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研究生:彭台珠
研究生(外文):Peng Tai Chu
論文名稱:建立清醒鼠固定血量持續失血休克模式探討器官損傷之生理病理變化
論文名稱(外文):Pathophysiological Alterations of Multiple OrganDysfunctions Following Continuous Hemorrhagic Shock in Conscious Rats
指導教授:張芙美張芙美引用關係
學位類別:博士
校院名稱:慈濟大學
系所名稱:醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2006
畢業學年度:94
語文別:中文
論文頁數:113
中文關鍵詞:非約束性器官損傷失血性休克清醒鼠模式
外文關鍵詞:unrestrainedorgan injuryconscious rathemorrhagic shock
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在許多的失血性休克動物實驗中,常需使用到麻醉劑,由於麻醉劑會干擾到實驗動物之生理表現,因此無法模擬臨床病人之情境。在非控制性失血休克模式則必須考慮如何控制失血的量與速度,若保持實驗動物清醒狀態時,則必須考慮如何約束實驗動物。目前大多數的失血性休克動物模式,無法長時間連續監測實驗動物之生理參數超過24小時。
本研究主要在建立一能反應臨床病患實際病況,且能連續監測失血後24小時以上生理指標變化之動物實驗模式,以探討失血後之生理病理變化,作為醫護人員對失血性休克病人病情進展與採行相關醫護處置時之參考依據,協助護理人員掌握病患病情變化。
實驗設計主要策略為:(一)實驗過程中動物不麻醉全程保持清醒;(二)實驗動物仍能上下左右活動,採用尾部約束;(三)使用固定血量失血;(四)採用連續24小時持續慢性失血。實驗動物共分成三組,以股動脈插管之方式進行失血,在初次失血時第一組失血量為全血之40 ﹪、第二組失血30 ﹪、第三組失血0 ﹪。
實驗結果顯示,本模式失血40 ﹪與30 ﹪組之兩天存活率皆為87.5﹪,本模式可觀察累積失血量與Hct之變化來判斷失血達到 50 ﹪之時間點,同時Lactic acid於失血 40 ﹪組因代償失調,由第9小時開始升高,於第18小時達到3倍,比失血30 ﹪組較高。
失血性休克促使TNF-α �n與 IL1-β 的分泌,使neutrophil 黏附到內皮細胞上,在系統性發炎上扮演一重要的角色。本研究失血40 ﹪組WBC 於失血後第1到6小時逐漸減少,TNF-α �n與 IL1-β 於失血後第1到 9 小時逐漸增高,可明顯看出失血與發炎反應之關係。
於失血第6小時後血清AST、ALT、BUN、LDH 和 CK-MB值逐漸升高,反應出肝臟、腎臟與心臟之早期損傷,於失血48小時後,由組織病理切片進一步可看出肝臟、腎臟、心臟、肺臟與小腸在失血後組織層次均出現損傷,未來將以初次失血量40 ﹪之方式作為後續相關研究之基準,亦可利用本模式,進一步作SIRS 與 MODS 之相關研究。同時護理人員於休克早期能經由觀察Hct、Lactic acid與血清生化值之變化,了解病患失血與器官損傷之程度,有效掌握病情變化。
Animal models utilizing anesthesia have been used in a number of studies of hemorrhagic shock. The anesthetic drugs may interfere with the physiologic course of hemorrhagic shock and make the animal impossible to simulate the clinical situations. On the other hand, in previous uncontrolled hemorrhagic shock animal models, the rate and the volume of blood loss couldn’t be adequately controlled. So that the animal models would prolonged anesthetic or a fasting state. In addition, these models can not measure physiologic parameters continuously at given intervals for a prolonged period.
The experiments were designed to establish an animal model based on the clinical situation to study hemorrhagic shock. Hemorrhagic shock was induced by withdrawing blood from a femoral arterial catheter. The blood volume withdrawn was 40 ﹪of the total blood volume for group 1 and 30 ﹪for group 2 and 0 ﹪for group 3 at the first blood withdrawal.
