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Savage, S. A., Fitzpatrick, C. M., Kashyap, V. S., Clouse, W. D. & Kerby, J. D. Endothelial dysfunction after lactated Ringer’s solution resuscitation for hemorrhagic shock. J. Trauma 59, 284–290. https://doi.org/10.1097/01.ta.0000179453.89769.1c (2005).
Park, J. B., Charbonneau, F. & Schiffrin, E. L. Correlation of endothelial function in large and small arteries in human essential hypertension. J. Hypertens. 19, 415–420 (2001).
Rizzoni, D. et al. Structural alterations in subcutaneous small arteries of normotensive and hypertensive patients with non-insulin-dependent diabetes mellitus. Circulation 103, 1238–1244. https://doi.org/10.1161/01.CIR.103.9.1238 (2001).
Monnink, S. H. J. et al. Endothelial dysfunction in patients with coronary artery disease: A comparison of three frequently reported tests. J. Investig. Med. 50, 19–24. https://doi.org/10.2310/6650.2002.33513 (2002).
Landmesser, U. et al. Vascular oxidative stress and endothelial dysfunction in patients with chronic heart failure. Circulation 106, 3073–3078. https://doi.org/10.1161/01.CIR.0000041431.57222.AF (2002).
Bolton, C. H. et al. Endothelial dysfunction in chronic renal failure: Roles of lipoprotein oxidation and pro-inflammatory cytokines. Nephrol. Dial. Transplant. 16, 1189–1197. https://doi.org/10.1093/ndt/16.6.1189 (2001).
Wang, P., Ba, Z. F. & Chaudry, I. H. Endothelial cell dysfunction occurs very early following trauma-hemorrhage and persists despite fluid resuscitation. Am. J. Physiol. 265, H973–H979. https://doi.org/10.1152/ajpheart.1993.265.3.H973 (1993).
Moreira, N. J. D. et al. Acute renal denervation normalizes aortic function and decreases blood pressure in spontaneously hypertensive rats. Sci. Rep. 10, 21826. https://doi.org/10.1038/s41598-020-78674-8 (2020).
Mendez-Barbero, N., Gutierrez-Munoz, C. & Blanco-Colio, L. M. Cellular crosstalk between endothelial and smooth muscle cells in vascular wall remodeling. Int. J. Mol. Sci. 22, 7284. https://doi.org/10.3390/ijms22147284 (2021).
Liu, L.-M., Ward, J. A. & Dubick, M. A. Hemorrhage-induced vascular hyporeactivity to norepinephrine in select vasculatures of rats and the roles of nitric oxide and endothelin. Shock 19, 208–214 (2003).
Liu, L. M. & Dubick, M. A. Hemorrhagic shock-induced vascular hyporeactivity in the rat: Relationship to gene expression of nitric oxide synthase, endothelin-1, and select cytokines in corresponding organs. J. Surg. Res. 125, 128–136. https://doi.org/10.1016/j.jss.2004.12.008 (2005).
Ratz, P. H., Miner, A. S., Huang, Y., Smith, C. A. & Barbee, R. W. Vascular smooth muscle desensitization in rabbit epigastric and mesenteric arteries during hemorrhagic shock. Am. J. Physiol. Heart Circ. Physiol. 311, H157–H167. https://doi.org/10.1152/ajpheart.00926.2015 (2016).
Ince, C. et al. The endothelium in sepsis. Shock 45, 259–270. https://doi.org/10.1097/shk.0000000000000473 (2016).
Woodcock, T. E. & Woodcock, T. M. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: An improved paradigm for prescribing intravenous fluid therapy. Br. J. Anaesth. 108, 384–394. https://doi.org/10.1093/bja/aer515 (2012).
Alphonsus, C. S. & Rodseth, R. N. The endothelial glycocalyx: A review of the vascular barrier. Anaesthesia 69, 777–784. https://doi.org/10.1111/anae.12661 (2014).
Florian, J. A. et al. Heparan sulfate proteoglycan is a mechanosensor on endothelial cells. Circ. Res. 93, e136–e142. https://doi.org/10.1161/01.RES.0000101744.47866.D5 (2003).
Johansson, P. I., Stensballe, J., Rasmussen, L. S. & Ostrowski, S. R. A high admission syndecan-1 level, a marker of endothelial glycocalyx degradation, is associated with inflammation, protein C depletion, fibrinolysis, and increased mortality in trauma patients. Ann. Surg. 254, 194–200. https://doi.org/10.1097/SLA.0b013e318226113d (2011).
Christensen, K. L. & Mulvany, M. J. Mesenteric arcade arteries contribute substantially to vascular resistance in conscious rats. J. Vasc. Res. 30, 73–79. https://doi.org/10.1159/000158978 (1993).
Reilly, P. M., Wilkins, K. B., Fuh, K. C., Haglund, U. & Bulkley, G. B. The mesenteric hemodynamic response to circulatory shock: An overview. Shock 15, 329–343 (2001).
