Impaired glycocalyx barrier properties and increased capillary tube haematocrit

Chappell, Daniel; Jacob, Matthias; Paul, Oliver; Mehringer, L.; Newman, Walter; Becker, Bernhard F.

doi:10.1113/jphysiol.2008.160648

Cited by 12 publications

(9 citation statements)

References 6 publications

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“…For example, Chappell and colleagues (18) proposed changes to the classic equation in a “revised Starling principle”, to incorporate the relevance of the glycocalyx by establishing the pressures Π p and Π if to Π esl (oncotic pressure within the endothelial surface layer) and Π b (oncotic pressure beneath the endothelial surface layer). The glycocalyx is the inner lining of the vascular endothelium and presents therefore the second important barrier line beside the endothelial cells (20,21). Chappell et al further summarize that the endothelial glycocalyx can bind free plasma and they form together the endothelial surface layer and that an oncotic gradient seems to be present directly across the endothelial surface layer, that defines finally vascular integrity, so that the presence of this layer should be the basic requirement for a physiologic barrier function (21).…”

Section: Discussionmentioning

confidence: 99%

“…The glycocalyx is the inner lining of the vascular endothelium and presents therefore the second important barrier line beside the endothelial cells (20,21). Chappell et al further summarize that the endothelial glycocalyx can bind free plasma and they form together the endothelial surface layer and that an oncotic gradient seems to be present directly across the endothelial surface layer, that defines finally vascular integrity, so that the presence of this layer should be the basic requirement for a physiologic barrier function (21). Additionally Svensen et al, (22) showed that in septic and burn-injured sheep that the intravascular retention of infused fluid is paradoxically maintained despite increased microvascular protein permeability and a reduced plasma-to-tissue oncotic gradient (22).…”

Section: Discussionmentioning

confidence: 99%

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Isoproternenol Increases Vascular Volume Expansion And Urinary Output After a Large Crystalloid Bolus in Healthy Volunteers

Asmussen¹,

Salter²,

Prough³

et al. 2014

Shock

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Background The primary goal of fluid therapy is to maintain fluid homeostasis. Commonly used isotonic crystalloids are only marginally effective and contribute to fluid excess syndrome. In patients with decreased cardiovascular reserve, fluid therapy alone is not sufficient to maintain end-organ perfusion. Therefore, inotropes or vasoactive drugs are used to supplement fluid infusion. Recent animal data suggests that co-infusion of adrenergic agents modulate the distribution of fluid between the vascular and extravascular/interstitial compartments after a fluid bolus. We sought to determine if this effect would translate in humans by co-administering a beta (β)-adrenergic agonist with fluid. Methods Nine healthy volunteers (age 21–50 yrs) were randomly paired and received either a continuous isoproterenol infusion (ISO:0.05μg/kg/min) or 0.9% saline (control(CON)) 30min prior to a 25mL/kg 0.9% NaCl fluid bolus. Hemodynamics, ventricular volume and function and microcirculatory determinants (capillary filtration coefficient (CFC) and oncotic pressure) were measured. Vascular and extra-vascular volume (EVV) and fluid balance were determined. Results Compared to CON, ISO significantly increased heart rate (CON:64.2 ±4.1 bpm vs. ISO:97.4±5.7 bpm) and cardiac output (CON 4.4±0.7L/min vs. ISO:10.2±0.9) before fluid bolus. ISO significantly increased urinary output (ISO: 10.86±1.95 vs Control: 6.53±1.45 mL/kg) and reduced EVV (7.98±2.0 vs 14.15±1.1mL/kg). ISO prevented an increase in CFC (1.74±0.4 vs 3.21±0.4 mL/min/mmHg•10−3). Conclusion Isoproterenol, a non-selective β-adrenergic agonist, augments vascular volume expansion and eliminates EVV via enhanced diuresis, which may in part be due to enhanced endothelial barrier function.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Isoproternenol Increases Vascular Volume Expansion And Urinary Output After a Large Crystalloid Bolus in Healthy Volunteers

Asmussen¹,

Salter²,

Prough³

et al. 2014

Shock

View full text Add to dashboard Cite

show abstract

“…This concept describes the EG as a second competent barrier for fluid and protein shifts 10 . According to this model there are two competent barriers in the vascular system: the EG and the endothelial cell line, which can also act against extravasation especially in case of a damaged EG 14,30 . The EG is probably a particularly fragile structure and the vascular barrier would be too vulnerable, if this structure alone would be responsible for the complete integrity of the vasculature.…”

