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Advances in Experimental Medicine and... 2006Previous studies showed that endothelial alterations caused by physical stress worsened the hemorheological parameters mainly in patients affected by ischemic vascular... (Review)
Review
Previous studies showed that endothelial alterations caused by physical stress worsened the hemorheological parameters mainly in patients affected by ischemic vascular diseases: major vascular alterations have been found in patients with very high endothelial dysfunction indexes: these indexes are given by the various substances produced by the endothelium, but it is very difficult to have a value which clearly identifies the real state of the endothelial alteration. The function of the NO, an endogenous vasodilator whose synthesis is catalyzed by NOs, can be determined by the Citrulline/Arginine ratio, which represents the level of activity of the enzyme. A very good index of the endothelial dysfunction is asymmetric dimethylarginine (ADMA), a powerful endogenous inhibitor of NOs; in fact several studies have demonstrated a strong relationship between ischemic vascular disease and high levels of plasmatic ADMA. Our recent studies on heart failure and on ischemic cerebrovascular diseases evaluate endothelial dysfunctions and hemorheological parameters.
Topics: Animals; Endothelium, Vascular; Hemorheology; Humans; Microcirculation
PubMed: 16927678
DOI: 10.1007/0-387-29540-2_17 -
Critical Care Medicine Mar 2009
Topics: Animals; Erythrocytes; Erythrocytes, Abnormal; Microcirculation
PubMed: 19237948
DOI: 10.1097/CCM.0b013e318196fd86 -
Critical Care Medicine Sep 2007
Topics: Animals; Arginine Vasopressin; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Microcirculation; Swine
PubMed: 17713379
DOI: 10.1097/01.CCM.0000281638.21573.C4 -
Hypertension (Dallas, Tex. : 1979) Dec 2006
Topics: Animals; Antihypertensive Agents; Arterioles; Humans; Hypertension; Microcirculation; Muscle Contraction; Muscle, Smooth, Vascular; Vascular Resistance
PubMed: 17060505
DOI: 10.1161/01.HYP.0000249510.20326.72 -
Clinical and Experimental Pharmacology... 20021. Hyperglycaemia in the vast majority of humans with diabetes mellitus is the end result of profound insulin resistance secondary to obesity. For patients in treatment,... (Review)
Review
1. Hyperglycaemia in the vast majority of humans with diabetes mellitus is the end result of profound insulin resistance secondary to obesity. For patients in treatment, hyperglycaemia is usually not sustained but, rather, occurs intermittently. In in vivo studies of the rat intestinal microcirculation, endothelial impairment occurs within 30 min at D-glucose concentrations > or = 300 mg/dL. Endothelial-dependent dilation to acetylcholine and constriction to noradrenaline is impaired. Vasodilation to exogenous nitric oxide (NO) remains normal. 2. When initiated before hyperglycaemia, suppression of oxygen radicals by both scavenging and pretreatment with cyclo-oxygenase blockade to prevent oxygen radical formation minimized endothelial impairments during hyperglycaemia. Neither treatment was effective in restoring endothelial function once it was damaged by hyperglycaemia. 3. A mechanism that may initiate the arachidonic acid- oxygen radical process is activation of specific isoforms of protein kinase C (PKC). De novo formation of diacylglycerol during hyperglycaemia activates PKC. Blockade of the beta II PKC isoform with LY-333531 prior to hyperglycaemia protected NO formation within the arteriolar wall, as judged with NO-sensitive microelectrodes. Furthermore, once suppression of endothelial dilation was present in untreated animals, PKC blockade could substantially restore endothelial-dependent dilation. 4. These results indicate that acute hyperglycaemia is far from benign and, in the rat, causes rapid endothelial impairment. Both oxygen radical scavenging and cyclo-oxygenase blockade prior to bouts of hyperglycaemia minimize endothelial impairment with limited side effects. Blockade of specific PKC isozymes protects endothelial function both as a pre- or post-treatment during moderately severe hyperglycaemia.