The data showed that the survival rate was 87.5% at the 48 h in both blood withdrawal groups. In which the experiment extends the blood withdrawal from the femoral artery catheter length of time to 48 hous. Moreover, without anesthesia and restraint the animals, conscious and perceived no pain, did not struggle when their blood was withdrawn.
In our model, we can observe the cumulative volume of blood withdrawal and Hct concentration to decide when blood loss reached to 50 ﹪.Meanwhile, cumulative hemorrhage resulted in an twofold increase of plasma lactic acid at 9 h and threefold increase at 18 h in group 1, whose increase was higher and earlier than group 2. This could be caused by decompensation.
TNF-α �nand IL1-βplay a major role in systemic inflammatory response. They also enhance leukocyte-endothelial cell adhesion, stimulate chemokine secretion, and induce neutrophil activation. In the present study, the number of WBC decreases within the first 6 hours of blood withdrawal, and the TNF-α �nand IL-1βincrease �nwithin the first 9 hours of blood withdrawal in group 1, which suggests a stronger inflammatory response after hemorrhage.
After hemorrhage, the blood AST、ALT、BUN、LDH and CK-MB concentrations significantly increased in starting the 6 h in group 1 and the pathological HE stain also shows the lesion on liver、kidney、heart and lung. The results suggest that hemorrhagic shock model is associated with multiple organ dysfunctions and may be useful for the study of SIRS and MODS.
Nurse practitioners can benefit from the observation of the changes of Hct、lactic acid and biochemistry levels in the early stage of hemorrhagic shock, to understand the extent of blood loss and MODS of the patients, and eventually take quick actions to help the patients.
中文提要..........................

英文提要..........................

縮寫表..........................

目錄............................
ⅩI
表目錄...........................
ⅩⅢ
圖目錄...........................
ⅩⅣ
第一章 緒論........................
1
一、前言
2
二、現有失血性休克動物實驗模式
2
三、失血與多重器官損傷
6
四、研究目的
7
第二章 文獻探討.......................
8
一、休克之定義....................
9
二、低血容性休克之定義.................
10
三、失血性休克的分級..................
10
四、失血性休克的分期..................
12
五、休克時之生理反應................
12
第三章 影響動物實驗血液樣本血球生化測量值準確度之因素探討
22
一、研究背景.....................
23二、實驗設計.....................
24
三、材料與方法....................
26
四、統計與分析....................
28
五、結果與討論....................
29
六、結論.......................
32
第四章 建立清醒鼠固定血量持續失血休克模式.........
55
一、研究背景......................
56
二、實驗設計......................
59
三、材料與方法.....................
60
四、統計與分析.....................
62
五、結果........................
62
六、討論........................
65
七、結論........................
67
第五章 探討固定血量持續失血休克模式對清醒鼠之器官損傷...
75
一、研究背景.....................
76
二、實驗設計.....................
79
三、材料與方法....................
80
四、統計與分析....................
81
五、結果.......................
82
六、討論.......................
83
七、結論.......................
84
第六章 總結論.......................
98
參考文獻..........................
100
已發表之論文相關著作
112
中華民國急重症護理學會(2004).東區急重症案例教學研討會手冊。
中華民國胸腔暨重症加護醫學會(1998)重症醫學.台北:金名。
李建賢、王立敏、黃睦順(1999).急診醫學.台北:金名。
何邵中、林梅香、黃人珍(2002).重症護理學.台北:偉華。
何敏夫(1994).臨床化學原理與實驗.台北:合記。
趙克然、楊毅俊、曹道俊(2002).氧自由基與臨床.台北:合記。
鄭隆賓(1999).急症醫學.台北:合記。
Arthur EB, Eugen F, Donald EF: Multiple organ failure. New York, NY: Springer-Verlag, p176-187, 2000.
