The role of renal hypoperfusion in development of renal microcirculatory dysfunction in endotoxemic rats

To study the role of renal hypoperfusion in development of renal microcirculatory dysfunction in endotoxemic rats. Rats were randomized into four groups: a sham group (n = 6), a lipopolysaccharide (LPS) group (n = 6), a group in which LPS administration was followed by immediate fluid resuscitation which prevented the drop of renal blood flow (EARLY group) (n = 6), and a group in which LPS administration was followed by delayed (i.e., a 2-h delay) fluid resuscitation (LATE group) (n = 6). Renal blood flow was measured using a transit-time ultrasound flow probe. Microvascular perfusion and oxygenation distributions in the renal cortex were assessed using laser speckle imaging and phosphorimetry, respectively. Interleukin (IL)-6, IL-10, and tumor necrosis factor (TNF)-α were measured as markers of systemic inflammation. Furthermore, renal tissue samples were stained for leukocyte infiltration and inducible nitric oxide synthase (iNOS) expression in the kidney. LPS infusion worsened both microvascular perfusion and oxygenation distributions. Fluid resuscitation improved perfusion histograms but not oxygenation histograms. Improvement of microvascular perfusion was more pronounced in the EARLY group compared with the LATE group. Serum cytokine levels decreased in the resuscitated groups, with no difference between the EARLY and LATE groups. However, iNOS expression and leukocyte infiltration in glomeruli were lower in the EARLY group compared with the LATE group. In our model, prevention of endotoxemia-induced systemic hypotension by immediate fluid resuscitation (EARLY group) did not prevent systemic inflammatory activation (IL-6, IL-10, TNF-α) but did reduce renal inflammation (iNOS expression and glomerular leukocyte infiltration). However, it could not prevent reduced renal microvascular oxygenatio

Pathophysiology of microcirculatory dysfunction and the pathogenesis of septic shock

Multiple experimental and human trials have shown that microcirculatory alterations are frequent in sepsis. In this review, we discuss the various mechanisms that are potentially involved in their development and the implications of these alterations. Endothelial dysfunction, impaired inter-cell communication, altered glycocalyx, adhesion and rolling of white blood cells and platelets, and altered red blood cell deformability are the main mechanisms involved in the development of these alterations. Microcirculatory alterations increase the diffusion distance for oxygen and, due to the heterogeneity of microcirculatory perfusion in sepsis, may promote development of areas of tissue hypoxia in close vicinity to well-oxygenated zones. The severity of microvascular alterations is associated with organ dysfunction and mortality. At this stage, therapies to specifically target the microcirculation are still being investigated

Microcirculatory blood flow as a new tool for perioperative fluid management

Microcirculatory alterations often occur in the perioperative setting under the influence of multiple factors including hypovolemia, impaired cardiac function, vasoplegia, anesthetic agents, surgical trauma, ischemia/reperfusion injury, and sepsis. The severity and duration of these alterations have been related to the outcome of these patients. This systematic review will report to which extent these microvascular abnormalities can be affected by fluid administration. Administration of fluids usually improves microvascular dysfunction by increasing the perfused capillary density. Importantly, there is a significant variability among the patients. Timing of the intervention has a huge impact, as early interventions often lead to an improved microvascular perfusion, while delayed intervention often fails to improve the microcirculation. Of note, the impact of fluids on the microcirculation is relatively dissociated from its systemic effects and can thus not be predicted by changes in cardiac output or blood pressure. Changes in lactate or in venoarterial PCO2 gradients can be useful to indirectly evaluate the microvascular effects of fluids. Even though colloids are often associated with greater effects than crystalloids in experimental settings, this has not been confirmed in patients. Finally, the impact of red blood cell transfusions is highly variable and may depend on the severity of microvascular alterations at baseline.SCOPUS: ch.binfo:eu-repo/semantics/publishe

Monitoring the microcirculation.

One of the main goals of hemodynamic support is to preserve tissue perfusion. However issue perfusion is related more to microvascular perfusion than aortic blood flow. Monitoring the microcirculation has long been difficult. Recent technologic advances have made feasible monitoring of the microcirculation at bedside of critically ill patients. In this review, we will discuss the relevance of the various tools available to monitor the microcirculation. Videomicroscopic devices such as sidestream darkfield imaging are the most appropriate techniques to evaluate the microcirculation, taking into account the heterogeneous aspect of diseased microcirculation, as in sepsis. The microcirculation can also be indirectly assessed by measuring tissue PCO2. Transcutaneous PCO2 measurement at ear lobe is particularly promising. Finally, near infrared spectroscopy can also provide interesting information, especially using vascular occlusion tests which reactivity of the microcirculation to a transient hypoxic insult. These different devices have provided important data helping us to better understand the pathophysiology of sepsis and multiple organ failure.Journal ArticleReviewinfo:eu-repo/semantics/publishe

Monitoring the microcirculation in the critically ill patient: current methods and future approaches.

To discuss the techniques currently available to evaluate the microcirculation in critically ill patients. In addition, the most clinically relevant microcirculatory alterations will be discussed.Journal ArticleReviewSCOPUS: re.jinfo:eu-repo/semantics/publishe