Toung, T., Reilly, P. M., Fuh, K. C., Ferris, R. & Bulkley, G. B. Mesenteric vasoconstriction in response to hemorrhagic shock. Shock 13, 267–273. https://doi.org/10.1097/00024382-200004000-00003 (2000).
Mitsuoka, H., Kistler, E. B. & Schmid-Schönbein, G. W. Generation of in vivo activating factors in the ischemic intestine by pancreatic enzymes. Proc. Natl. Acad. Sci. 97, 1772–1777. https://doi.org/10.1073/pnas.97.4.1772 (2000).
Kistler, E. B., Hugli, T. E. & Schmid-Schönbein, G. W. The pancreas as a source of cardiovascular cell activating factors. Microcirculation 7, 183–192. https://doi.org/10.1111/j.1549-8719.2000.tb00119.x (2000).
Savoye, G., Tamion, F., Richard, V., Varin, R. & Thuillez, C. Hemorrhagic shock resuscitation affects early and selective mesenteric artery endothelial function through a free radical-dependent mechanism. Shock 23, 411–416. https://doi.org/10.1097/01.shk.0000159928.49620.67 (2005).
Mitsuoka, H., Kistler, E. B. & Schmid-Schönbein, G. W. Protease inhibition in the intestinal lumen: Attenuation of systemic inflammation and early indicators of multiple organ failure in shock. Shock 17, 205–209 (2002).
Dos Santos, F. et al. Enteral gabexate mesilate improves volume requirements and autonomic cardiovascular function after experimental trauma/hemorrhagic shock in the absence of blood reperfusion. Am. J. Transl. Res. 14, 7391–7402 (2022).
Aletti, F. et al. Continuous enteral protease inhibition as a novel treatment for experimental trauma/hemorrhagic shock. Eur. J. Trauma Emerg. Surg. 48, 1579–1588. https://doi.org/10.1007/s00068-020-01591-y (2022).
Aird, W. C. Endothelium as an organ system. Crit. Care Med. 32, S271–S279. https://doi.org/10.1097/01.ccm.0000129669.21649.40 (2004).
Gulati, A. Vascular endothelium and hypovolemic shock. Curr. Vasc. Pharmacol. 14, 187–195. https://doi.org/10.2174/1570161114666151202210221 (2016).
Piton, G. & Capellier, G. Biomarkers of gut barrier failure in the ICU. Curr. Opin. Crit. Care 22, 152–160. https://doi.org/10.1097/MCC.0000000000000283 (2016).
Alsaigh, T., Chang, M., Richter, M., Mazor, R. & Kistler, E. B. In vivo analysis of intestinal permeability following hemorrhagic shock. World J. Crit. Care Med. 4, 287–295. https://doi.org/10.5492/wjccm.v4.i4.287 (2015).
Kistler, E. B., Alsaigh, T., Chang, M. & Schmid-Schonbein, G. W. Impaired small-bowel barrier integrity in the presence of lumenal pancreatic digestive enzymes leads to circulatory shock. Shock 38, 262–267. https://doi.org/10.1097/SHK.0b013e31825b1717 (2012).
Lipowsky, H. H. Protease activity and the role of the endothelial glycocalyx in inflammation. Drug Discov. Today Dis. Model. 8, 57–62. https://doi.org/10.1016/j.ddmod.2011.05.004 (2011).
Sieve, I., Münster-Kühnel, A. K. & Hilfiker-Kleiner, D. Regulation and function of endothelial glycocalyx layer in vascular diseases. Vascul. Pharmacol. 100, 26–33. https://doi.org/10.1016/j.vph.2017.09.002 (2018).
Zha, D., Fu, M. & Qian, Y. Vascular endothelial glycocalyx damage and potential targeted therapy in COVID-19. Cells 11, 1972 (2022).
Tarbell, J. M. & Cancel, L. M. The glycocalyx and its significance in human medicine. J. Intern. Med. 280, 97–113. https://doi.org/10.1111/joim.12465 (2016).
Cooper, S., Emmott, A., McDonald, K. K., Campeau, M.-A. & Leask, R. L. Increased MMP activity in curved geometries disrupts the endothelial cell glycocalyx creating a proinflammatory environment. PLoS One 13, e0202526. https://doi.org/10.1371/journal.pone.0202526 (2018).
Colburn, P., Kobayashi, E. & Buonassisi, V. Depleted level of heparan sulfate proteoglycan in the extracellular matrix of endothelial cell cultures exposed to endotoxin. J. Cell. Physiol. 159, 121–130. https://doi.org/10.1002/jcp.1041590116 (1994).
Subramanian, S. V., Fitzgerald, M. L. & Bernfield, M. Regulated shedding of syndecan-1 and -4 ectodomains by thrombin and growth factor receptor activation. J. Biol. Chem. 272, 14713–14720. https://doi.org/10.1074/jbc.272.23.14713 (1997).
Schmidt, A., Echtermeyer, F., Alozie, A., Brands, K. & Buddecke, E. Plasmin- and thrombin-accelerated shedding of syndecan-4 ectodomain generates cleavage sites at Lys(114)-Arg(115) and Lys(129)-Val(130) bonds. J. Biol. Chem. 280, 34441–34446. https://doi.org/10.1074/jbc.M501903200 (2005).
