Abstract
A number of vascular-disease processes damage resistance microvessels. These include acute’ and chronic hypertension,2 diabetes mellitus 3,4 some connective tissue diseases 5 burn6 and frostbite7 injuries, and injury from ischemia followed by reperfusion 8-11 Damage to microvessels poses a precarious insult to the organism because the microvasculature is ultimately responsible for oxygen delivery to the tissues. It has recently been shown that autocoid products of the endothelium, such as endothelium-derived relaxing factor(s) (EDRF), play an important regulatory role in microvascular tone.12,13 This endothelial control of vascular smooth-muscle function is now known to be an active component of microvascular resistance and is therefore an important regulator of blood flow for critical metabolic processes. It is now postulated that, in a number of disease states, microvascular endothelial dysfunction, structural damage to the endothelium of microvessels, or abnormal endo-thelium—blood-component interactions (e.g., of endothelial cells of the microcirculation with platelets and neutrophils) are crucial pathophysiologic events that lead to microvascular damage and the death of cells dependent on the microvasculature blood flow. Oxygen radicals have been implicated as a mechanism of vascular injury in a number of diverse disease states. Recently the interaction between oxy radicals and microvascular endothelium-dependent function has gained considerable interest. Below, we review some of the acute mechanisms that damage resistance blood vessels.
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Marshall, J.J., Kontos, H.A. (1991). Acute-Microvascular-Injury Mechanisms. In: Bevan, J.A., Halpern, W., Mulvany, M.J. (eds) The Resistance Vasculature. Vascular Biomedicine. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-4612-0403-9_22
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