Blockade of Stellate Ganglion Remediates Hemorrhagic Shock–Induced Intestinal Barrier Dysfunction

Zhang, Jing; Lin, Xue-Rong; Zhang, Yuping; Zhang, Limin; Du, Hui-Bo; Jiang, Lina; Zhao, Zi‐Gang; Niu, Chun‐Yu

doi:10.1016/j.jss.2019.06.007

Cited by 10 publications

(18 citation statements)

References 34 publications

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“…Because the animals lose blood in the conscious state, this model is more likely to mimic the acute blood loss in human. Moreover, the current finding that SGB improved the intestinal mucosal barrier in conscious rats with hemorrhagic shock is consistent with the results of acute blood loss in anesthetized rats [5] which advances the experimental method in studying the hemorrhagic shock in conscious animals.…”

Section: Discussionsupporting

confidence: 86%

“…The rats were divided into the Sham, Shock, Sham+SGB, Shock+SGB, Shock+4-phenylbutyric acid (4-PBA) (Shock plus 4-PBA treatment), and Shock+SGB+tunicamycin (TM) (Shock+SGB plus TM administration) groups, with n=6 for each group. According to the methods in our lab [5], right SGB was performed before hemorrhagic shock. In the SGB group, 0.25% ropivacaine hydrochloride (AstraZeneca AB, Sweden 2018-05 2021-04 LBKT) in 0.2 mL saline was injected into the body surface landmarks of the right stellate ganglion after isoflurane inhalation anesthesia, and the rats were naturally awakened to observe whether there was Horner syndrome.…”

Section: Methodsmentioning

confidence: 99%

“…Stellate ganglion block (SGB) is widely used in clinical analgesia. Previous study [5] demonstrated that SGB can reduce intestinal injury and improve the survival condition of animals after hemorrhagic shock. Also, sympathetic transection simulated by SGB reduces organ injury in septic rats [6].…”

Section: Ivyspringmentioning

confidence: 96%

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Stellate Ganglion Blockade repairs Intestinal Mucosal Barrier through suppression of Endoplasmic Reticulum Stress following Hemorrhagic Shock

Yin

Wang

et al. 2020

Int. J. Med. Sci.

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Background: Hemorrhagic shock-induced ischemia and hypoxia elicit endoplasmic reticulum stress (ERS) that leads to cell apoptosis, tissue structural damage and organ dysfunction and failure. Stellate ganglion blockade (SGB) has been demonstrated to improve intestinal barrier dysfunction induced by hemorrhagic shock. The present study sought to investigate whether the beneficial effect of SGB on the intestinal mucosal barrier function is via suppression of ERS. Materials and methods: A conscious rat model of hemorrhagic shock (40 ±2 mmHg for 1 hour, followed by resuscitation) was established. The parameters reflecting intestinal morphology and intestinal mucosal barrier function including wet-dry ratio (W/D), intestinal permeability, D-lactic acid (D-LA) and intestinal fatty acid binding protein (I-FABP) in plasma, and expressions of ATF6α, PERK, and IRE1α in intestinal tissues were then observed. Furthermore, the effects of either SGB or ERS inhibitor, 4-phenylbutyric acid (4-PBA), on these parameters in rats with hemorrhagic shock were assessed. The effect of ERS agonist tunicamycin (TM) on the rats subjected with both SGB and hemorrhagic shock was also determined. Results: Either SGB or administration of ERS inhibitor, 4-PBA, alleviated hemorrhagic shock-induced adverse effects such as intestinal mucosal barrier dysfunction and excessive autophagy, which were characterized by damaged intestinal tissue, enhanced intestinal permeability and D-LA and I-FABP levels in plasma, and increased expressions of ATF6α, PERK, IRE1α in intestinal tissue. In contrast, administration of ERS agonist, TM, suppressed the beneficial effects of SGB on intestinal tissue and function during hemorrhagic shock. Conclusion: The SGB repairs intestinal mucosal barrier through suppression of ERS following hemorrhagic shock.

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Section: Discussionsupporting

confidence: 86%

Section: Methodsmentioning

confidence: 99%

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Stellate Ganglion Blockade repairs Intestinal Mucosal Barrier through suppression of Endoplasmic Reticulum Stress following Hemorrhagic Shock

Yin

Wang

et al. 2020

Int. J. Med. Sci.

