Schmidt W, Tinelli M, Secchi A, Gebhard M, Martin E, Schmidt H
Department of Anesthesiology, University of Heidelberg, Im Neuenheimer Feld 110, D-69120 Heidelberg, Germany.
Int J Surg Investig. 2001;2(5):359-67.
The objective of this study was to determine the effects of a continuous infusion of the phosphodiesterase inhibitor enoximone on mucosal villus blood flow in a normotensive model of endotoxemia.
Twenty-four anesthetized and ventilated rats underwent laparotomy and a ileal portion was exteriorized and opened by an antimesenteric incision. The ileal segment was fixed on a plexiglass stage with the mucosal surface upward. Microcirculatory parameters were assessed by intravital videomicroscopy. The animals were randomly assigned to receive one of three treatments: infusion of Escherichia coli lipopolysaccharides (LPS, 2 mg/kg/h) without phosphodiesterase inhibitor pretreatment (LPS group); or infusion of LPS with enoximone pretreatment (10 microg x kg(-1) x min(-1), start 30 min before LPS infusion, enoximone group), or infusion of an eqivalent volume of NaCl 0.9% (control group). Macrohemodynamic parameters (MAP, HR) and microhemodynamic parameters of ileal mucosa (mean diameter of central arterioles = DA, and mean erythrocyte velocity within the arterioles = VE) were measured 30 min before and at 0, 60, and 120 min after induction of endotoxemia. Mucosal villus blood flow was calculated from DA and VE.
In this normotensive endotoxemia model MAP remained stable in the control and the LPS group but significantly decreased in the enoximone group. The endotoxin-induced decrease of VE and DE of central arterioles of mucosal villi could be prevented. Thus, mucosal villus blood flow did not decrease compared to the LPS group.
Our results indicate that enoximone during an early stage of sepsis contributes to systemic hypotension but prevents mucosal hypoperfusion.
本研究的目的是确定在正常血压的内毒素血症模型中持续输注磷酸二酯酶抑制剂依诺昔酮对黏膜绒毛血流的影响。
24只麻醉并通气的大鼠接受剖腹手术,将一段回肠经肠系膜对侧切口外置并打开。将回肠段黏膜面朝上固定在有机玻璃台上。通过活体显微镜评估微循环参数。动物被随机分配接受三种处理之一:输注大肠杆菌脂多糖(LPS,2mg/kg/h)且无磷酸二酯酶抑制剂预处理(LPS组);或输注LPS并进行依诺昔酮预处理(10μg·kg⁻¹·min⁻¹,在LPS输注前30分钟开始,依诺昔酮组),或输注等量的0.9%氯化钠(对照组)。在内毒素血症诱导前30分钟以及诱导后0、60和120分钟测量宏观血流动力学参数(平均动脉压、心率)和回肠黏膜的微观血流动力学参数(中央小动脉平均直径 = DA,小动脉内平均红细胞速度 = VE)。根据DA和VE计算黏膜绒毛血流。
在这个正常血压的内毒素血症模型中,对照组和LPS组的平均动脉压保持稳定,但依诺昔酮组显著降低。内毒素诱导的黏膜绒毛中央小动脉的VE和DE降低可被预防。因此,与LPS组相比,黏膜绒毛血流没有减少。
我们的结果表明,脓毒症早期使用依诺昔酮会导致全身低血压,但可预防黏膜灌注不足。