Assaly R, Olson D, Hammersley J, Fan PS: Initial evidence of endothelial cell apoptosis as a mechanism of systemic capillary leak syndrome. Chest 120:1301-1308, 2001.
Baker JW, Deitch EA, Li M, Berg RD, Specian RD: Hemorrhagic shock induces bacterial translocation from the gut. J Trauma 28:896-906, 1988
Barbee RW, Kline JA, Watts JA: A comparison of resuscitation with packed red blood cells and whole blood following hemorrhagic shock in canines. Shock 12:449-453, 1999.
Baue AE: Multiple organ failure, multiple organ dysfunction syndrome,and the systemic inflammatory response syndrome –where do we stand? Shock
2:385-397, 1994.
Bitterman H, Reissman P, Bitterman N, Melamed Y, Cohen L: Oxygen therapy in hemorrhagic shock. Circ Shock 33:183-191, 1991.
Bone RC, Balk RA, Cerra FB: Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 101:1644-1655, 1992.
Capone A, Safar P, Stezoski SW: Uncontrolled hemorrhagic shock outcome model in rats. Resuscitation 29:143-152, 1995.
Chen HI, Kao SJ, Wang D, Lee RP, Su CF: Acute respiratory distress syndrome. J Biomed Sci 10:588-592, 2003.
Chintala MS, Jandhyala BS: Comparative evaluation of the effects of felodipine, hydralazine, and naloxone on the survival rate in rats subjected to a "fixed volume" model of hemorrhagic shock. Circ Shock 32:219-229, 1990.
Claridge JA, Enelow RI, Young JS: Hemorrhage and resuscitation induce delayed inflammation and pulmonary dysfunction in mice. J Surg Res 92:206-213, 2000.
Copstead LC, Banasik JL: Pathophysiology: Biological and behavioral perspectives. philadelphia: W.B. Saunders, 2nd, p 482-501, 2000.
Collins JA, Stechenberg L: The effects of the concentration and function of hemorrhage on the survival of rats after hemorrhage. Surgery 85:412-418, 1979.
Crippen D, Safar P, Snyder C, Porter L: Dying pattern in volume-controlled hemorrhagic shock in awake. Resuscitation 21:259-270, 1991.
Darovic GO: Hemodynamic monitoring: Invasive and nonvasive clinical application. Piladelphia: W.B.Sounders Company, 3rd, p 361-401, 2002.
Deitch EA: Animal models of sepsis and shock: A review and lessons learned. Shock. 9:1-11, 1998.
Durham RM, Moran JJ, Mazuski JE, Shapiro MJ, Baue AE, Flint LM: Multiple organ failure in trauma patients. J Trauma 55:608-616, 2003.
Dunham CM, Siegel JH, Weireter L, Fabian M, Goodarzi S, Guadalupi P, Gettings L, Linberg SE, Vary TC: Oxygen debt and metabolic acidemia as quantitative predictors of mortality and the severity of the ischemic insult in hemorrhagic shock. Crit Care Med 19:231-243, 1991.
Flohe S, Ackermann M, Reuter M, Nast-Kolb D, Schade FU: Sublethal hemorrhagic shock reduces tumor necrosis factor-alpha-producing capacity in different cell compartments. Eur Cytokine Netw 11:420-426, 2000.
Friedman SG, Pearce FJ, Drucker WR: The role of blood glucose in defense of plasma volume during hemorrhage. J Trauma 22:86-91, 1982.
Gonzalez RJ, Moore EE, Ciesla DJ, Biffl WL, Johnson JL, Silliman CC: Mesenteric lymph is responsible for post-hemorrhagic shock systemic neutrophil priming. J Trauma 51:1069-1072, 2001.
Guyton AC, Hall JE: Cardiac output and circulation shock. Human Physiology and mechanisms of disease, 6th edition, editor by Chuan LL., print Farseeing publishing Co., Ltd; pp247-262,1998.
Hampton MB, Kettle AJ, Winterbourn CC: Inside the neutrophil phagosome: Oxidants,myeloperoxidase,and bacterial killing. Blood 92:3007-3010, 1998.
