Microvascular blood flow alterations are frequent in animal models of sepsis and may impair tissue oxygenation. We hypothesized that alterations of the microcirculation are present in patients with sepsis. We used an orthogonal polarization spectral imaging technique to investigate the sublingual microcirculation in 10 healthy volunteers, 16 patients before cardiac surgery, 10 acutely ill patients without sepsis (intensive care unit control subjects), and 50 patients with severe sepsis. The effects of topical application of acetylcholine (10(-2) M) were tested in 11 patients with sepsis. In each subject, five to seven sublingual areas were recorded and analyzed semiquantitatively. Data were analyzed with nonparametric tests and are presented as medians (25th-75th percentiles). No significant difference in microvascular blood flow was observed between healthy volunteers and patients before cardiac surgery or intensive care unit control subjects. The density of all vessels was significantly reduced in patients with severe sepsis (4.5 [4.2-5.2] versus 5.4 [5.4-6.3]/mm in volunteers, p < 0.01). The proportion of perfused small (< 20 microm) vessels was reduced in patients with sepsis (48 [33-61] versus 90 [89-92]% in volunteers, p < 0.001). These alterations were more severe in nonsurvivors. The topical application of acetylcholine totally reversed these alterations. In conclusion, microvascular blood flow alterations are frequent in patients with sepsis and are more severe in patients with a worse outcome.

Microvascular Blood Flow Is Altered in Patients with Sepsis

Objective:To characterize the time course of microcirculatory alterations and their relation to outcome in patients with septic shock.Design:Prospective, observational study.Setting:Thirty-one-bed, medico-surgical intensive care unit in a university hospital.Patients:Forty-nine patients with septic

Persistent microcirculatory alterations are associated with organ failure and death in patients with septic shock.

Previous studies have demonstrated the presence of myocardial depression in clinical and experimental septic shock. This depression is associated with the presence of a circulating myocardial depressant substance with physical characteristics consistent with cytokines. The present study utilized an in vitro myocardial cell assay to examine the role of various human recombinant cytokines, including tumor necrosis factor (TNF)alpha and interleukin (IL)1beta, in depression of cardiac myocyte contractile function induced by serum from humans with septic shock. The extent and velocity of electrically paced rat cardiac myocytes in tissue culture was quantified by a closed loop video tracking system. Individually, TNF-alpha and IL-1beta each caused significant concentration-dependent depression of maximum extent and peak velocity of myocyte shortening in vitro. In combination, TNF-alpha and IL-1beta induced depression of myocardial cell contractility at substantially lower concentrations consistent with a synergistic effect. Using immunoabsorption, removal of both TNF-alpha and IL-1beta (but not either alone) from the serum of five patients with acute septic shock and marked reversible myocardial depression resulted in elimination of serum myocardial depressant activity. IL-2, -4, -6, -8, -10, and interferon gamma failed to cause significant cardiac myocyte depression over a wide range of concentrations. These data demonstrate that TNF-alpha and IL-1beta cause depression of myocardial cell contraction in vitro and suggest that these two cytokines act synergistically to cause sepsis-associated myocardial depression in humans.

https://rupress.org/jem/article-pdf/183/3/949/1108067/949.pdf

Tumor necrosis factor alpha and interleukin 1beta are responsible for in vitro myocardial cell depression induced by human septic shock serum.

The microcirculation is a complex and integrated system that supplies and distributes oxygen throughout the tissues. The red blood cell (RBC) facilitates convective oxygen transport via co-operative binding with hemoglobin. In the microcirculation oxygen diffuses from the RBC into neighboring tissues, where it is consumed by mitochondria. Evidence suggests that the RBC acts as deliverer of oxygen and 'sensor' of local oxygen gradients. Within vascular beds RBCs are distributed actively by arteriolar tone and passively by rheologic factors, including vessel geometry and RBC deformability. Microvascular oxygen transport is determined by microvascular geometry, hemodynamics, and RBC hemoglobin oxygen saturation. Sepsis causes abnormal microvascular oxygen transport as significant numbers of capillaries stop flowing and the microcirculation fails to compensate for decreased functional capillary density. The resulting maldistribution of RBC flow results in a mismatch of oxygen delivery with oxygen demand that affects both critical oxygen delivery and oxygen extraction ratio. Nitric oxide (NO) maintains microvascular homeostasis by regulating arteriolar tone, RBC deformability, leukocyte and platelet adhesion to endothelial cells, and blood volume. NO also regulates mitochondrial respiration. During sepsis, NO over-production mediates systemic hypotension and microvascular reactivity, and is seemingly protective of microvascular blood flow.

/pdf/bench-to-bedside-review-microvascular-dysfunction-in-sepsis-b8wgnkk9jb.pdf

Bench-to-bedside review: Microvascular dysfunction in sepsis –hemodynamics, oxygen transport, and nitric oxide

Myocardial dysfunction in septic shock.

Lipopolysaccharide, tumor necrosis factor, and interleukin-1 interact to cause hypotension.

Capillary blood cell velocity was measured in a group of normotensive febrile patients as a basis for further study into the microvascular physiology of febrile hypotensive patients with sepsis. Television videomicroscopy was used to record the capillary blood cell movement in the finger nailfold. Analysis of all moving gaps in the red cell column seen during a minimum of 2 minutes was done by the frame-by-frame technique and mean blood cell velocity derived. Core (external auditory meatus) and skin (finger) temperature were also measured. Subjects (n = 6) were sex and skin temperature matched to controls. Although the mean skin temperature of subjects [28.73-degrees-C, SD = 0.28] was not significantly different to controls [30.63-degrees-C, SD = 3.11; p < 0.05] the mean velocity was significantly reduced in the febrile subject group [0.28 mm/sec, SD = 0.17] as compared with controls [0.56 mm/sec, SD = 0.22; p < 0.05]. It is likely therefore that these skin vessels vasoconstrict as part of the integrated response to reduce heat loss.

Capillary blood cell velocity is reduced in fever without hypotension.

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Lipopolysaccharide, tumor necrosis factor, and interleukin-1 interact to cause hypotension.

Capillary blood cell velocity is reduced in fever without hypotension.