Revised Starling equation predicts pulmonary edema formation during fluid loading in the critically ill with presumed hypovolemia

Woodcock, Thomas; Woodcock, Thomas

doi:10.1097/ccm.0b013e31825ae6c9

Cited by 16 publications

(4 citation statements)

References 5 publications

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“…As a result of this model, there is now re‐examination of some of the long standing controversies in fluid therapy (crystalloids alone vs. crystalloids containing oncotic agents) guided by understanding of the revised Starling Principle (Aman et al . , Woodcock & Woodcock ,b).…”

Section: Determinants Of Normal Permeability: Molecular Insights Intomentioning

confidence: 99%

Tonic regulation of vascular permeability

Curry

Adamson

2013

Acta Physiologica

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Our major theme is that the layered structure of the endothelial barrier requires continuous activation of signaling pathways regulated by S1P and intracellular cAMP. These pathways modulate the adherens junction, continuity of tight junction strands, and the balance of synthesis and degradation of glycocalyx components. We evaluate recent evidence that baseline permeability is maintained by constant activity of mechanisms involving the small GTPases Rap1 and Rac1. In the basal state, the barrier is compromised when activities of the small GTPases are reduced by low S1P supply or delivery. With inflammatory stimulus, increased permeability can be understood in part as the action of signaling to reduce Rap1 and Rac1 activation. With the hypothesis that microvessel permeability and selectivity under both normal and inflammatory conditions are regulated by mechanisms that are continuously active it follows that when S1P or intracellular cAMP are elevated at the time of inflammatory stimulus, they can buffer changes induced by inflammatory agents and maintain normal barrier stability. When endothelium is exposed to inflammatory conditions and subsequently exposed to elevated S1P or intracellular cAMP, the same processes restore the functional barrier by first reestablishing the adherens junction, then modulating tight junctions and glycocalyx. In more extreme inflammatory conditions, loss of the inhibitory actions of Rac1 dependent mechanisms may promote expression of more inflammatory endothelial phenotypes by contributing to the up-regulation of RhoA dependent contractile mechanisms and the sustained loss of surface glycocalyx allowing access of inflammatory cells to the endothelium.

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Section: Determinants Of Normal Permeability: Molecular Insights Intomentioning

confidence: 99%

Tonic regulation of vascular permeability

Curry

Adamson

2013

Acta Physiologica

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“…These results should be taken into account considering the physical determinants of capillary filtration, described by the revised Starling principle [30,35]:…”

Section: Discussionmentioning

confidence: 99%

Kinin B1 receptor: a potential therapeutic target in sepsis-induced vascular hyperpermeability

et al. 2020

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Background: In sepsis, the endothelial barrier becomes incompetent, with the leaking of plasma into interstitial tissues. VE-cadherin, an adherens junction protein, is the gatekeeper of endothelial cohesion. Kinins, released during sepsis, induce vascular leakage and vasodilation. They act via two G-protein coupled receptors: B1 (B1R) and B2 (B2R). B1R is inducible in the presence of pro-inflammatory cytokines, endotoxins or after tissue injury. It acts at a later stage of sepsis and elicits a sustained inflammatory response. The aim of our study was to investigate the relationships between B1R and VE-cadherin destabilization in vivo in a later phase of sepsis. Methods: Experimental, prospective study in a university research laboratory. We used a polymicrobial model of septic shock by cecal ligation and puncture in C57BL6 male mice or C57BL6 male mice that received a specific B1R antagonist (R-954). We studied the influence of B1R on sepsis-induced vascular permeability 30 h after surgery for several organs, and VE-cadherin expression in the lung and kidneys by injecting R-954 just before surgery. The 96-h survival was determined in mice without treatment or in animals receiving R-954 as a "prophylactic" regimen (a subcutaneous injection of 200 µg/kg, prior to CLP and 24 h after CLP), or as a "curative" regimen (injection of 100 µg/kg at H6, H24 and H48 post-surgery). Results: B1R inactivation helps to maintain MAP above 65 mmHg but induces different permeability profiles depending on whether or not organ perfusion is autoregulated. In our model, VE-cadherin was destabilized in vivo during septic shock. At a late stage of sepsis, the B1R blockade reduced the VE-cadherin disruption by limiting eNOS activation. The survival rate for mice that received R-954 after sepsis induction was higher than in animals that received an antagonist as a prophylactic treatment. Conclusions: B1R antagonizing reduced mortality in our model of murine septic shock by limiting the vascular permeability induced by VE-cadherin destabilization through maintenance of the macrohemodynamics, consequently limiting organ dysfunctions.

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“…Indeed, there has been no evidence showing that interstitial fluids can be reabsorbed into the venular site of the vessel through oncotic pressure gradient [15]. More than a major regulator of the plasma fluid filtration [4,16], the ESL has proven to be important in providing vascular protection [17] and regulation of microvascular blood flow [18,19]. It mediates sheer stress from the blood flow through the endothelial cells [20] and prevents leukocyte-endothelium and platelet-endothelial adhesion [21].…”

Section: Vascular Fluid Homeostasismentioning

confidence: 99%

Intravenous Fluids and Acute Kidney Injury

2017

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Over 50% of the human body is comprised of fluids that are distributed in defined compartments. Although compartmentalized, these fluids are dynamically connected. Fluids, electrolytes, and acid-base balance in each compartment are tightly regulated, mostly in an energy-dependent manner to achieve their designed functions. For over a century, our understanding of the microvascular fluid homeostasis has evolved from hypothesized Ernest Starling principle to evidence-based and the revised Starling principle, incorporating the functional endothelial surface layer. The kidney is a highly vascular and encapsulated organ that is exquisitely sensitive to inadequate (insufficient or excess) blood flow. The kidney is particularly sensitive to venous congestion, and studies show that reduced venous return triggers a greater degree of kidney damage than that from lacking arterial flow. Thus, fluid overload can induce severe and sustained kidney injury. In the setting of established acute kidney injury, fluid management can be challenging. Impaired capacity of urine output and urine concentration and dilution should be taken into consideration when designing fluid therapy. Video Journal Club ‘Cappuccino with Claudio Ronco' at http://www.karger.com/?doi=452702.

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Revised Starling equation predicts pulmonary edema formation during fluid loading in the critically ill with presumed hypovolemia

Cited by 16 publications

References 5 publications

Tonic regulation of vascular permeability

Tonic regulation of vascular permeability

Kinin B1 receptor: a potential therapeutic target in sepsis-induced vascular hyperpermeability

Intravenous Fluids and Acute Kidney Injury

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