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American Journal of Physiology. Heart... Jul 2007Whereas large arteries dampen oscillations resulting from intermittent ventricular ejection, small arteries steadily deliver optimal blood flow to various organs as the... (Review)
Review
Whereas large arteries dampen oscillations resulting from intermittent ventricular ejection, small arteries steadily deliver optimal blood flow to various organs as the heart. The transition from pulsatile to steady pressure is influenced by several factors as wave travel, damping, and reflections, which are mainly determined by the impedance mismatch between large vessels and arteriolar bifurcations. The mechanism(s) behind the dampening of pressure wave in the periphery and the links between central and peripheral pulsatile pressure (PP) may determine cardiac damage. Active pathways participate to pulse widening and changes in pulse amplitude in microvessels. Steady and cyclic stresses operate through different transduction mechanisms, the former being focal adhesion kinase and the latter being free radicals and oxidative stress. Independently of mechanics, calcifications and attachment molecules contribute to enhance vessel wall stiffness through changes in collagen cross-links, proteoglycans, integrins, and fibronectin. Enhanced PP transmission may thus occur and precipitate organ damage at each time that autoregulatory mechanisms, normally protecting the heart from vascular injury, are blunted. Such circumstances, observed in old subjects with systolic hypertension and/or Type 2 diabetes mellitus, particularly under high-sodium diet, cause cardiac damage and explain why increased PP and arterial stiffness are significant predictors of morbidity and mortality in the elderly.
Topics: Animals; Blood Pressure; Heart; Heart Diseases; Humans; Microcirculation; Models, Cardiovascular; Pulsatile Flow
PubMed: 17369469
DOI: 10.1152/ajpheart.00063.2007 -
Minerva Anestesiologica Apr 2006The recent onset of orthogonal polarization spectral (OPS) imaging techniques has allowed the direct visualization of the microcirculation at the bedside of critically... (Review)
Review
The recent onset of orthogonal polarization spectral (OPS) imaging techniques has allowed the direct visualization of the microcirculation at the bedside of critically ill patients. A systematic review with particular emphasis on recent findings and implications in pathophysiological processes is presented. Using OPS techniques various investigators have observed microcirculatory alterations in critically ill patients, and especially in patients with severe sepsis and septic shock. These alterations include a decrease in vessel density and an increased proportion of non perfused or intermittently perfused capillaries, and these alterations can be fully reversed by the topical application of acetylcholine. Similar alterations are observed in patients with septic and cardiogenic shock. Persistent microvascular alterations are associated with the development of organ failure and death. In addition, the reversal of these alterations during resuscitation procedures is highly predictive of outcome. Unfortunately, the effects of many therapeutic interventions usually performed in critically ill patients are still not well defined, even though evidence coming from animal experiments is sometimes available. In particular, the role of fluid resuscitation, red blood cell transfusions, inotropic, vasoactive and anesthetic agents should be investigated. Microcirculation plays an important role in the pathogenesis of shock and organ dysfunction, especially in sepsis. The microcirculatory effects of various therapeutic interventions have still to be reported. OPS technique may become a valuable tool to monitor patients with circulatory failure.
Topics: Critical Care; Critical Illness; Humans; Microcirculation
PubMed: 16570031
DOI: No ID Found -
The Yale Journal of Biology and Medicine 1992When the barrier to acid back-diffusion is disrupted, there is a protective increase in gastric mucosal blood flow to help remove the back-diffusing acid. Only recently... (Review)
Review
When the barrier to acid back-diffusion is disrupted, there is a protective increase in gastric mucosal blood flow to help remove the back-diffusing acid. Only recently has the mechanism for calling forth this protective hyperemia been determined. The gastric mucosa and submucosa are innervated by many capsaicin-sensitive sensory nerve fibers containing vasodilator peptides. The gastric mucosal sensory neurons monitor for acid back-diffusion, and, when this process occurs, signal for a protective increase in blood flow via release of calcitonin gene-related peptide from the submucosal periarteriolar fibers. The endothelium-derived vasodilator, nitric oxide, plays an important role both in the maintenance of basal gastric mucosal blood flow and in the increase in blood flow that accompanies pentagastrin-stimulated gastric acid secretion. It also interacts with the capsaicin-sensitive sensory nerves in the modulation of the microcirculation to maintain mucosal integrity. Finally, it has been shown that neutrophils play an important role in various forms of mucosal injury. The leukocytes adhere to the vascular endothelium and contribute to injury by reducing blood flow via occlusion of microvessels, as well as by releasing mediators of tissue damage.
