Regulatory mechanisms, prophylaxis and treatment of vascular leakage following severe trauma and shock

Duan, Chenyang; Zhang, Jie; Wu, Huiling; Li, Tao; Liu, Liangming

doi:10.1186/s40779-017-0117-6

Cited by 21 publications

(28 citation statements)

References 81 publications

(79 reference statements)

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“…In accordance, we showed that plasma obtained after standard treatment did not affect in vitro endothelial permeability and that in vitro endothelial resistance was positively associated with in vivo microcirculatory perfusion. Taken together, these results support endothelial hyperpermeability as underlying problem in the development of microcirculatory perfusion disturbances [23].…”

Section: Discussionsupporting

confidence: 71%

In vitro endothelial hyperpermeability occurs early following traumatic hemorrhagic shock

Leeuwen

Naumann

Dekker

et al. 2020

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BACKGROUND: Endothelial hyperpermeability is suggested to play a role in the development of microcirculatory perfusion disturbances and organ failure following hemorrhagic shock, but evidence is limited. OBJECTIVE: To study the effect of plasma from traumatic hemorrhagic shock patients on in vitro endothelial barrier function. METHODS: Plasma from traumatic hemorrhagic shock patients was obtained at the emergency department (ED), the intensive care unit (ICU), 24 h after ICU admission and from controls (n = 8). Sublingual microcirculatory perfusion was measured using incident dark field videomicroscopy at matching time points. Using electric cell-substrate impedance sensing, the effects of plasma exposure on in vitro endothelial barrier function of human endothelial cells were assessed. RESULTS: Plasma from traumatic hemorrhagic shock patients collected at ED admission induced a 19% loss of in vitro endothelial resistance compared to plasma from controls (p < 0.001). This loss was due to reduced cell-cell contacts (p < 0.01). Plasma withdrawn at later time points did not affect endothelial barrier function (p > 0.99). Interestingly, in vitro endothelial resistance showed a positive association with in vivo microcirculatory perfusion (r = 0.56, p < 0.01). CONCLUSIONS: Plasma from traumatic hemorrhagic shock patients obtained following ED admission, but not at later stages, induced in vitro endothelial hyperpermeability. This coincided with in vivo microcirculatory perfusion disturbances.

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Section: Discussionsupporting

confidence: 71%

In vitro endothelial hyperpermeability occurs early following traumatic hemorrhagic shock

Leeuwen

Naumann

Dekker

et al. 2020

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“…The extent of tissue injury is associated with the extent of oxygen deprivation and the duration of the ischemic period 5 . In the early stages of ischemia, vasoconstriction in the skin and viscera is prominent due to activity in the sympathetic-adrenal medullary system, which compensates for the decrease in blood pressure to maintain adequate blood flow to the heart and brain 6 . In the latestage ischemia, vascular hyporeactivity with a progressive decrease in blood pressure may cause multiple organ dysfunction, and even death 7 .…”

Section: Introductionmentioning

confidence: 99%

Drp1 regulates mitochondrial dysfunction and dysregulated metabolism in ischemic injury via Clec16a-, BAX-, and GSH- pathways

et al. 2020

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The adaptation of mitochondrial homeostasis to ischemic injury is not fully understood. Here, we studied the role of dynamin-related protein 1 (Drp1) in this process. We found that mitochondrial morphology was altered in the early stage of ischemic injury while mitochondrial dysfunction occurred in the late stage of ischemia. Drp1 appeared to inhibit mitophagy by upregulating mito-Clec16a, which suppressed mito-Parkin recruitment and subsequently impaired the formation of autophagosomes in vascular tissues after ischemic injury. Moreover, ischemia-induced Drp1 activation enhanced apoptosis through inducing mitochondrial translocation of BAX and thereby increasing release of Cytochrome C to activate caspase-3/-9 signalling. Furthermore, Drp1 mediated metabolic disorders and inhibited the levels of mitochondrial glutathione to impair free radical scavenging, leading to further increases in ROS and the exacerbation of mitochondrial dysfunction after ischemic injury. Together, our data suggest a critical role for Drp1 in ischemic injury.

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“…Intercellular junctions play an important role in vascular leakage [3]. In this study, we found that HBOC protects against vascular permeability by upregulating the expression of the intercellular junction proteins ZO-1, VE-cadherin and occludin after haemorrhagic shock; however, it remains unclear how these effects are achieved.…”

Section: Discussionmentioning

confidence: 77%

“…Vascular leakage results in the leakage of macromolecules and proteins into tissue gaps and tissue edoema, which is an important cause of lung injury. Therefore, it is essential to choose an effective treatment for preventing pulmonary vascular leakage during fluid resuscitation [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

“…Many factors participate in the regulation of vascular permeability, with intercellular junctions being a key factor. Previous studies found that haemorrhagic shock and hypoxia could result in decreased expression of intercellular junction proteins, an increase in intercellular space and enhanced transmembrane transport of proteins and other macromolecules [3]. Moreover, the endothelial glycocalyx plays an important role in maintaining the vascular barrier.…”

Section: Introductionmentioning

confidence: 99%

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Protective effects of HBOC on pulmonary vascular leakage after haemorrhagic shock and the underlying mechanisms

Zhao

Zhang

Zhu

et al. 2020

Artificial Cells, Nanomedicine, and Biotechnology

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Volume resuscitation is an important early treatment for haemorrhagic shock. Haemoglobin-based oxygen carrier (HBOC) can expand the volume and provide oxygen for tissues. Vascular leakage is common complication in the process of haemorrhagic shock and resuscitation. The aim of this study was to observe the effects of HBOC (a bovine-derived, cross-linked tetramer haemoglobin oxygen-carrying solution, 0.5 g/L) on vascular leakage in rats after haemorrhagic shock. A haemorrhagic shock rat model and hypoxic vascular endothelial cells (VECs) were used. The role of intercellular junctions and endothelial glycocalyx in the protective effects of HBOC and the relationship with mitochondrial function were analysed. After haemorrhagic shock, the pulmonary vascular permeability to FITC-BSA, Evans Blue was increased, endothelial glycocalyx was destroyed and the expression of intercellular junction proteins was decreased. After haemorrhagic shock, a small volume of HBOC solution (6 ml/kg) protected pulmonary vascular permeability, increased structural thickness of endothelial glycocalyx, the levels of its components and increased expression levels of the intercellular junction proteins ZO-1, VE-cadherin and occludin. Moreover, HBOC significantly increased oxygen delivery and consumption in rats, improved VEC mitochondrial function and structure. In conclusion, HBOC mitigates endothelial leakage by protecting endothelial glycocalyx and intercellular junctions through improving mitochondrial function and tissue oxygen delivery.

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Regulatory mechanisms, prophylaxis and treatment of vascular leakage following severe trauma and shock

Cited by 21 publications

References 81 publications

In vitro endothelial hyperpermeability occurs early following traumatic hemorrhagic shock

In vitro endothelial hyperpermeability occurs early following traumatic hemorrhagic shock

Drp1 regulates mitochondrial dysfunction and dysregulated metabolism in ischemic injury via Clec16a-, BAX-, and GSH- pathways

Protective effects of HBOC on pulmonary vascular leakage after haemorrhagic shock and the underlying mechanisms

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