Diet-induced obesity prevents the development of acute traumatic coagulopathy

被引:7
|
作者
McCully, Belinda H. [1 ]
Dean, Rondi K. [1 ]
McCully, Sean P. [1 ]
Schreiber, Martin A. [1 ]
机构
[1] Oregon Hlth & Sci Univ, Trauma Res Inst Oregon, Div Trauma Crit Care & Acute Care Surg, Portland, OR 97219 USA
来源
JOURNAL OF TRAUMA AND ACUTE CARE SURGERY | 2014年 / 77卷 / 06期
关键词
Obesity; acute traumatic coagulopathy; hemorrhage; rats; RAT MODEL; RISK; SENSITIVITY; MORTALITY;
D O I
10.1097/TA.0000000000000461
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
BACKGROUND: Obesity and hemorrhagic shock following trauma are predictors of mortality but have conflicting effects on coagulation. Following hemorrhage, tissue injury and hypoperfusion lead to acute traumatic coagulopathy (ATC), producing a hypocoagulable state. Inversely, obesity promotes clotting and impairs fibrinolysis to yield a hypercoagulable state. High rates of venous thromboembolism, organ failure, and early mortality may be caused by hypercoagulability in obese patients. We hypothesize that obesity prevents the development of ATC following injury-induced hemorrhagic shock. METHODS: Male Sprague-Dawley rats (250-275 g) were fed a high-fat diet (32% kcal from fat) for 4 weeks to 6 weeks and diverged into obesity-resistant (OR, n = 9) and obesity-prone (OP, n = 9) groups. Age-matched control (CON) rats were fed normal diet (10% kcal from fat, n = 9). Anesthetized rats were subjected to an uncontrolled hemorrhage by a Grade V splenic injury to a mean arterial pressure (MAP) of 40 mm Hg. Hypotension (MAP, 30-40 mm Hg) was maintained for 30 minutes to induce shock. MAP, heart rate, lactate, base excess, cytokines, blood loss, and thrombelastography (TEG) parameters were measured before and after hemorrhagic shock. RESULTS: At baseline, OP rats exhibited a shorter time to 20-mm clot (K), and higher rate of clot formation (alpha angle), clot strength (maximal amplitude), and coagulation index, compared with the CON rats (p < 0.05), indicating enhanced coagulation. Physiologic parameters following shock were similar between groups. In the CON and OR rats, shock prolonged the time to clot initiation (R) and K and decreased a. angle and coagulation index (all p < 0.05 vs. baseline). In contrast, shock had no effect on these TEG parameters in the OP rats. Maximal amplitude was the only TEG parameter affected by shock in the OP rats, which was decreased in all groups. CONCLUSION: Obesity prevents the development of ATC following hemorrhage shock. Complications associated with obesity following hemorrhagic shock may be attributed to the preserved hypercoagulable state. (Copyright (C) 2014 by Lippincott Williams & Wilkins)
引用
收藏
页码:873 / 877
页数:5
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