Topics: Animals; Gastrointestinal Diseases; Humans; Microcirculation; Regional Blood Flow; Stomach
PubMed: 1341071
DOI: No ID Found -
American Journal of Veterinary Research Dec 2023To investigate the effects of hemorrhagic shock and fresh whole blood resuscitation on the microcirculation and endothelial glycocalyx using sidestream dark field (SDF)...
OBJECTIVE
To investigate the effects of hemorrhagic shock and fresh whole blood resuscitation on the microcirculation and endothelial glycocalyx using sidestream dark field (SDF) imaging and plasma biomarkers.
ANIMALS
8 purpose-bred dogs.
METHODS
Pressure-targeted hemorrhagic shock was induced in anesthetized dogs. SDF measurement of perfused boundary region and microcirculatory variables (RBC flow, total vessel density, and relative and absolute capillary blood volume), biomarker measurement (heparan sulfate, hyaluronan, VE-cadherin, and syndecan-1), mean arterial blood pressure, and cardiac output measurement were performed before anesthesia (TP0), after induction (TP1), after hemorrhagic shock (TP2), and after 50% retransfusion (TP3) and 100% retransfusion (TP4).
RESULTS
At TP1, TP2, TP3, and TP4, mean arterial blood pressure was 74.25 ± 7.17 mm Hg, 49.50 ± 13.74 mm Hg, 63.50 ± 13.29 mm Hg, and 71.38 ± 8.77 mm Hg, and cardiac output was 2.57 ± 1.01 L/min, 0.8 ± 0.36 L/min, 1.81 ± 0.57 L/min, and 2.93 ± 1.22 L/min, respectively. Heparan sulfate, hyaluronan, syndecan-1, and VE-cadherin ranges were 24.80 to 77.72 ng/mL, 5.77 to 105.06 ng/mL, below detection to 1,545.69 pg/mL, and 0 to 2.52 ng/mL, respectively. Perfused boundary region, RBC flow, total vessel density, and relative and absolute capillary blood volume ranges were 1.75 to 2.68 µm, 89.6 to 584.5 µm/s, 51.7 to 1,914.3 mm/m2, 0.94 to 1.53 103 μm3, and 1.50 to 94.30 103 μm3, respectively. Heparan sulfate decreased significantly over time (P = .016). No significant differences were found for microcirculatory variables, perfused boundary regions, or other biomarkers.
CLINICAL RELEVANCE
This was the first study to assess microvascular dysfunction and endothelial shedding in a canine hemorrhagic shock model using SDF microscopy (Glycocheck) and plasma biomarkers. Further studies are needed to determine clinical relevance.