Hsu YH, Kao SJ, Lee RP, Chen HI: Acute pulmonary oedema:Rare causes and possible mechanisms. Clin Sci 104:259-264, 2003.
Hsu BG, Yang FL, Lee RP, Peng TC, Harn HJ Chen HI: N-acetylcysteine ameliorated lipopolysaccharide induced organ damage in conscious rats. J Biomed Sci 11:152-162, 2004.
Inada T, Taniuchi S, Shingu K, Kobayashi Y, Fujisawa J, Nakao S: Propofol depressed neutrophil hydrogen peroxide production more than midazolan. Whereas adhesion molecule expression was minimally affected by both
anesthetics in rats with abdominal sepsis. Anesth & Analgesia 92:437-441, 2001.
James M, Lan R, Phillip E: Fluid resuscitation strategies: A systematic review of animal trials. J Trauma 55:571-589, 2003.
Jernigan TW, Croce MT, Fabian TC: Apoptosis and Necrosis in the Development of Acute Lung Injury After Hemorrhagic Shock The American Sur 170:1094-1099, 2004.
Johnson KB, Egan TD, Kern SE, White JL, McJames SW, Syroid N, Whiddon D, Church T: The influence of hemorrhagic shock on propofol: A pharmacokinetic and pharmacodynamic analysis. Anesthesiology 99:409-420, 2003.
Kalff JC, Omert L, Tsukada K: Interleukin-6 production in hemorrhagic shock is accompanied by neutrophil recruitment and lung injury. American Journal of Physiology. Lung cellular and molecular physiology:Bethesda 19:611-622, 1998.
Kao SJ, Peng TC, Lee RP, Hsu K, Chen CF, Hung YK, Wang D, Chen HI: Nitric oxide mediates lung injury induced by ischemia -reperfusion in rats. J Biomed Sci 10:58-64, 2003.
Kelbela I, Weiss M: Anaesthetics and immune function. Anaesthesiology.
14:685-691, 2001.
Knaus W, Wagner D: Multiple systems organ failure: Epidemiology and prognosis. Crit Care Clin 5:221-232, 1989.
Kohlstaedt K, Page I: Hemorrhagic hypotension and its treatment by intra-arterial and intravenous infusion of blood. Arch Surg 47:178-191, 1943.
Kotani N, Hashimoto H, Sessler DI: Intraoperative modulation of alveolar macrophage function during isoflurane and propofol anesthesia. Anesthesiol 89:1125-1132, 1998.
Kotani N, Hashimoto H, Sessler DI: Expression of genes for proinflammatory cytokines in alveolar macrophages during propofol and isoflurane anesthesia. Anesth Analg. 89:1250-1256, 1999.
Kumar V, Abbars A, Fausto N: Pathologic basis of disease. philadelphia: Elsevier, 7th, 2004.
Laplace C, Huet O, Vicaut E, Ract C: Endothelial oxidative stress induced by serum from patients with severe trauma hemorrhage. Intensive Care Med 31:1171-1180, 2005.
Lamson P, Deturk W: Studies on shock induced by hemorrhge. J Pharmacol Exp Ther 83:250-252, 1945.
Lee RP, Wang D, Lin NT, Chen HI: A modified technique for tail-cuff pressure measurement in unrestrained rats at conscious state. J Biomed Sci 9:424-427, 2002.
Lee RP, Wang D, Lin NT, Chen HI: Physiological and chemical indicators for early and late stages of sepsis in conscious rats. J Biomed Sci 9:613-621, 2002.
Lee RP, Wang D, Kao SJ, Chen HI: The lung is the major site that produces nitric oxide to induce acute pulmonary oedema in endotoxin shock. Clin Exp Pharmacol Physiol 28:315-320, 2001.
Loeb AL, Godeny I, Longnecker DE: Anesthestics alter relative contributions of NO and EDHF in rat cremaster muscle microcirculation. Am J Physiol Heart Circ Physiol. 273:618-627, 1997.