Topics: Animals; Humans; Hyperglycemia; Intestinal Mucosa; Microcirculation; Rats
PubMed: 11906473
DOI: 10.1046/j.1440-1681.2002.03617.x -
Journal Des Maladies Vasculaires Apr 2001Three main types of approaches are currently used for the exploration of the microcirculation in man: Clinimetric measurements of the cutaneous temperature... (Review)
Review
Three main types of approaches are currently used for the exploration of the microcirculation in man: Clinimetric measurements of the cutaneous temperature (thermometry), skin color (chromametry) and tissue volume (leg or foot volumetry) allow a quantification of clinical indexes of skin blood flow, blood volume and edema that are useful in therapeutic trials. Global parameters evaluating the hemodynamic or nutritional efficacy of the microcirculation in a tissue sample (laser Doppler and TcPO(2)) are easy to perform in clinical routine. TcPO(2) measurements through Clarke electrodes or fluorescence lifetime imaging technology evaluate the nutritional efficacy of the microcirculation. Laser Doppler devices are producing a semi-quantitative index of superficial tissue perfusion, that can be split into a volumic and a velocimetric components; its high sensitivity makes it a valuable tool for clinical research, mainly for dynamic measurements of reactivity of the superficial microcirculation to various stimuli. New instruments are able to use two different frequencies in order to compare tissue perfusion at different depths beneath the skin surface. The combination of a laser probe and a small automate can produce a two-dimensional image allowing the evaluation of spatial heterogeneity in tissue perfusion. Visualization of the skin capillary bed, i.e. capillaroscopy, was recently improved by the emergence of flexible videomicroscopes easily allowing the exploration of the whole body skin surface and not only the classical site of the nailfold. The use of the method was therefore broadened from vascular acrosyndromes and connective tissue diseases to the whole spectrum of skin trophic changes of the extremities. Combination with digital image analysis systems allows the quantification of the microvascular and microlymphatic structure (quantitative appraisal of microangiopathies) and function (capillary hemodynamics and exchange). Laser-doppler and capillaroscopy can also be combined for the measurement of red blood cell velocity in single capillaries.
Topics: Capillaries; Hemodynamics; Humans; Laser-Doppler Flowmetry; Microcirculation; Regional Blood Flow; Skin; Skin Temperature
PubMed: 11319422
DOI: No ID Found -
Acta Physiologica (Oxford, England) Apr 2010Physiologically, macro- and microcirculation differ markedly as macrocirculation deals with pulsatile pressure and flow and microcirculation with steady pressure and...
Physiologically, macro- and microcirculation differ markedly as macrocirculation deals with pulsatile pressure and flow and microcirculation with steady pressure and flow. Various such haemodynamic aspects correspond to a large heterogeneity in the structure and function of the vascular tree. In the past, diseases such as hypertension and diabetes mellitus were classified on the basis of the structure and function of small and large arteries. The purpose of this paper is to review the cross-talk between the micro- and macrocirculation. We shall discuss this cross-talk from the perspective of the development, physiology and pathology of the entire arterial tree.
Topics: Antihypertensive Agents; Diabetes Mellitus; Microcirculation; Models, Biological; Regional Blood Flow; Rheology; Speech
PubMed: 20050837
DOI: 10.1111/j.1748-1716.2009.02073.x -
Klinika Oczna Mar 1983
Review
Topics: Humans; Microcirculation; Optic Nerve; Optic Neuritis
PubMed: 6355637
DOI: No ID Found -
Intensive Care Medicine Nov 2010
Topics: Fluid Therapy; Hemodynamics; Humans; Microcirculation; Sepsis
PubMed: 20725822
DOI: 10.1007/s00134-010-1973-7 -
Chest Apr 1992
Review
Topics: Animals; Humans; Lung; Microcirculation; Models, Cardiovascular; Pulsatile Flow; Rheology
PubMed: 1555433
DOI: 10.1378/chest.101.4.1135