Topics: Dogs; Animals; Shock, Hemorrhagic; Microcirculation; Syndecan-1; Glycocalyx; Hyaluronic Acid; Biomarkers; Heparitin Sulfate; Dog Diseases
PubMed: 38041946
DOI: 10.2460/ajvr.23.06.0134 -
The Keio Journal of Medicine Sep 1990Pial arterioles of mice are studied by in vivo TV microscopy. Focal endothelial injury is produced by a laser/Evans blue technique. Moderate damage results in local... (Review)
Review
Pial arterioles of mice are studied by in vivo TV microscopy. Focal endothelial injury is produced by a laser/Evans blue technique. Moderate damage results in local platelet aggregation. Very slight damage, without electron microscopic evidence of injury, results in loss of many endothelium derived vasoactive factors. These include "EDRFs" for acetylcholine, bradykinin and calcium ionophore, and "EDCFs" for histamine and serotonin. In the cases of acetylcholine, histamine and serotonin, each agonist possesses an additional opposing action which is independent of endothelium. The latter action is unmasked by the endothelial injury. The balance between simultaneously acting endothelium dependent and endothelium independent actions is a determinant of the response to an agonist with two opposing actions. This balance is partly dependent upon initial tone. Thus the effect of the agonist depends on initial tone. One of the determinants of initial tone may be basal release of one or more EDRFs or EDCFs. Evidence in pial arterioles for the basal release of EDRF for acetylcholine, comes from our data showing that L-NMMA constricts these arterioles. L-NMMA is a known inhibitor of synthesis of "classical" EDRF from L-arginine. The response to L-ARG is relaxation. Both the response to L-NMMA and the response to L-ARG are abolished by laser/dye injury of the endothelium. Thus these agents are really acting via an endothelial mechanism in brain arterioles, just as has been reported for their actions in conductance vessels. Finally mild injury associated with loss of "EDRFs" is also accompanied by a reduced ability of pial arteriolar endothelium to repell activated platelets.
Topics: Animals; Brain; Endothelium, Vascular; Male; Mice; Mice, Inbred ICR; Microcirculation
PubMed: 2255125
DOI: 10.2302/kjm.39.137 -
Kidney International Apr 1998Developmental assembly of the renal microcirculation is a precise and coordinated process now accessible to experimental scrutiny. Although definition of the cellular... (Review)
Review
Developmental assembly of the renal microcirculation is a precise and coordinated process now accessible to experimental scrutiny. Although definition of the cellular and molecular determinants is incomplete, recent findings have reframed concepts and questions about the origins of vascular cells in the glomerulus and the molecules that direct cell recruitment, specialization and morphogenesis. New findings illustrate principles that may be applied to defining critical steps in microvascular repair following glomerular injury. Developmental assembly of endothelial, mesangial and epithelial cells into glomerular capillaries requires that a coordinated, temporally defined series of steps occur in an anatomically ordered sequence. Recent evidence shows that both vasculogenic and angiogenic processes participate. Local signals direct cell migration, proliferation, differentiation, cell-cell recognition, formation of intercellular connections, and morphogenesis. Growth factor receptor tyrosine kinases on vascular cells are important mediators of many of these events. Cultured cell systems have suggested that basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF) promote endothelial cell proliferation, migration or morphogenesis, while genetic deletion experiments have defined an important role for PDGF beta receptors and platelet-derived growth factor (PDGF) B in glomerular development. Receptor tyrosine kinases that convey non-proliferative signals also contribute in kidney and other sites. The EphB1 receptor, one of a diverse class of Eph receptors implicated in neural cell targeting, directs renal endothelial migration, cell-cell recognition and assembly, and is expressed with its ligand in developing glomeruli. Endothelial TIE2 receptors bind angiopoietins (1 and 2), the products of adjacent supportive cells, to signals direct capillary maturation in a sequence that defines cooperative roles for cells of different lineages. Ultimately, definition of the cellular steps and molecular sequence that direct microvascular cell assembly promises to identify therapeutic targets for repair and adaptive remodeling of injured glomeruli.
