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Oncotic Pressure (oncotic + pressure)
Selected AbstractsThe rapidly adapting receptors in mammalian airways and their responses to changes in extravascular fluid volumeEXPERIMENTAL PHYSIOLOGY, Issue 4 2006C. Tissa Kappagoda In this short review, we shall focus on some recent findings on the physiological stimulus for the rapidly adapting receptors (RAR) of the airways. They are readily activated by a sustained inflation of the lungs and they are usually identified by their rapid adaptation to this stimulus. They are also activated by both tactile stimuli and irritant gases applied to the epithelium of the airways. The investigations reviewed here suggest that these receptors are activated by changes in extravascular fluid volume. The principal factors governing fluid flux from the microcirculation are identified in the Starling equation. These are the hydrostatic pressure, plasma oncotic pressure and capillary permeability. Findings from recent studies suggest that all these factors increase the activity of RAR. In addition, these receptors are also activated by obstruction of lymph drainage from the lung. Evidence is presented to show that manipulation of Starling forces also increases the extravascular fluid volume of the airways in areas where the RAR are located. On the basis of these findings, it is suggested that, along with mechanosensitivity to stimuli such as stretch, inflation and deflation, another physiological stimulus to the RAR is a change in extravascular fluid volume in the regions of the airways where these receptors are located. [source] Colloid Osmotic Pressure of Parenteral Nutrition Components and Intravenous FluidsJOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 4 2001Daniel L. Chan DVM Abstract Objective:Parenteral nutrition is an important part of therapy for critically ill animals that cannot tolerate enteral feedings. It has been hypothesized that parenteral nutrition might also play a role in increasing colloid osmotic pressure (COP). The purpose of this study was to measure COP of various parenteral nutrition components and compare them to the COP of commonly used intravenous solutions. Design:Membrane colloid osmometry was used to measure the COP of parenteral nutrition components (lipids, Abstractamino acids, dextrose solutions) and of synthetic colloids, crystalloids, and blood products. Main Results:Parenteral nutrition components and all crystalloid solutions had COP measurements < 1 mm Hg. Great variation in COP was found in the different artificial colloids and blood products. The COP of the artificial colloids tested ranged from 32.7 ± 0.2 mm Hg for hetastarch to 61.7 ± 0.5 mm Hg for dextran 70. Conclusions:The results of this in vitro study suggest that parenteral nutrition does not directly contribute to an increase in oncotic pressure. Further studies are needed to determine whether parenteral nutrition may indirectly influence COP in vivo. Knowing the COP of a fluid, along with its other properties, is useful in making appropriate therapeutic decisions. [source] Oxygen infusions (hemoglobin-vesicles and albumin-hemes) based on nano-molecular sciences,POLYMERS FOR ADVANCED TECHNOLOGIES, Issue 2-3 2005Professor Eishun Tsuchida Abstract Since the discovery of a red-colored saline solution of a heme derivative that reversibly binds and releases oxygen (1983), significant efforts have been made to realize an oxygen infusion as a red cell substitute based on the sciences of both molecular assembling phenomena and macromolecular metal complexes. The authors have specified that hemoglobin (Hb)-vesicles (HbV) and recombinant human serum albumin-hemes (rHSA-heme) would be the best systems that meet the clinical requirements. (A) Hb is rigorously purified from outdated, donated red cells via pasteurization and ultrafiltration, to completely remove blood type antigen and pathogen. The HbV encapsulates thus purified concentrated Hb solution with a phospholipid bimolecular membrane (diameter, 250,nm,), and its solution properties can be adjusted comparable with blood. Surface modification of HbV with a water-soluble polymer ensures stable dispersion state and storage over a year at 20°C. In vivo tests have clarified the efficacy for extreme hemodilution and