Correction

Abstract

HomeCirculationVol. 124, No. 24Correction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection Originally published13 Dec 2011https://doi.org/10.1161/CIR.0b013e31823f9206Circulation. 2011;124:e901–e903This article corrects the followingBiological Basis of Therapeutic LymphangiogenesisIn the article by Norrmén et al, “Biological Basis of Therapeutic Lymphangiogenesis,” which published in the March 29, 2011 issue of the journal (Circulation. 2011;123:1335–1351), the authors included an outdated view on fluid balance in the microcirculation. In the second paragraph of their article, the sentence:“Most of the extravasated interstitial fluid is absorbed back by colloid osmotic pressure into the blood capillaries on the venous side of the capillary bed, while the remaining fluid and macromolecules are taken up by the lymphatic vessels (Figure 1).”Has been revised to state the following:“Most of the extravasated interstitial fluid and macromolecules are absorbed back by the lymphatic vessels, whereas some reabsorption may also occur in the venules, depending on the tissue (Figure 1).”Figure 1 has also been replaced to reflect this correction. The correct figure appears as follows:Download figureDownload PowerPointFigure 1. Contributions of the blood and lymphatic vascular systems to tissue fluid homeostasis. A through D, Mechanisms leading to tissue edema1. Normal fluid homeostasis in tissues is schematically illustrated in A: Colloid proteins and associated water are constantly filtrated from the arterial side of the capillary bed into the interstitial space (red arrows). The majority of the filtrate is collected by the lymphatic capillaries (green arrows); some of the fluid may be reabsorbed into the capillaries on the venous side of the capillary bed (blue arrows). B, Under the conditions of increased blood vascular permeability, such as in inflammation, the amount of filtrate is dramatically increased. Although the lymphatic vessels have a remarkable capacity to increase their drainage, sometimes the system is overwhelmed and net edema remains. C, Obstruction of the veins, for example, due to venous thrombosis or venous insufficiency will impair reabsorption (Reabs) and increase blood pressure within the capillary bed, leading to increased filtration (Filtr). Again, the lymphatic vessels are capable of increasing drainage, yet net edema is generated. D, Inherited or acquired damage to the lymphatic vessels, such as surgery or radiation therapy, blocks lymphatic drainage. This will lead to gradual accumulation of edematous fluid in tissues. The units in the bar graphs are arbitrary. Note that only the underlying reasons for edema formation are given in each figure, and secondary effects due to, for example, increased interstitial fluid pressure in edematous conditions are not accounted for.The Legend to Figure 1 has also been updated and now reads:Reference 1, which is cited in the Figure legend, has also been updated. It now refers to: Lick JR, Michel CC. Microvascular fluid exchange and the revised starling principle. Cardiovasc Res. 2010;87:198–210.These changes have been made to the current online version of the manuscript. The authors regret the errors. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesBiological Basis of Therapeutic LymphangiogenesisCamilla Norrmén, et al. Circulation. 2011;123:1335-1351 December 13, 2011Vol 124, Issue 24 Advertisement Article InformationMetrics © 2011 American Heart Association, Inc.https://doi.org/10.1161/CIR.0b013e31823f9206 Originally publishedDecember 13, 2011 PDF download Advertisement SubjectsStatements and Guidelines