Chagnon Frederic, Bentourkia M'hamed, Lecomte Roger, Lessard Michel, Lesur Olivier
Groupe de Recherche en Physiopathologie Respiratoire, Université de Sherbrooke, PQ, Canada.
Crit Care Med. 2006 Jan;34(1):127-33. doi: 10.1097/01.ccm.0000190622.02222.df.
The pathophysiology of sepsis-induced myocardial dysfunction is still controversial. Whether microcirculatory hypoperfusion together with capillary leakage can occur in the heart wall also remains a matter of debate. The objective was to evaluate the impact of fluid resuscitation on endotoxin-induced myocardial dysfunction.
Adult rats were given intraperitoneal injection of endotoxin (lipopolysaccharide, Escherichia coli, 10 mg/kg) or phosphate-buffered solution, followed up by echocardiography and acetate micro-positron emission tomography scan imaging, together with final hemodynamic, biochemical, and pathologic evaluations up to 48 hrs.
University laboratory.
Pathogen-free male Wistar rats (350 g).
Influence of isovolumic fluid infusion type (saline vs. pentastarch) on these variables was assessed in 11 groups of six animals including an unchallenged control one.
Endotoxin injection induced a) myocardial dysfunction (decrease of approximately 15-20% in left ventricular ejection fraction); b) ventricular enlargement (approximately 1.5- to 1.7-fold increase in left ventricular systolic volume); c) cardiac output increase (10-15%); d) myocardial hypoperfusion ( approximately 1.5- to 2-fold decrease in acetate k1 constant rate); e) increased oxygen consumption (k2); and f) interstitial wall increase. Endotoxin injection also enhanced levels of arterial lactates and troponin I. Colloid (pentastarch) over crystalloid (saline) fluid resuscitation significantly reversed echocardiographic changes, some positron emission tomography imaging alterations, and lactate and troponin I levels without further enhancing interstitial spaces.
Endotoxin can induce reversible myocardial alterations with evidence of coronary hypoperfusion and heart wall enlargement/damage, some of which can be prevented by fluid resuscitation. The use of crystalloids is less beneficial than pentastarch.
脓毒症诱发的心肌功能障碍的病理生理学仍存在争议。心脏壁是否会同时出现微循环灌注不足和毛细血管渗漏也尚无定论。本研究旨在评估液体复苏对内毒素诱发的心肌功能障碍的影响。
成年大鼠腹腔注射内毒素（脂多糖，大肠杆菌，10mg/kg）或磷酸盐缓冲溶液，随后进行超声心动图和醋酸盐微正电子发射断层扫描成像，并在48小时内进行最终的血流动力学、生化和病理学评估。
大学实验室。
无特定病原体的雄性Wistar大鼠（350g）。
在11组每组6只动物（包括未接受挑战的对照组）中评估等容液体输注类型（生理盐水与羟乙基淀粉）对这些变量的影响。
注射内毒素可导致：a）心肌功能障碍（左心室射血分数降低约15%-20%）；b）心室扩大（左心室收缩容积增加约1.5-1.7倍）；c）心输出量增加（10%-15%）；d）心肌灌注不足（醋酸盐k1常数率降低约1.5-2倍）；e）氧消耗增加（k2）；f）间质壁增厚。注射内毒素还会提高动脉血乳酸和肌钙蛋白I水平。胶体液（羟乙基淀粉）复苏比晶体液（生理盐水）复苏能更显著地逆转超声心动图变化、一些正电子发射断层扫描成像改变以及乳酸和肌钙蛋白I水平，且不会进一步增加间质间隙。
内毒素可诱发可逆性心肌改变，表现为冠状动脉灌注不足和心脏壁扩大/损伤，其中一些改变可通过液体复苏预防。使用晶体液不如羟乙基淀粉有益。
