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肠道在脓毒症早期引发高动力反应中的重要作用。

The important role of the gut in initiating the hyperdynamic response during early sepsis.

作者信息

Yang S, Koo D J, Chaudry I H, Wang P

机构信息

Center for Surgical Research, Brown University School of Medicine, Providence, Rhode Island 02903, USA.

出版信息

J Surg Res. 2000 Mar;89(1):31-7. doi: 10.1006/jsre.1999.5807.

Abstract

BACKGROUND

Although the initial response to sepsis includes a hyperdynamic phase and although the increased hepatic perfusion in early sepsis is due solely to the increased portal blood flow, it remains unknown whether the gut plays an important role in producing such a response.

MATERIALS AND METHODS

Adult male Sprague-Dawley rats underwent a complete enterectomy (ER) before being subjected to sepsis by cecal ligation and puncture (CLP; the cecum was excised from the removed gut and stitched to the posterior peritoneum in ER groups) or sham operation. At 2 h after CLP (i.e., the early, hyperdynamic phase of sepsis), cardiac output and heart performance (+/-dP/dt(max)), as well as hepatic and renal blood flow, were measured. Systemic and regional oxygen delivery (DO(2)) and oxygen consumption (VO(2)) were also determined.

RESULTS

Cardiac output, heart performance, organ blood flow, as well as DO(2) and VO(2), increased significantly 2 h after CLP. ER prior to the onset of sepsis, however, prevented the elevation of those parameters. ER in sham animals did not alter the measured parameters with the exception that portal blood flow decreased by 85% and hepatic arterial blood flow increased by 368%, resulting in no significant reduction in hepatic DO(2) and VO(2). There were no changes in circulating blood volume among groups, indicating that the effect of ER on hemodynamics after CLP was not due to alterations in blood volume.

CONCLUSION

Since ER immediately before the onset of sepsis prevents the increase in cardiac output and regional hemodynamics, the gut appears to play an important role in producing the hyperdynamic response during the early stage of polymicrobial sepsis.

摘要

背景

尽管对脓毒症的初始反应包括高动力阶段,且早期脓毒症时肝脏灌注增加仅归因于门静脉血流增加,但肠道在产生这种反应中是否起重要作用仍不清楚。

材料与方法

成年雄性Sprague-Dawley大鼠在进行盲肠结扎和穿刺以诱发脓毒症(CLP;在进行全肠切除术的组中,将盲肠从切除的肠道中取出并缝合到后腹膜)或假手术之前先接受全肠切除术(ER)。在CLP后2小时(即脓毒症的早期高动力阶段),测量心输出量和心脏功能(±dP/dt(max)),以及肝和肾血流量。还测定了全身和局部的氧输送(DO(2))和氧消耗(VO(2))。

结果

CLP后2小时,心输出量、心脏功能、器官血流量以及DO(2)和VO(2)均显著增加。然而,在脓毒症发作前进行ER可阻止这些参数的升高。假手术动物进行ER除门静脉血流减少85%和肝动脉血流增加368%外,未改变所测参数,导致肝DO(2)和VO(2)无显著降低。各组间循环血量无变化,表明ER对CLP后血流动力学的影响不是由于血容量改变所致。

结论

由于在脓毒症发作前立即进行ER可阻止心输出量和局部血流动力学的增加,肠道似乎在多微生物脓毒症早期产生高动力反应中起重要作用。

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