| BackgroundTrauma has been one of the most important factors of the increasing mortality of young people. There are three major causes of death of trauma: (1)failure of resuscitation of severe traumatic shock. (2)severe organ injury. (3)Development of immunosuppression, sepsis and MODS after trauma. Many severe traumatic/hemorragic shock and insufficient fluid resuscitation initiate systemic inflammatory process and alter the physiologic immune balance. Adequate volume replacement is paramount in the treatment of traumatic/hemorragic shock patients. However, controversy is still remaining on the volume therapy.Crystalloids are freely permeable to the vascular membrane and are therefore distributed mainly in the interstititial and/or intercellular compartment. Only 25% of the infused crystalloid solution remains in the intravascular space and subsequently lead to tissue edema. That's why even a massive crystalloid resuscitation is less likely to achieve adequate restoration of microcirculation blood flow compared to a colloid-based volume replacement strategy. After world war II, a large variety of nature and synthetic colloid preparations are used world-wide. An infusion of albumin can not raise colloid osmotic and the pressure gradient of colloid osmotic-pulmonary arterial wedge pressure(PAWP). It was shown that the infusion of albumin resulted respiratory failure, especially in patients with sever shock compared to patients who did not receive albumin. This appears to be due to increased leakage into the interstitial pace. Whereas in inflammatory-related capillary leaks, hydroxyethyl starch (HES) has been reported to have "occlusive" effect on damaged capillaries, and subsequently limit the extravasation of fluid. In a recent clinical study, intravascular volume replacement with HES130/0.4 versus crystalloid solution improved tissue oxygenation in patients undergoing abdominal surgery. Meantime, the use of HES may result in less endothelial cell damage and improve microcirculation, andconsequently reduced the inflammatory response.Depressed T-cell activity has been a consistent finding during the development of immunosuppression after severe traumatic/hemorragic shock . Many reports show a shift to Th2 subset with resultant overproduction of IL-10 and IL-4. It has been suggested to be a pivotal contributor to post injury immunosuppression. On the otherwise exaggerate lymphocyte apoptosis is present in peripheral blood of patients with traumatic/hemorragic shock, and leads rapidly to a profound and persistent lymphocyte loss. Since HES may reduce inflammatory response in traumatic/hemorragic shock, can it prevent the development of immunosuppression versus other resuscitation fluid. This is the main goal of our study.Objects and methods1. T/HS animal model: SD rats underwent internal jugular vessel cannulation. The T/HS model involved: (1)femoral bone mutilation , (2) a controlled retrieval of blood, maintaining mean blood pressure at 30±5mmHg during 30 minutes. (3)resuscitation with lactated Ringer's (control 1), HES130/0.4 (experimental) and 5%human albumin (control 2)(twice the blood volume retrieved)plus their shed blood.2. Evaluate Serum lactate , potassium, and creatinine level; PH, PO2 and sBE in arterial blood; and pathological change in tissue of lung and kidney in control group to evaluate the stability of the T/HS animal model.3. Determination of CD4+ and CD8+ lymphocyte subsets by dual parameter flow cytometry at time of 24, 48 hours after resuscitation (control group versus experimental group).4. Determination of TH1 and TH2 lymphocyte subset by detection of intracytoplasmic cytokine (IL-4, γ-IFN) using flow cytometry at time of 24, 48 hours after resuscitation (control group versus experimental group).5. Determination of apoptosis of CD4+ lymphocyte in spleen by detection of phosphatidylserine expression on early apoptotic cells using fluorescein labelled Annexin V with Flow cytometric at time of 24, 48 hours after resuscitation (control group versus experimental group).6. Determination of apoptosis of PBMC of marrow by detection of phosphatidylserine expression on early apoptotic cells using fluorescein labelled Annexin V with Flow cytometric at time of 24,48 hours after resuscitation (control group versus experimental group).7. Apoptosis of PBMC of marrow was assessed through terminal deoxynucleotide transferase-mediated dUTP nick-end labeling assay at time of 24, 48 hours after resuscitation (control group versus experimental group).Result1. T/HS animal model was established successfully. Through a controlled retrieving of blood from jugular vessel the mean arterial pressure was reduced to 30 mmHg and kept this level for 30 mins. Biochemical indicator such as serum lactate , potassium, and creatinine level; PH, PO2 and sBE in arterial blood; and pathological change in tissue of lung and kidney at time of 24,48 hours after resuscitation indicate the stability of the T/HS animal model in control group.2. The percentage area of CD3+,CD4+ T cell decreased obviously at time of 24 hours after resuscitation in each group, and risen quickly at time of 48 hours only in experimental group (HES130/0.4).3. The ratio of TH1/TH2 decreased obviously in control group 1 (Ringer's) at time of 48 hours after resuscitation. This difference did not occur in experimental group at any time.4. Control group 1(Ringer's) showed a striking increased number of apoptosis cells in CD4+T cell at 24 hours after resuscitation versus HES and albumin groups.5. A significantly increased number of apoptosis cells in PBMC of bone marrow was observed in control group1,2(Ringer's and albumin) and not in experimental group(HES130/0.4).ConclusionsMany significant changes such as the decrease of percentage area of CD3+,CD4+T cell and ratio of TH1/TH2 and the increase number of apoptosis immunologic cell was observed after traumatic/hemorragic shock. HES130/0.4 as a resuscitation fluid may prevent those changes occurred in immunological function.
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