resuscitation from hemorrhagic shock, and safety in terms of biodistribution, metabolism in reticuloendothelial system (RES), clinical chemistry, blood coagulation, etc. The HbV does not induce vasoconstriction thus maintains blood flow and tissue oxygenation. (B) rHSA is now manufactured in Japan as a plasma-expander. The rHSA can incorporate eight heme derivatives (axial base substituted hemes) as oxygen binding sites, and the resulting rHSA-heme is a totally synthetic O2 -carrier. Hb binds endothelium-derived relaxation factor, NO, and induces vasoconstriction. The rHSA-heme binds NO as Hb does, however, it does not induce vasoconstriction due to its low pI (4.8) and the resulting low permeability across the vascular wall (1/100 of Hb). A 5%-albumin solution possesses a physiologic oncotic pressure. Therefore, to increase the O2 -transporting capacity, albumin dimer is effective. Albumin dimer can incorporate totally 16 hemes with a regulated oncotic pressure. The rHSA-heme is effective not only as a red cell substitute but also for oxygen therapeutics (e.g. oxygenation for tumor). Significant efforts have been made to produce HbV and rHSA-heme with a facility of Good Manufacturing Practice (GMP) standard, and to start preclinical and finally clinical trials. Copyright © 2005 John Wiley & Sons, Ltd. [source] Liposome-Encapsulated Hemoglobin Alleviates Brain Edema After Permanent Occlusion of the Middle Cerebral Artery in RatsARTIFICIAL ORGANS, Issue 2 2009Akira T. Kawaguchi Abstract Liposome-encapsulated hemoglobin (LEH) was proven to be protective in cerebral ischemia/reperfusion injury. The present study evaluated LEH in a rat model of permanent middle cerebral artery (MCA) occlusion to clarify its effect during ischemia and reperfusion. Five minutes after thread occlusion of the MCA, rats were infused with 10 mL/kg of LEH (LEH, n = 13), and compared with normal controls (n = 11). Additional animals received the same MCA occlusion with no treatment (CT, n = 11), saline (saline, n = 10), empty liposome solution (EL, n = 13), or washed red blood cells (RBC, n = 7). Severity of brain edema was determined 24 h later by signal strength in T2-weighted magnetic resonance imaging of the cortex, striatum, hippocampus, and pyriform lobe. The results showed that brain edema/infarction observed in any vehicle-infused control was significantly more severe than in LEH-treated rats. There was a tendency toward aggravated edema in rats receiving ELs. LEH infusion at a dose of 10 mL/kg significantly reduced edema formation as compared to other treatments in a wide area of the brain 24 h after permanent occlusion of the MCA. Low oncotic pressure of EL and LEH solution (vehicle solution) appeared to cause nonsignificant aggravation of edema and reduced protective effects of LEH. [source] Diabetic macular oedema: physical, physiological and molecular factors contribute to this pathological processACTA OPHTHALMOLOGICA, Issue 3 2010Rita Ehrlich Abstract. Diabetic macular oedema (DMO) is an important cause of vision loss in patients with diabetes mellitus. The underlying mechanisms of DMO, on both macrocellular and microcellular levels, are discussed in this review. The pathophysiology of DMO can be described as a process whereby hyperglycaemia leads to overlapping and inter-related pathways that play a role not only in the initial vascular events, but also in the continued tissue insult that leads to chronic DMO. On a macrocellular level, DMO is believed to be in part caused by alterations in hydrostatic pressure, oxygen tension, oncotic pressure and shear stress. Three key components of the microvascular pathways include angiogenic factor expression, inflammation and oxidative stress. These molecular mediators, acting in conjunction with macrocellular factors, which are all stimulated in part by the hyperglycaemia and hypoxia, can have a direct endothelial effect leading to hyperpermeability, disruption of vascular endothelial cell junctions, and leukostasis. The interactions, signalling events and feedback loops between the various molecules are complicated and are not completely understood. However, by attempting to understand the pathways involved in DMO, we can help guide new treatment options targeted towards specific factors or mediators. [source] | ||||||||||