Majde JA: Animal models for hemorrhage and resuscitation research. J Trauma. 54:s100-s105, 2003.
Marshall JC: Inflammation, coagulopathy, and the pathogenesis of multiple prgan dysfunction syndrome. Crit Care Med 29:s99-s106, 2001.
Mayeux PR: Pathobiology of lipopolysaccharide. J Toxicol Environ Health 51:415-435, 1997.
McCance KL, Huether SE: Pathophysiology:The biologic basis for disease inadults and children. St.Louis, Missouri USA: Mosby,Inc., 4th, 1483-1512, 2002.
Molina PE: Opiate modulation of hemodynamic, hormonal, and cytokine responses to hemorrhage. Shock 15:471-478, 2001.
Molina PE: Endogenous opioid analgesia in hemorrhagic shock. J Trauma 54:S126-132, 2003.
Moore KE, Murtaugh RJ: Pathophysiologic characteristics of hypovolemic shock. Vet Clin North Am Small Anim Pract 31:1115-1128, 2001.
Raedler C, Voelckel WG, Wenzel V: Treatment of uncontrolled hemorrhagic shock after liver trauma: Fatal effects of fluid resuscitation versus improved outcome after vasopressin. Anesth Analg. 98:1759-1766, 2000.
Ramos-Kelly JR, Toledo-Pereyra LH, Jordan J, Rivera-Chavez F, Rohs T, Holevar M, Dixon RA, Yun E, Ward PA: Multiple selectin blockade with a small molecule inhibitor downregulates liver chemokine expression and neutrophil infiltration after hemorrhagic shock. J Trauma 49:92-100, 2000.
Redl H, Schlag G: Pathophysiology of multiorgan failure-inflammatory factors and mediators. Clin intensive care 2:16-27, 1991.
Redl H, Gasser H, Schlag G, Marzi I: Involvement of oxygen radicals in shock related cell injury. Br Med Bull 49:556-565, 1993.Rhee P, Waxman K, Clark L, Kaupke CJ, Vaziri ND, Tominaga G, Scannell G: Tumor necrosis factor and monocytes are released during hemorrhagic shock. Resuscitation 25:249-255, 1993.
Rixen D, Raum M, Holzgraefe B: A pig hemorrhagic shock model: Oxygen debt and metabolic acidemia as indicators of severity. Shock. 16:239-244, 2001.
Sayeed MM, Baue AE: Mitochondrial metabolism of succinate, b-hydroxybutyrate, and a-ketoglutarate in hemorrhagic shock. Am J Physiol 220:1275-1281, 1971.
Schadt JC, Ludbrook J: Hemodynamic and neurohumoral resposes to acute hypovolemia in conscious mammals. Am J Physiol 260:H305-H318, 1991.
Schlag G, Redl H: Pathophysiology of shock, sepsis, and organ failure. New York: Springer-Verlag, p 371-383,1993.
Shibata K, Yamamoto Y, Kobayashi T, Murakami S: Beneficial effect of upper thoracic epidural anesthesia in experimental hemorrhagic shock in dogs: Influence of circulating catecholamines. Anesthesiol 74:303-308, 1991.
Singh G, Chaudry KI, Chaudry IH: Crystalloid is as effective as blood in the resuscitation of hemorrhagic shock. Ann. Surg. 215:377-382, 1992.
Solomonov E, Hirsh M, Yahiya A, Krausz MM: The effect of vigorous fluidresuscitation in uncontrolled hemorrhagic shock after massive splenic injury. Crit Care Med 28:749-754, 2000.
Stevens A, Abrams K, Brazier J, Fitzpatrick R, Lilford R: Methods in evidence based healthcare. Thousand Oaks, California: SAGE publications Inc, 1st, 2001.
