The effects of lipopolysaccharide-induced endotoxic shock on the intestinal microcirculatory perfusion: an experimental study in pigs

Abstract Background Impairment of microcirculatory tissue perfusion is a central element of sepsis. Unfortunately, monitoring microcirculatory tissue perfusion to detect microcirculatory dysfunction at the bedside remains challenging. Therefore, the effects of sepsis and systemic infection on the intestinal microcirculatory tissue perfusion remain poorly understood. Methods In this experimental study, lipopolysaccharide was infused in six healthy female adult Yorkshire cross-breed pigs to induce endotoxic shock. Subsequently, animals were primarily resuscitated using fluids and subsequently with additional norepinephrine. The intestinal microcirculation was monitored using videomicroscopy with incident dark field imaging and quantified using the microvascular flow index. We primarily analyzed changes of the intestinal microvascular flow index. Additionally, we investigated the relationship between the intestinal microvascular flow index and other hemodynamic variables using repeated measures correlation r rm ( n ). Results The median (25th to 75th percentile) intestinal microvascular flow index decreased from 3.0 (2.9 to 3.0) at baseline to 2.5 (1.5 to 2.6) during endotoxic shock ( P = 0.027). After resuscitation with fluids, the intestinal microvascular flow index increased to 2.8 (2.8–2.9) and after additional norepinephrine administration to 3.0 (2.9–3.0). Intestinal heterogeneity index increased from 0.1 (0 to 0.1) to 0.4 (0.4 to 0.5) during endotoxic shock and returned to baseline levels 0 (0 to 0.1) after resuscitation with fluids and norepinephrine. The correlation between the microvascular flow index and mean arterial pressure was r rm (32) = 0.39 (95% CI 0.054 to 0.64; P = 0.024), and between the microvascular flow index and cardiac o utput r rm (32) = 0.21 (95% CI − 0.133, 0.515; P = 0.223). Conclusions In line with previous experimental studies, lipopolysaccharide-induced endotoxic shock impaired intestinal microcirculatory tissue perfusion and increased intestinal flow heterogeneity, both of which recovered after resuscitation with fluids and norepinephrine in this porcine model. Macrohemodynamic variables remained impaired after resuscitation and, therefore, correlated only weakly with the intestinal microvascular flow index. Thus, macrohemodynamic variables should not be used as a surrogate for microcirculatory tissue perfusion during endotoxic shock.