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“…According to the conventional method in our laboratory [15,16] , the left side stellate ganglion was blocked by injecting 0.5% ropivacaine hydrochloride (AstraZeneca AB, Sweden). After the rat spontaneously waked up, the appearance of ptosis is the sign of the success of SGB.…”

Section: Sgb Protocolmentioning

confidence: 99%

“…It also regulates immune response and suppresses acute post-traumatic in ammation [13,14] . Studies have shown that SGB pretreatment signi cantly reduces the intestinal barrier damage after hemorrhagic shock, which is related to the inhibition of endoplasmic reticulum stress [15,16] . However, it is not clear whether SGB post-processing can also reduce intestinal barrier damage after hemorrhagic shock, which is pivotal to expand the clinical application of SGB.…”

Section: Introductionmentioning

confidence: 99%

SGB Postconditioning Improves Intestinal Barrier Function by Inhibiting Autophagy in Conscious Rats Following Hemorrhagic Shock and Resuscitation

Li¹,

Wang²,

Sun³

et al. 2021

Preprint

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Background Intestinal barrier dysfunction is the critical link of distant organ injury caused by hemorrhagic shock. The role of autophagy in ischemic intestinal injury has been paid more and more attention. Prophylactic treatment of stellate ganglion block (SGB) reduces intestinal barrier dysfunction induced by haemorrhagic shock. This study investigated the role of SGB post-processing on improved bowel barrier function and autophagy-related mechanisms of action after haemorrhagic shock. Methods The model of hemorrhagic shock in conscious rats was established, and the rats were treated with SGB, autophagy inhibitor 3- methyladenine (3-MA) at the time of fluid resuscitation. We detected the survival rate, intestinal loop blood flow, intestinal barrier permeability, intestinal morphology, wet/dry ratio (W/D), the intestinal barrier and autophagy marker proteins. Simultaneously, we also observed the effect of autophagy activator rapamycin (RAPA) on SGB. Results SGB postconditioning significantly prolonged the overall survival and enhanced survival rate of 72 hours in rats after hemorrhagic shock. SGB post-processing and 3-MA administration improved the intestinal morphology and intestinal permeability, increased the intestinal loop blood flow and expression of ZO1, Occludin and Claudin-1, and decreased the intestinal W/D and LC3 and Beclin-1 expressions, expected for increased P62. Meanwhile, RAPA partially inhibited the effect of SGB on above indices in haemorrhagic shock rats. Conclusion SGB postconditioning alleviates the intestinal barrier dysfunction caused by haemorrhagic shock, which is related to the inhibition of excessive autophagy.

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Stellate Ganglion Block Improves the Proliferation and Function of Splenic CD4 + T Cells Through Inhibition of Posthemorrhagic Shock Mesenteric Lymph–Mediated Autophagy

Jiang

et al. 2021

Inflammation

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Background and objectiveSevere hemorrhagic shock leads to excessive in ammation and immune dysfunction, which resulted in high mortality related to mesenteric lymph return. Recent study showed that stellate ganglion block (SGB) increased survival rate in rats suffered hemorrhagic shock. However, whether SGB ameliorates immune dysfunction induced by hemorrhagic shock, it remains unknown. The aim of present study is therefore to verify the favorable effect of SGB on the proliferation and function of splenic CD4 + T cells isolated from rats underwent hemorrhagic shock, and investigate its mechanism focusing autophagy and PHSML. Materials and methodsMale rats underwent SGB or sham SGB pretreatment and conscious acute hemorrhage followed by resuscitation and multiple treatments. After three hours of resuscitation, splenic CD4 + T cells were isolated for the measurements of proliferation and cytokine production following stimulation with ConA in vitro. Furthermore, the CD4 + T cells isolated from normal rats were treated with post-hemorrhagic shock mesenteric lymph (PHSML) drained from rats treated with SGB or not. And the proliferation, cytokine production and autophagy biomarkers were detected. ResultsHemorrhagic shock reduced CD4 + T cells proliferation and function to produce interleukin (IL)-2, IL-4 and tumor necrosis factor-α-induced protein 8 like 2 (TIPE2). SGB pretreatment or administration of autophagy inhibitor 3-methyladenine (3-MA) signi cantly normalized these indicators. In contrast, administration of autophagy agonist rapamycin (RAPA) or intravenous injection of PHSML inhibited the bene cial effect of SGB on CD4 + T cells obtained from hemorrhagic shocked rats. Furthermore, PHSML incubation decreased the proliferation and cytokine production, increased LC3 II/I and Beclin-1 expressions, and reduced p-PI3K and p-Akt expressions of normal CD4 + T cells. More critically, these adverse effects of PHSML were abolished by 3-MA administration, as well as incubation with PHSML obtained from SGB treated rats. ConclusionsSGB improves splenic CD4 + T cells function following hemorrhagic shock, which is related to the inhibition of PHSML-mediated autophagy.

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Blockade of Stellate Ganglion Remediates Hemorrhagic Shock–Induced Intestinal Barrier Dysfunction

Cited by 10 publications

References 34 publications

Stellate Ganglion Blockade repairs Intestinal Mucosal Barrier through suppression of Endoplasmic Reticulum Stress following Hemorrhagic Shock

Stellate Ganglion Blockade repairs Intestinal Mucosal Barrier through suppression of Endoplasmic Reticulum Stress following Hemorrhagic Shock

SGB Postconditioning Improves Intestinal Barrier Function by Inhibiting Autophagy in Conscious Rats Following Hemorrhagic Shock and Resuscitation

Stellate Ganglion Block Improves the Proliferation and Function of Splenic CD4 + T Cells Through Inhibition of Posthemorrhagic Shock Mesenteric Lymph–Mediated Autophagy

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