The microcirculation is highly responsive to, and a vital participant in, the inflammatory response. All segments of the microvasculature (arterioles, capillaries, and venules) exhibit characteristic phenotypic changes during inflammation that appear to be directed toward enhancing the delivery of inflammatory cells to the injured/infected tissue, isolating the region from healthy tissue and the systemic circulation, and setting the stage for tissue repair and regeneration.
The best characterized responses of the microcirculation to inflammation include impaired vasomotor function, reduced capillary perfusion, adhesion of leukocytes and platelets, activation of the coagulation cascade, and enhanced thrombosis, increased vascular permeability, and an increase in the rate of proliferation of blood and lymphatic vessels. A variety of cells that normally circulate in blood (leukocytes, platelets) or reside within the vessel wall (endothelial cells, pericytes) or in the perivascular space (mast cells, macrophages) are activated in response to inflammation.
The activation products and chemical mediators released from these cells act through different well-characterized signaling pathways to induce the phenotypic changes in microvessel function that accompany inflammation. Drugs that target a specific microvascular response to inflammation, such as leukocyte–endothelial cell adhesion or angiogenesis, have shown promise in both the preclinical and clinical studies of inflammatory disease. Future research efforts in this area will likely identify new avenues for therapeutic intervention in inflammation.
source: Inflammation and the Microcirculation. D. Neil Granger and Elena Senchenkova. San Rafael (CA): Copyright © 2010 by Morgan & Claypool Life Sciences.
The microcirculation, comprised of the most distal segments of the vascular system, proceeds from an active network of arterioles to capillaries and venules in the periphery. Together, these vascular beds function to regulate blood flow and perfusion pressure. The microcirculation is responsible for optimizing the supply of nutrients and oxygen to various organs, while simultaneously removing metabolic waste products.
Consequently, the rate of blood flow through these beds is tightly controlled by the metabolic demands of the tissue they pervade and is finely tuned by the more proximal small arteries and resistance arterioles. It is widely acknowledged that the small arteries and arterioles account for the majority (80%) of vascular resistance to blood flow [1–3]. They also serve to protect downstream capillaries from the potential damaging effects of high perfusion pressure and, in turn, prevent end-organ damage [4]. Arteriolar lumen size can vary dramatically depending on various species, distinct vascular beds and intrinsic contractile status.
However, the common feature shared by arterioles across all vascular beds and species is the fact that they only possess one or two layers of smooth muscle cells in their arterial wall, which play a remarkably effective and fundamental role in regulating vascular contractility and local perfusion. Regulation of arteriolar diameter and blood flow in the microcirculation is a dynamic and well-controlled process that integrates signals from mechanical, chemical, hormonal and neuronal stimuli. This is also achieved by an ensemble of responses elicited by endothelial cells and smooth muscle cells [1,2]. Impaired arteriolar function, as observed in various cardiovascular pathologies such as hypertension, diabetes, stroke and aging, leads to vascular remodeling, tissue ischemia and organ damage [3,5–8]. Emerging evidence has shown that changes in the oxidative environment are often accompanied by the aforementioned vascular dysfunction and cardiovascular diseases in the microcirculation [6,9–12]. As a primary source for oxidative stress and reactive oxygen species (ROS) in vascular cells, the contribution of NADPHoxidases (Noxs) to the cardiovascular system in health and disease has been investigated in a plethora of studies [9–11,13–15]. In the microcirculation, Noxs are implicated in a variety of vascular pathologies including arteriolar remodeling [16,17] and endothelial dysfunction [18,19] in systemic microvessels, as well as impaired neurovascular coupling [20] and disrupted blood-brain barrier (BBB) integrity [21] in the cerebral circulation. The current review aims not to be an exhaustive review on the roles of all sources of oxidases in the microcirculation. Rather, the goal here is to survey what is known of the roles of Noxs in ROS generation in resistance arterioles and to summarize their contributions to microvascular physiology and pathophysiology in both cerebral and systemic microcirculation.
The microcirculation is a functionally independent entity that encompasses of arterioles, venules, and capillaries, with diameters ranging from 5 μm to 100 μm. The primary goal of the microcirculation is to adjust blood flow to match the changing nutritional needs of parenchymal cells and to remove byproducts of metabolism. Although the primary purpose of the microcirculation is to facilitate the delivery of oxygen and nutrients to the tissues, its endogenous vasomotor activity also influences.
source: A Review on Microvascular Hemodynamics: The Control of Blood Flow Distribution and Tissue Oxygenation> Author links open overlay panel Carlos J. Munoz MS, Alfredo Lucas MS, Alexander T. Williams BS, Pedro Cabrales PhD. Department of Bioengineering, University of California, 9500 Gilman Drive, La Jolla, CA 92093-0412, USA. Available online 10 February 2020, Version of Record 12 March 2020.
We use cookies to analyze website traffic and optimize your website experience. By accepting our use of cookies, your data will be aggregated with all other user data.