Abstract
The microcirculation is not merely a passive conduit for red cell transport, nutrient and gas exchange, but is instead a dynamic participant contributing to the multiple processes involved in the maintenance of metabolic homeostasis and optimal end-organ function. The microcirculation's angioarchitechture and surface properties influence conduit function and flow dynamics over a wide spectrum of conditions, accommodating many different mechanical, pathological or organ-specific responses. The endothelium itself plays a critical role as the interface between tissues and blood components, participating in the regulation of coagulation, inflammation, vascular tone, and permeability. The complex nitric oxide pathways affect vasomotor tone and influence vascular conduit caliber and distribution density, alter thrombotic propensity, and modify adhesion molecule expression. Nitric oxide pathways also interact with red blood cells and free hemoglobin moieties in normal and pathological conditions. Red blood cells themselves may affect flow dynamics. Altered rheology and compromised NO bioavailability from medical storage or disease states impede microcirculatory flow and adversely modulate vasodilation. The integration of the microcirculation as a system with respect to flow modulation is delicately balanced, and can be readily disrupted in disease states such as sepsis. This review will provide a description of these varied and intricate functions of the microvasculature.
Original language | English (US) |
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Pages (from-to) | 61-68 |
Number of pages | 8 |
Journal | Transfusion and Apheresis Science |
Volume | 43 |
Issue number | 1 |
DOIs | |
State | Published - Aug 2010 |
Bibliographical note
Funding Information:We apologize for not having been able to cite all relevant studies. We wish to acknowledge Jean Kulander and James Kiley for manuscript assistance. This work was support by the Vikings Children’s Fund and University Pediatrics Foundation Grant (to A. Somani) and by the National Institutes of Health (PO1-HL55552 to R.P. Hebbel). We have no conflicts of interest to declare.