Takasu A, Prueckner S, Tisherman SA, Stezoski SW, Stezoski J, Safar P: Effects of increased oxygen breathing in a volume controlled hemorrhagic shock outcome model in rats. Resuscitation 45:209-220, 2000.
Van Zutphen LMF, Baumans V, Beynen AC: Principles of laboratory animal science:A contribution to the humane use and care of animals to the quality of experiment results. Amsterdam: Elservier 1st ,P 17-74, 1993.
Wang D, Wei J, Hsu K, Jau JC, Lieu MW, Chao TJ, Chen HI: Effects of nitric oxide synthase inhibitors on systemic hypotension,cytokines and inducible nitric oxide synthase expression and lung injury following endotoxin administration in rats. J Biomed Sci 6:28-35, 1999.
Wang JD: Basic principles and practical applications in epidemiological research. New Jersey: World Scientific, 1st, 2002.
Wiggers CJ: The present status of the shock problem. Physiol Rev 22:74-123, 1942.
Xu H, Aibiki M, Yokono S: Dose-depenndent effects of propofol on renal sympathetic nerve activity, blood pressure and heart rate in urethane-anesthetized rabbits. Eur J Pharmacol. 387:79-85, 2000.
Yao YM, Sheng ZY, Tian HM, Wang YP, Yu Y, Fu XB, Lu LR, Wang DW, Ma YY: Gut-derived endotoxemia and multiple system organ failure following gunshot wounds combined with hemorrhagic shock: An experimental study in the dog. J Trauma 38:742-746, 1995.
Zingarelli B, Squadrito F, Altavilla D: Role of tumor necrosis factor-alpha in acute hypovolemic hemorrhagic shock in rats. Am J Physiol 266:H1512-1515, 1994.
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1. 朱天文,〈電影,小說的敵人!〉,台北:《聯合文學》第5卷第7期,1989年5月,頁56-57。
2. 朱天文,〈牧羊橋畔〉,台北:《聯合文學》第12卷第12期,1996年10月,頁16-17。
3. 朱天文,〈過站不停〉,台北:《印刻文學生活誌》第10期,2004年6月,頁14。
4. 朱天文,〈往事並不如煙〉,台北:《印刻文學生活誌》第11期,2004年7月,頁18。
5. 朱天文,〈巫事〉,台北:《印刻文學生活誌》第13期,2004年9月,頁60-90。
6. 朱天心,〈流水十九年〉,台北:《幼獅文藝》第76卷第2期,1992年8月,頁40-41。
7. 黃秋芳,〈在文學之外—朱天文走過「炎夏之都」〉,《自由青年》,台北:自由青年社,1988年1月,頁40。
8. 黃錦樹,〈悼祭之書〉,收入:朱天心著,《漫遊者》,台北:聯合文學出版社,2000年11月,頁6-25。
9. 王怡,〈胡蘭成其人其事〉,台北:《傳記文學》第403期,1995年12月,頁87-90。
10. 江弱水,〈胡蘭成的人格與文體—讀《今生今世》〉,台北:《讀書人》第24期,1997年2月,頁54-59。
11. 邱貴芬,〈想我(自我)放逐的(兄弟)姊妹們:閱讀第二代「外省」(女)作家朱天心〉,台北:《中外文學》第22卷第3期,1993年8月,頁94-115。
12. 張茂桂,〈台灣最棘手的政治問題—國家認同、族群平等「難分難解」〉,台北:《財訊》第168期,1996年3月,頁152-160+162-163。
13. 張瑞芬,〈一枝花語•話一枝花—論張愛玲、胡蘭成與朱天文〉,台北:《印刻文學生活誌》第11期,2004年7月,頁107-119。
14. 陳光達,〈朱天心:我不屬於台灣,要屬於哪裡?〉,台北:《新新聞》第559期,1997年11月19-11月24日,頁90+93-94。
15. 陳國偉,〈遺失地址的理想國—朱天心小說中的記憶烏托邦〉,台北:《淡水牛津文藝》創刊號,1998年10月,頁45-71。