Contrasting effects of colloid and crystalloid resuscitation fluids on cardiac vascular permeability
ABSTRACT Fluid extravasation may lead to myocardial edema and consequent reduction in ventricular function. Albumin is presumed to interact with the endothelial glycocalyx. The authors' objective was to compare the impact of different resuscitation fluids (human albumin, hydroxyethyl starch, saline) on vascular integrity.
In an isolated perfused heart model (guinea pig), Krebs-Henseleit buffer was augmented with colloids (one third volume 5% albumin or 6% hydroxyethyl starch 130/0.4) or crystalloid (0.9% saline). Perfusion pressure and vascular fluid filtration (epicardial transudate formation) were assessed at different flow rates. After global, stopped-flow ischemia (37 degrees C, 20 min), hearts were reperfused with the same resuscitation fluid additives. In a second series, the authors applied the respective perfusates after enzymatic digestion of the endothelial glycocalyx (heparinase, 10 U over 15 min).
Both 5% albumin and 6% hydroxyethyl starch decreased fluid extravasation versus saline (68.4 +/- 5.9, 134.8 +/- 20.5, and 436.8 +/- 14.7 microl/min, respectively, at 60 cm H(2)O perfusion pressure; P < 0.05), the corresponding colloid osmotic pressures being 2.95, 5.45, and 0.00 mmHg. Digestion of the endothelial glycocalyx decreased coronary integrity in both colloid groups. After ischemia, a transient increase in vascular leak occurred with Krebs-Henseleit buffer containing hydroxyethyl starch and saline, but not with albumin. The authors observed no difference between intravascular and bulk interstitial colloid concentration in the steady state. Notwithstanding, electron microscopy revealed an intact endothelial glycocalyx and no interstitial edema in the albumin group.
Ex vivo, albumin more effectively prevented fluid extravasation in the heart than crystalloid or artificial colloid. This effect was partly independent of colloid osmotic pressure and may be attributable to an interaction of albumin with the endothelial glycocalyx.
SourceAvailable from: Nadine Regenscheit[Show abstract] [Hide abstract]
ABSTRACT: To (1) review the development and medical applications of hydroxyethyl starch (HES) solutions with particular emphasis on its physiochemical properties; (2) critically appraise the available evidence in human and veterinary medicine, and (3) evaluate the potential risks and benefits associated with their use in critically ill small animals. Human and veterinary original research articles, scientific reviews, and textbook sources from 1950 to the present. HES solutions have been used extensively in people for over 30 years and ever since its introduction there has been a great deal of debate over its safety and efficacy. Recently, results of seminal trials and meta-analyses showing increased risks related to kidney dysfunction and mortality in septic and critically ill patients, have led to the restriction of HES use in these patient populations by European regulatory authorities. Although the initial ban on the use of HES in Europe has been eased, proof regarding the benefits and safety profile of HES in trauma and surgical patient populations has been requested by these same European regulatory authorities. The veterinary literature is limited mostly to experimental studies and clinical investigations with small populations of patients with short-term end points and there is insufficient evidence to generate recommendations. Currently, there are no consensus recommendations regarding the use of HES in veterinary medicine. Veterinarians and institutions affected by the HES restrictions have had to critically reassess the risks and benefits related to HES usage based on the available information and sometimes adapt their procedures and policies based on their reassessment. Meanwhile, large, prospective, randomized veterinary studies evaluating HES use are needed to achieve relevant levels of evidence to enable formulation of specific veterinary guidelines. © Veterinary Emergency and Critical Care Society 2015.01/2015; 25(1):20-47. DOI:10.1111/vec.12283
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ABSTRACT: The endothelial glycocalyx has a profound influence at the vascular wall on the transmission of shear stress, on the maintenance of a selective permeability barrier and a low hydraulic conductivity, and on attenuating firm adhesion of blood leukocytes and platelets. Major constituents of the glycocalyx, including syndecans, heparan sulphates and hyaluronan, are shed from the endothelial surface under various acute and chronic clinical conditions, best characterised being ischaemia and hypoxia, sepsis and inflammation, atherosclerosis, diabetes, renal disease and haemorrhagic viral infections. Damage has also been detected by in vivo microscopic techniques. Matrix metalloproteases may shed syndecans, and heparanase released from activated mast cells cleaves heparan sulphates from core proteins. According to new data, not only hyaluronidase but also the serine proteases thrombin, elastase, proteinase 3 and plasminogen, as well as cathepsin B lead to loss of hyaluronan from the endothelial surface layer, suggesting a wide array of potentially destructive conditions. Appropriately, pharmacological agents such as inhibitors of inflammation, antithrombin and inhibitors of metalloproteases display potential to attenuate shedding of the glycocalyx in various experimental models. Also, plasma components, especially albumin, stabilize the glycocalyx and contribute to the endothelial surface layer. Though symptoms of the above listed diseases and conditions correlate to sequelae expected from disturbance of the endothelial glycocalyx (oedema, inflammation, leukocyte and platelet adhesion, low-reflow), therapeutic studies to prove a causal connection have yet to be designed. With respect to studies on humans, some clinical evidence exists for benefits from application of sulodexide, a preparation delivering precursors of the glycocalyx constituent heparan sulphate. At present, the simplest option for protecting the glycocalyx seems to be ensuring for an adequate level of albumin. However, also in this case, definite proof of causality needs to be delivered. This article is protected by copyright. All rights reserved.British Journal of Clinical Pharmacology 03/2015; DOI:10.1111/bcp.12629 · 3.69 Impact Factor
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ABSTRACT: Endothelial glycocalyx degradation induced by fluid overload adds to the concern of a detrimental effect of uncontrolled fluid resuscitation and the risk of unnecessary fluid infusion. As a consequence, the use of new tools for monitoring response to fluids appears promising. From that perspective, the monitoring of plasma concentration of glycocalyx degradation markers could be useful.Critical care (London, England) 01/2014; 18(6):707. DOI:10.1186/s13054-014-0707-6