Mild hypothermia Immunity T lymphocyte subsets
CLC: R641
Type: Master's thesis
Year: 2008
Downloads: 106
Quote: 1
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Abstract

Severe trauma (AIS gt; 3) a higher incidence of infection is the second leading cause of death led to the death of trauma patients. Severe trauma patients with immune dysfunction, infection simple anti-infective poor efficacy. T lymphocyte subsets in the output of the cells from the thymus with special signs, perform cell immune effector immune regulatory function, including CD4 and CD8 T-cell subsets mutual restraint, self-stabilizing cellular immunity depends on this pair the balance between the subsets. IL-2 is mainly produced by T lymphocytes, and plays an important role in the immune response and regulation. Tumor necrosis factor TNF-α has a wide range of biological activity may be involved in inflammation and immune responses. TNF-α levels significantly increased post-traumatic, such as uncontrolled release can cause inflammatory reaction \The immunoglobulin is a globulin, having antibody activity and has an extremely important role in humoral immune anti-infection. With the deepening understanding of mild hypothermia and advances in technology, a growing number of experimental and clinical study reports affirmed the brain protective effect of mild hypothermia. The implementation of the of traumatic hemorrhagic animals and patients the purpose of body cooling, lower metabolic rate, reduce tissue injury, inhibiting the inflammatory response, extended trauma patients, especially massive blood loss in patients with first-aid \Mild hypothermia little impact studies of immune function in severe trauma. The experimental rat model of hemorrhagic shock, traumatic explore hypothermia treatment of immune function after severe trauma, and provide laboratory basis for the study of the protective mechanism of mild hypothermia on the body after severe trauma. Methods: 60 SD rats (weighing 200 to 280 g, male or female), were randomly divided into three groups, the experiment 10 deaths due to trauma, blood loss, low temperature, and other factors, the remaining 50. (1) control group: rats are not the trauma and blood loss (n = 10); production traumatic hemorrhagic shock model (2) in the normothermic group: normal body temperature, 6h, 24h two when phase detection indicators (n = 20) respectively; ⑶ hypothermia group: production traumatic hemorrhagic shock model of mild hypothermia, respectively, 6h, 24h two time points detection index (n = 20). ⑴ group of experimental animals, 3% sodium pentobarbital 30 mg / kg intraperitoneal anesthesia, the double midfemoral closed fractures, femoral artery bled to blood pressure 40 mmHg made traumatic hemorrhagic shock model. Reinfusion of blood loss and 2 times the amount of Ringer's solution for 1 h. 2cm rectum temperature was measured from the anus. Normothermic group with a heat lamp irradiation to maintain rectal temperature in rats at 38 to 39 ℃, continuous 3h; hypothermia group with ice water to cool, to maintain rat rectal temperature was 32.5 ~ 33.5 ℃, sustained 3h. Completed after 6h, 24h blood in the abdominal aorta, to take 1.6ml plasma, for the determination of T cell subsets (FCM method) in traumatic hemorrhagic shock model. Taken 4 ml of plasma was centrifuged, the supernatant at -20 ℃ save for peripheral immune globulin IgG assay (ELISA). Spleen and cultured spleen lymphocytes, using a double antibody sandwich ELISA kit in accordance with the requirements of ConA-stimulated spleen lymphocytes secrete cytokines IL-2, TNF-α. And observed mortality for each group of experimental animals. Results: 1. Traumatic hemorrhagic shock, peripheral blood CD4 significantly reduced (P lt; 0.01), CD8 elevated (P lt; 0.05), CD4 / CD8 decreased significantly (P lt; 0.01). Post-traumatic mild hypothermia group compared with the normothermic group, 6h significant difference (P gt; 0.05); increased in peripheral blood of 24h in CD4 (P lt; 0.05), CD8 decreased (P lt; 0.05), CD4 / CD8 elevated (P lt; 0.01). Traumatic hemorrhagic shock, stimulated by ConA spleen lymphocytes secrete cytokines IL-2 lower (P lt; 0.01), elevated TNF-α (P lt; 0.01). Post-traumatic hypothermia group compared with the normothermic group cytokines IL-2 increased (P lt; 0.05), TNF-α reduce (P lt; 0.01). Compared with the normal control group, the rats with traumatic hemorrhagic shock after peripheral blood immunoglobulin IgG no significant difference (P gt; 0.05). Post-traumatic hypothermia group compared with the normothermic group, peripheral blood immunoglobulin IgG no statistically significant difference (P gt; 0.05). Experiment control group without the death of the animal, the hypothermia group and the normal body temperature of animals have animal deaths, mortality differences, but no statistical significance (P gt; 0.05). Conclusion: 1. Early after traumatic hemorrhagic shock (24h within) rat model of suppression of cellular immune function, and performance: the elevated peripheral T lymphocyte subsets CD8, CD4, CD4 / CD8 significantly reduced; ConA-stimulated spleen lymphocyte secretion of cytokines IL-2 was significantly reduced, and TNF-α was significantly higher. Hypothermia therapy, T lymphocyte subsets CD8 reduce, CD4, CD4 / CD8 elevated; IL-2 increased, TNF-α decreased significantly, suggesting that mild hypothermia may improve the body after severe traumatic hemorrhagic shock early cellular immune function suppression. 2 early, peripheral blood immunoglobulin IgG did not change significantly after traumatic hemorrhagic shock, hypothermia therapy no significant change. Hypothermia treatment may improve the cellular immune function suppression, but the early survival of the animals and did not significantly improve.

The Influence of Therapeutic Mild Hypothermia on Immune Function of Rats with Hemorrhagic Shock Induced by Severe Injury

Abstract

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