Shock/Sepsis/Trauma/Critical CareBlockade of Stellate Ganglion Remediates Hemorrhagic Shock–Induced Intestinal Barrier Dysfunction
Introduction
The crucial role of gut barrier dysfunction has recently been demonstrated in the progression of critical diseases.1, 2, 3 Sympathetic–adrenal–medullary system (SAS) activation in the episode of hemorrhagic shock results in a sustained disproportionate constriction and blood hypoperfusion of gut circulation, which leads to gut ischemic hypoxia and consequent necrosis or apoptosis of enterocytes to a different extent. Combined with inappropriate or excessive fluid resuscitation causing reperfusion injury, these insults jointly induce hyperpermeability of gut mucosa and gut-derived bacterial–endotoxin translocation. The adverse effects of gut barrier dysfunction would serve as a trigger to further induce distant organs injury after severe hemorrhagic shock.4 Therefore, the preservation of gut barrier function is essential for the rescue of hemorrhagic shock individuals.
Stellate ganglion blockade (SGB) has been widely used in the clinical treatments of painful diseases, such as headaches, faciocervical neuralgia, herpes zoster or postherpetic neuralgia, complex regional pain syndrome, and so on.5, 6 In recent years, scholars have initiated new studies on the therapeutic effects of SGB in other diseases, such as posttraumatic stress disorder syndrome.7 The study of CO2 pneumoperitoneum in elderly patients has shown that the right SGB reduced the concentration of catecholamine in the blood and the occurrence of postoperative cardiovascular events. The results suggest that the beneficial effect of SGB on cardiovascular function is attributed to the suppressive action on the excessive excitation of sympathetic nerves.8
In the process of hemorrhagic shock, the excitation of SAS not only has a certain compensatory effect on maintaining blood perfusion of vital organs, including heart and brain, but also induces the hypoperfusion of some other organs, including kidney, spleen, gut, and so on. The sustaining and serious blood hypoperfusion in these organs would lead to gut ischemic damage and enterogenic infection. This prompts one to raise a question on how to reduce the adverse effects induced by the hypoperfusion during hemorrhagic shock. Thus, we hypothesized that the implementation of SGB could inhibit the SAS excitation after severe traumatic hemorrhage to a certain extent, thereby reducing gut injury and restoring intestinal barrier function. To test it, SGB technique was used to investigate the effects of SGB on survival time, intestinal barrier function, cytoskeleton protein and junction protein in intestinal tissue in rats subjected to hemorrhagic shock.
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Animals and experimental procedures
Forty-eight male-specific pathogen-free Wistar rats (Laboratory Animal Center of the Academy of Military Medical Sciences, Beijing, China) weighing 210 ± 20 g were used in the present experiments. The animals were housed in accordance with the guidelines of Hebei North University for the Care and Use of Laboratory Animals. All surgery was performed under anesthesia, and every effort was made to minimize suffering, and the experiments were approved by the Hebei North University Animal ethics
Effect of SGB on the survival rate in rats after hemorrhagic shock
The results showed that the survival rates for 24, 48, and 96 h in the Shock group were 83.3%, 25.0%, and 8.3%, respectively. In contrast, the survival rates were 100%, 75.0%, and 66.7% in the Shock + SGB group, correspondingly. The median survival times in the Shock and Shock + SGB group were 32.5 and 96 h, respectively. These data revealed that SGB treatment significantly enhanced the survival time and survival rate of the rats subjected to acute hemorrhage and resuscitation (P < 0.05). The
Discussion
It is established that acute hemorrhage-induced excessive excitation of SAS induces gut hypoperfusion and barrier dysfunction, thereby leading to multiple organ injuries and high mortality. In this study, we found that SGB treatment before acute hemorrhage significantly improved animal survival and attenuated hemorrhagic shock–induced intestinal barrier injury. The results suggest that SGB may be a potential therapy to effectively treat severe hemorrhagic shock.
At present, there are many
Acknowledgment
The authors greatly appreciate and thank Dr Xue Bao-Jian (Department of Psychological and Brain Sciences, University of Iowa, Iowa) and Dr Gao Si-Qi (Institute of Microcirculation, Hebei North University, China) for reviewing the article.
This study was supported by the National Natural Science Foundation of China (No. 81770492).
Authors' contributions: J.Z., X.L., Y.Z., L.Z., H.D., and L.J., performed the majority of the animal experiment and laboratory work; J.Z. acquired and analyzed the data;
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