Section: The Vascular Barrier and The Endothelial Glycocalyx – Two Simentioning

confidence: 99%

“…It is more likely that the classical third space does not exist and that perioperative fluid shifts into the interstitial space, the functional extracellular compartment, with the result of a clinically relevant interstitial edema 55 . The EG with its barrier function plays a key role for avoiding fluid losses into the interstitial space 30 . It can be assumed that by maintaining an intact ESL an excessive shift towards the interstitial space can be avoided.…”

Section: Insensible Perioperative Fluid And/or Protein Shifts – To Bementioning

confidence: 99%

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The role of the glycocalyx in transvascular fluid shifts

Paptistella

Chappell

Hofmann-Kiefer

et al. 2010

Transfusion Alternatives in Transfusion Medicine

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SUMMARY Perioperative fluid management and fluid shifting have been main topics of debate in the recent years. Liberal fluid application is still a common practice and fluid overload believed to be a minor problem. Recent studies, however, have shown that liberal fluid management facilitates fluid shifts into the interstitial space especially in the context of major abdominal surgery. Consequently, the integrity of the vascular barrier is a rediscovered target of research. The endothelial glycocalyx, which covers the endothelial cells on the luminal side of every healthy vessel, plays a key role concerning the barrier properties of healthy blood vessels. Together with bound plasma proteins the glycocalyx forms the endothelial surface layer with a thickness of about 1 µm. With these packed proteins, this layer has its own colloid osmotic force. Damage of the endothelial glycocalyx can lead to protein extravasation and tissue edema. The endothelial glycocalyx is also important concerning leukocyte and platelet adhesion and shear‐stressed nitric oxide‐release and therefore, very probably, with regard to the pathophysiology of diseases like sepsis and ischemia/reperfusion injury. The purpose of this review is to elucidate the physiological and functional impact of the endothelial glycocalyx in transvascular fluid shifts.

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Endothelial glycocalyx and coronary vascular permeability: the fringe benefit

2010

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Current concepts of vascular permeability are largely still based on the Starling principle of 1896. Starling's contribution to understanding vascular fluid homeostasis comes from realising that the transport of fluid to and from the interstitial space of peripheral tissues follows the balance between opposing oncotic and hydrostatic pressures. It is presumed that in peripheral tissues fluid is readily filtered from blood to tissues at the arterial/arteriolar side of the circulation and largely reabsorbed at the venular/venous aspect, excess fluid being removed from the tissue by the lymphatic system. This balance is determined particularly by the properties of the vascular barrier. Recent studies have shown that the endothelial glycocalyx, located with a thickness of at least 200 nm on the luminal side of healthy vasculature, plays a vital role in vascular permeability by constituting the vascular barrier together with the endothelial cells themselves. While water and electrolytes can freely pass through the glycocalyx, plasma proteins, especially albumin, interact strongly. Binding and intercalating plasma constituents with the structural elements of the glycocalyx creates the so-called endothelial surface layer. This is the actual interface between flowing blood and the endothelial cell membrane in vivo. The oncotic pressure difference pertinent to fluid homeostasis is not built up between the intravascular and the interstitial tissue spaces, but within a small protein-free zone beneath the glycocalyx surface layer. This explains why perturbation of the glycocalyx leads to a breakdown of both fluid and protein handling in the coronary vascular bed. Preventing damage to the glycocalyx seems to be a promising goal in cardioprotection in many clinical scenarios, including acute ischaemia, hypoxia and inflammation, and chronic vascular disease as in atherosclerosis, diabetes and hypertension.

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Impaired glycocalyx barrier properties and increased capillary tube haematocrit

Cited by 12 publications

References 6 publications

Isoproternenol Increases Vascular Volume Expansion And Urinary Output After a Large Crystalloid Bolus in Healthy Volunteers

Isoproternenol Increases Vascular Volume Expansion And Urinary Output After a Large Crystalloid Bolus in Healthy Volunteers

The role of the glycocalyx in transvascular fluid shifts

Endothelial glycocalyx and coronary vascular permeability: the fringe benefit

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