Abstract
DURING SEVERE ACUTE anaphylactic shock, circulating blood volume may decrease by as much as 50%. This has been attributed to an increased vascular permeability with a shift of intravascular fluid into the extravascular space within minutes, resulting in hypotension and hemoconcentration. In the systemic capillary leak syndrome (Clarkson disease), it has been proposed that the increased vascular permeability is caused by a transient endothelial dysfunction, but in the case of anaphylaxis, evidence for this hypothesis is lacking. Endothelial function can be assessed by measurement of the postocclusive reactive hyperemia (PORH) response. PORH refers to the reproducible transient increase in blood flow after the release of an arterial occlusion. When the occluding cuff is released, the sudden restoration of blood flow causes an endothelium-dependent, flow-mediated vasodilatation. The velocity and degree of flow restoration depend on the capacity of the microvasculature to recruit arterioles and capillaries, thereby reflecting the integrity of the microcirculation. PORH usually is assessed using Doppler flowmetry. Recently, near-infrared spectroscopy (NIRS) has been introduced as a way to quantify the endothelium-mediated changes in vascular tone, elicited by inducing PORH. NIRS has proved to provide excellent reproducibility, and a coherent directional change with simultaneously performed strain gauge plethysmography and radionuclide plethysmography. In a recent systematic review and meta-analysis, it has been demonstrated that NIRS-derived PORH variables allowed discrimination between normal and abnormal states of microcirculation. The authors report the PORH response assessed by NIRS in a case of acute anaphylaxis. The responses during this event were suggestive of the presence of transient impairment of microvascular reactivity.
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