Abstract
IntroductionDuring severe sepsis or septic shock, activation of the inflammatory and coagulatory systems can result in microcirculatory dysfunction as well as microvascular thrombosis, culminating in multiple organ dysfunction and death. Enoxaparin can inhibit factor Xa and attenuate endothelial damage. The primary purpose of this study was to investigate the effect of enoxaparin on intestinal microcirculation in endotoxemic rats.MethodsThirty male Wistar rats were divided into the following three groups: sham operated (OP); lipopolysaccharide (LPS); and LPS + Enoxaparin group. The rats received a midline laparotomy to exteriorize a segment of terminal ileum for microcirculation examination by full-field laser perfusion imager and sidestream dark field video microscope on mucosa, muscle, and Peyer's patch. In the LPS and LPS + Enoxaparin groups, 15 mg/kg LPS was administered intravenously to induce endotoxemia, and 400 IU/kg enoxaparin sodium was also administered in the LPS + Enoxaparin group.ResultsAt 240 minutes, the mean arterial pressure was higher in the LPS + Enoxaparin group than in the LPS group (93 ± 9 versus 64 ± 16 mm Hg, P < 0.001). Microcirculatory blood flow intensity was higher in the LPS + Enoxaparin group than in the LPS group as follows: mucosa (1085 ± 215 versus 617 ± 214 perfusion unit [PU], P < 0.001); muscle (760 ± 202 versus 416 ± 223 PU, P = 0.001); and Peyer's patch (1,116 ± 245 versus 570 ± 280 PU, P < 0.001). Enoxaparin inhibited LPS-induced reduction in perfused small vessel density and increase in heterogeneity of microcirculation.ConclusionsEnoxaparin can prevent intestinal microcirculatory dysfunction in endotoxemic rats by preventing microvascular thrombosis formation and maintaining normal mean arterial pressure.
Highlights
During severe sepsis or septic shock, activation of the inflammatory and coagulatory systems can result in microcirculatory dysfunction as well as microvascular thrombosis, culminating in multiple organ dysfunction and death
At 240 minutes, the mean arterial pressure was higher in the LPS + Enoxaparin group than in the LPS group (93 ± 9 versus 64 ± 16 mm Hg, P < 0.001)
At 240 minutes, the microcirculatory blood flow intensity was higher in the LPS + Enoxaparin group than in the LPS group as follows: mucosa (1,085 ± 215 versus 617 ± 214 perfusion unit (PU), P < 0.001); muscle (760 ± 202 versus 416 ± 223 PU, P = 0.001); and Peyer’s patch (1,116 ± 245 versus 570 ± 280 PU, P < 0.001)
Summary
During severe sepsis or septic shock, activation of the inflammatory and coagulatory systems can result in microcirculatory dysfunction as well as microvascular thrombosis, culminating in multiple organ dysfunction and death. Severe sepsis and septic shock are the leading causes of multiple organ dysfunction and death in patients admitted to ICUs. the Surviving Sepsis Campaign guidelines led to a decrease in hospital mortality [1], one-year mortality remains high ranging from 21.5% to 71.9% [2]. Increasing evidence supports the existence of an extensive cross-talk between inflammation and coagulation during sepsis [3], and activation of the inflammatory and coagulation systems and down regulation of endothelial-bound anticoagulant mechanisms can cause disseminated microvascular thrombosis [4]. The intestinal microcirculation provides an excellent site to investigate sepsis-related microcirculatory dysfunction [13,14]. A sidestream dark-field (SDF) video microscope has been used to visualize the small vessel and can calculate the small vessel density, microvascular flow index, and heterogeneity of microcirculation [8]
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