Chung, M.-C., Jorgensen, S. C., Popova, T. G., Bailey, C. L. & Popov, S. G. Neutrophil elastase and syndecan shedding contribute to antithrombin depletion in murine anthrax. FEMS Immunol. Med. Microbiol. 54, 309–318. https://doi.org/10.1111/j.1574-695X.2008.00480.x (2008).
Platt, J. L., Dalmasso, A. P., Lindman, B. J., Ihrcke, N. S. & Bach, F. H. The role of C5a and antibody in the release of heparan sulfate from endothelial cells. Eur. J. Immunol. 21, 2887–2890. https://doi.org/10.1002/eji.1830211135 (1991).
Peng, Z., Ban, K., LeBlanc, A. & Kozar, R. A. Intraluminal tranexamic acid inhibits intestinal sheddases and mitigates gut and lung injury and inflammation in a rodent model of hemorrhagic shock. J. Trauma Acute Care Surg. 81, 358–365. https://doi.org/10.1097/ta.0000000000001056 (2016).
Anderson, T. N. et al. Early tranexamic acid administration after traumatic brain injury is associated with reduced syndecan-1 and angiopoietin-2 in patients with traumatic intracranial hemorrhage. J. Head Trauma Rehabil. 35, 317–323. https://doi.org/10.1097/htr.0000000000000619 (2020).
Ebong, E. E., Lopez-Quintero, S. V., Rizzo, V., Spray, D. C. & Tarbell, J. M. Shear-induced endothelial NOS activation and remodeling via heparan sulfate, glypican-1, and syndecan-1. Integr. Biol. 6, 338–347. https://doi.org/10.1039/c3ib40199e (2014).
Pahakis, M. Y., Kosky, J. R., Dull, R. O. & Tarbell, J. M. The role of endothelial glycocalyx components in mechanotransduction of fluid shear stress. Biochem. Biophys. Res. Commun. 355, 228–233 (2007).
Becker, B. F., Chappell, D., Bruegger, D., Annecke, T. & Jacob, M. Therapeutic strategies targeting the endothelial glycocalyx: Acute deficits, but great potential†. Cardiovasc. Res. 87, 300–310. https://doi.org/10.1093/cvr/cvq137 (2010).
Zakaria, E. R., Spain, D. A., Harris, P. D. & Garrison, R. N. Resuscitation regimens for hemorrhagic shock must contain blood. Shock 18, 567–573. https://doi.org/10.1097/00024382-200212000-00014 (2002).
Mazor, R. et al. Involvement of toll-like receptor 4 in decreased vasopressor response following trauma/hemorrhagic shock. Crit. Care Explor. 3, e0469. https://doi.org/10.1097/CCE.0000000000000469 (2021).
Gericke, A., Martinka, P., Nazarenko, I., Persson, P. B. & Patzak, A. Impact of alpha1-adrenoceptor expression on contractile properties of vascular smooth muscle cells. Am. J. Physiol. Regul. Integr. Comp. Physiol. 293, R1215–R1221. https://doi.org/10.1152/ajpregu.00076.2007 (2007).
Santamaria, M. H. et al. Enteral tranexamic acid attenuates vasopressor resistance and changes in alpha1-adrenergic receptor expression in hemorrhagic shock. J. Trauma Acute Care Surg. 83, 263–270. https://doi.org/10.1097/TA.0000000000001513 (2017).
Mitsuoka, H., Kistler, E. B. & Schmid-Schonbein, G. W. Protease inhibition in the intestinal lumen: Attenuation of systemic inflammation and early indicators of multiple organ failure in shock. Shock 17, 205–209. https://doi.org/10.1097/00024382-200203000-00008 (2002).
Goodall, K. J., Poon, I. K., Phipps, S. & Hulett, M. D. Soluble heparan sulfate fragments generated by heparanase trigger the release of pro-inflammatory cytokines through TLR-4. PLoS One 9, e109596. https://doi.org/10.1371/journal.pone.0109596 (2014).
Szabó, C., Faragó, M., Horváth, I., Lohinai, Z. & Kovách, A. G. Hemorrhagic hypotension impairs endothelium-dependent relaxations in the renal artery of the cat. Circ. Shock 36, 238–241 (1992).
Aletti, F. et al. Continuous enteral protease inhibition as a novel treatment for experimental trauma/hemorrhagic shock. Eur. J. Trauma Emerg. Surg. https://doi.org/10.1007/s00068-020-01591-y (2021).
Jadeja, R. N., Rachakonda, V., Bagi, Z. & Khurana, S. Assessing myogenic response and vasoactivity in resistance mesenteric arteries using pressure myography. J. Vis. Exp. 101, e50997. https://doi.org/10.3791/50997 (2015).
Lawton, P. F. et al. VasoTracker, a low-cost and open source pressure myograph system for vascular physiology. Front. Physiol. 10, 99. https://doi.org/10.3389/fphys.2019.00099 (2019).
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