Topics: Animals; Kidney; Kidney Diseases; Microcirculation; Neovascularization, Physiologic
PubMed: 9551388
DOI: 10.1111/j.1523-1755.1998.00822.x -
British Journal of Anaesthesia Oct 2010
Topics: Anesthesia, General; Animals; Epinephrine; Gastrointestinal Tract; Humans; Microcirculation; Norepinephrine; Oxygen Consumption; Vasoconstrictor Agents
PubMed: 20837720
DOI: 10.1093/bja/aeq236 -
Critical Care (London, England) 2006Use of arginine vasopressin in the management of refractory vasodilatory shock has been associated with development of ischaemic skin lesions. Because of the increasing... (Review)
Review
Use of arginine vasopressin in the management of refractory vasodilatory shock has been associated with development of ischaemic skin lesions. Because of the increasing popularity of arginine vasopressin, it is important to evaluate its effects on microcirculatory blood flow. Such studies are crucial if we are to appreciate the microcirculatory consequences of our various resuscitation strategies. However, methodological issues must always be considered because they can significantly influence interpretation of the results. Some aspects of use of laser Doppler to evaluate the microcirculation are reviewed within the context of recent findings presented by Luckner and coworkers in this issue of Critical Care.
Topics: Arginine Vasopressin; Blood Flow Velocity; Humans; Infusion Pumps; Laser-Doppler Flowmetry; Microcirculation; Skin
PubMed: 16594988
DOI: 10.1186/cc4884 -
Hypertension (Dallas, Tex. : 1979) Jul 2014Over the past decade, increased aortic stiffness has emerged as an important risk factor for target organ damage and cardiovascular disease events. Aortic stiffness can...
Over the past decade, increased aortic stiffness has emerged as an important risk factor for target organ damage and cardiovascular disease events. Aortic stiffness can be assessed as pulse wave velocity (PWV), which is a measure of aortic wall stiffness, and pulse pressure (PP), which is affected by wall stiffness and the interaction between flow and diameter. Because these stiffness measures have different sensitivities to geometry and other factors, they are only moderately correlated and play a complementary role in risk prediction. Arterial stiffness has long been viewed as a complication of hypertension that integrates long-term adverse effects of elevated blood pressure and other risk factors. However, PWV is only modestly correlated with risk factors other than age and blood pressure, which likely explains the ability of PWV to add to standard risk prediction models and reclassify risk in a clinically relevant manner. Recent studies have demonstrated that stiffness can antedate and contribute to the pathogenesis of hypertension, raising the possibility that early assessment of arterial stiffness may provide insight into complications including hypertension that develop years later. The role that stiffness plays in the pathogenesis of hypertension and cardiovascular disease has sparked considerable interest in defining basic mechanisms that stiffen the aortic wall, increase PP and contribute to target organ damage with a hope that elucidation of these mechanisms will allow for development of more effective treatments.
Topics: Humans; Hypertension; Microcirculation; Vascular Stiffness
PubMed: 24752432
DOI: 10.1161/HYPERTENSIONAHA.114.00921 -
British Journal of Cancer Jan 2021During metastasis, tumour cells navigating the vascular circulatory system-circulating tumour cells (CTCs)-encounter capillary beds, where they start the process of... (Review)
Review
During metastasis, tumour cells navigating the vascular circulatory system-circulating tumour cells (CTCs)-encounter capillary beds, where they start the process of extravasation. Biomechanical constriction forces exerted by the microcirculation compromise the survival of tumour cells within capillaries, but a proportion of CTCs manage to successfully extravasate and colonise distant sites. Despite the profound importance of this step in the progression of metastatic cancers, the factors about this deadly minority of cells remain elusive. Growing evidence suggests that mechanical forces exerted by the capillaries might induce adaptive mechanisms in CTCs, enhancing their survival and metastatic potency. Advances in microfluidics have enabled a better understanding of the cell-survival capabilities adopted in capillary-mimicking constrictions. In this review, we will highlight adaptations developed by CTCs to endure mechanical constraints in the microvasculature and outline how these mechanical forces might trigger dynamic changes towards a more invasive phenotype. A better understanding of the dynamic mechanisms adopted by CTCs within the microcirculation that ultimately lead to metastasis could open up novel therapeutic avenues.
Topics: Animals; Humans; Microcirculation; Microfluidics; Neoplasm Invasiveness; Neoplastic Cells, Circulating
PubMed: 33257836
DOI: 10.1038/s41416-020-01176-x