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Mechanisms of organ failure and abnormal oxygen metabolism during sepsis

脓毒症期间器官衰竭和氧代谢异常的机制

基本信息

批准号：
16390515
负责人：
KUWAGATA Yasuyuki
金额：
$ 9.09万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2006
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16390515/
关键词：
circulatory shock oxygen delivery oxygen consumption sepsis cytokine 人工赤血球

项目摘要

This study was based on our previous findings that abnormal dependency of systemic oxygen consumption (VO_2) on systemic oxygen delivery (DO_2) occurred during the supply-independent range of DO_2 in a rabbit IL-1β-induced septic shock model (SHOCK 14:193-9,2000). In the present series of study, we identified the organ responsible for the development of the abnormal oxygen metabolism during sepsis. Hemodynamics during hyperdynamic sepsis was reproduced by 1 mg/kg i.v. administration of lipopolysaccharide (LPS) to rabbits. Each animal was monitored invasively with an arterial catheter, a Swan-Ganz catheter, and an ultrasonic probe placed on the superior mesenteric vein (SMV). In addition, mucosal blood flow of the ileum was monitored by the surface Doppler scan method. The animals developed hypotension with metabolic acidosis by 90 min after the administration of LPS in the presence of the consistent or somewhat increased cardiac output. This vasomotor shock persisted by 240 min after the administration of LPS. The SMV blood flow was increased approximately by 50% from the baseline value. In contrast, mucosal blood flow of the ileum was decreased initially by 67% from the baseline value approximately by 120 min after LPS, and returned gradually to the baseline value by 240 min. The heterogeneity of the blood flow assessed by a relative dispersion of the blood flow to an area of ileal mucosa was significantly increased after LPS regardless of a period of time. These results suggest a significant role of the gut tissue in the development of systemic abnormalities in hemodyamics and oxygen metabolism.

本研究是基于我们以前的研究结果（SHOCK 14：193- 9，2000），即在IL-1β诱导的感染性休克家兔模型中，在不依赖于氧供应的氧耗（VO_2）范围内，发生了体循环氧耗（VO_2）对体循环氧输送（DO_2）的异常依赖性。在本系列研究中，我们确定了在脓毒症期间负责发展异常氧代谢的器官。通过静脉注射脂多糖（LPS）1 mg/kg，复制了高动力性脓毒症时的血流动力学。用动脉导管、Swan-Ganz导管和放置在上级肠系膜静脉（SMV）上的超声探头侵入性监测每只动物。此外，通过表面多普勒扫描方法监测回肠粘膜血流。在心输出量持续增加或略有增加的情况下，动物在给予LPS后90分钟出现低血压伴代谢性酸中毒。这种血管性休克持续240分钟后，管理的LPS。SMV血流量较基线值增加约50%。与此相反，回肠的粘膜血流量最初下降了67%，从基线值约120分钟后，LPS，并逐渐返回到基线值240分钟。的异质性评估的血流相对分散的回肠粘膜面积的血流显着增加LPS后，无论一段时间。这些结果表明，肠道组织在血液动力学和氧代谢系统异常的发展中起着重要作用。