Sevoflurane Reduces Leukocyte and Platelet Adhesion after Ischemia-Reperfusion by Protecting the Endothelial Glycocalyx

Chappell, Daniel; Heindl, B.; Jacob, Matthias; Annecke, Thorsten; Chen, Congcong; Rehm, Markus; Conzen, P.; Becker, Bernhard F.

doi:10.1097/aln.0b013e3182289988

Cited by 132 publications

(104 citation statements)

References 53 publications

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“…26 The endothelial glycocalyx is a functional barrier and plays a critical role in maintaining the physiologically normal vascular permeability, and it can also prevent the adhesion of white blood cells and platelets to the walls of blood vessels. 7,16,27 Hence, the present study suggested that sevoflurane is likely to be therapeutically effective in reducing the liver tissue edema and inflammation induced by the ischemia-reperfusion injury. 17 Figure 1.…”

Section: Discussionmentioning

confidence: 98%

“…The time-dependent protective effects of sevoflurane on the shedding of HS and Syn-1 are likely dependent on the physiological association between these molecules and the endothelial glycocalyx, as well as the concentration of sevoflurane in the tissue.12,13 While HS is located on the surface of the endothelial glycocalyx and has a relatively loose association with the endothelial glycocalyx, Syn-1 is a core component of the endothelial glycocalyx and is located in its deeper layers. 3,8,10,16,[27][28][29] Therefore, when the endothelial glycocalyx is damaged, the peak of the HS release appeared earlier than that of Syn-1 (Figure 1a). Relatively loose association of HS with the endothelial glycocalyx likely contributes to the limited protective effect of sevoflurane on the shedding of HS at the beginning of the reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…Relatively loose association of HS with the endothelial glycocalyx likely contributes to the limited protective effect of sevoflurane on the shedding of HS at the beginning of the reperfusion. [11][12][13][14][15][16]18,29 Conversely, Syn-1 has a solid association with the endothelial glycocalyx. As a result, the peak of the Syn-1 release appeared much later during reperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…10 Some studies examined the effects of sevoflurane pretreatment on hepatic tissues following the ischemia-reperfusion injury. 12,13,[15][16][17][18] The available data on this issue are, however, limited and often inconclusive. In particular, there is little information on the effect of sevoflurane pretreatment on the endothelial glycocalix.…”

Section: Introductionmentioning

confidence: 99%

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Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Yuan

Zhao

et al. 2016

Int J Immunopathol Pharmacol

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The endothelial glycocalyx plays a critical role in the regulation of vascular structure and functions. Previous studies have demonstrated that sevoflurane, a volatile anesthetic, can preserve the endothelial glycocalyx in heart tissues against ischemia-reperfusion injury. However, little is known about the effects of sevoflurane pretreatment on the vascular structure and functions of liver tissues following ischemia-reperfusion injury. To this end, female Sprague-Dawley rats (n = 28) were anesthetized either with ketamine (80-120 mg/kg, i.p.) or with one minimum alveolar concentration (MAC) sevoflurane (2% v/v). Following in vivo hepatic ischemia procedure, the liver was isolated and reperfusion was produced. During the period of reperfusion, liver reperfusion samples were collected, and the concentrations of heparan sulfate and syndecan-1 (Syn-1), and the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzymes, were measured. The morphology of hepatocytes and endothelial glycocalyx were then assessed by using the light and electron microscopies, respectively. Ischemia-reperfusion increased the release of HS and Syn-1, and elevated the levels of ALT and AST in a time-dependent manner. However, sevoflurane pretreatment reduced the release of HS and Syn-1and attenuated the levels of ALT and AST, in a time-dependent manner, as compared with ketamine pretreatment. Furthermore, sevoflurane pretreatment decreased the shedding of endothelial glycocalyx and hepatocytes necrosis. Sevoflurane pretreatment preserved the endothelial glycocalyx in the liver tissue against ischemia-reperfusion injury. The effect appears to help protect hepatocytes against ischemia-reperfusion-induced necrosis.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Yuan

Zhao

et al. 2016

Int J Immunopathol Pharmacol

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“…However, this structure is quite vulnerable and tends to disintegrate after application of various stressors, such as endotoxins, ischemia/hypoxia/ reperfusion, oxidative stress, among others. Damage to and modification of the EG are observed in many diseases including diabetes, ischemia, chronic infectious diseases, atherosclerosis, and tumors (van den Berg et al, 2003;Reitsma et al, 2007;Weinbaum et al, 2007;Becker et al, 2010b;VanTeeffelen et al, 2010;Chappell et al, 2011). The disintegration of EG predisposes to tissue infiltration by polymorphonuclears, monocyte/macrophages, and lymphocytes.…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Restoration of Endothelial Glycocalyx in Sepsis

Song

Zullo

Liveris

et al. 2017

J Pharmacol Exp Ther

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Endothelial glycocalyx (EG) is disintegrated during sepsis. We have previously shown that this occurs very early in the course of sepsis and its prevention improves the survival of mice with sepsis. Here, we sought to investigate the possibility of pharmacologically accelerating the restoration of disintegrated EG in sepsis. We used a soilage injection model to induce polymicrobial sepsis in C57/BL6 mice and measured total body EG. En face aortic preparations were used for staining of markers of EG and atomic force microscopy was used to measure EG in vitro. In vitro studies were conducted in cultured endothelial cells either exposed to a lipopolysaccharide or enzymatically denuded of EG. Sulodexide (SDX), a heparin sulfate-like compound resistant to degradation by heparanase, accelerated EG regeneration in vitro and in vivo. The total volume of EG was drastically reduced in septic mice. Administration of SDX produced a dramatic acceleration of EG restoration. This effect, unrelated to any SDX-induced differences in microbial burden, was associated with better control of vascular permeability. Notably, SDX demonstrated not only a remarkable capacity for EG regeneration in vitro and in vivo but was also associated with improved animal survival, even when instituted 2 hours after induction of severe sepsis. In conclusion, 1) EG is disintegrated in sepsis, the event which contributes to high animal mortality; 2) pharmacologic acceleration of EG restoration can be achieved using SDX; and 3) SDX reduces vascular permeability, which is elevated in septic mice, and improves animal survival.

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2016

Rapid Perioperative Care

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Sevoflurane Reduces Leukocyte and Platelet Adhesion after Ischemia-Reperfusion by Protecting the Endothelial Glycocalyx

Abstract: Sevoflurane reduces glycocalyx shedding in the postischemic coronary bed, maintaining the natural cover for endothelial adhesion molecules and, thus, reducing cell adhesion. This may explain beneficial outcomes linked to clinical use of volatile anesthetics after ischemia-reperfusion.

Cited by 132 publications

References 53 publications

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Protective effects of sevoflurane in hepatic ischemia-reperfusion injury

Therapeutic Restoration of Endothelial Glycocalyx in Sepsis

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