Lymph Formation and Transport: Role in Trauma-Hemorrhagic Shock

Zhao, Zi‐Gang; Zhang, Yuping; Zhang, Limin; Guo, Yanping

doi:10.1007/978-981-13-3353-8_5

Cited by 1 publication

(1 citation statement)

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“…These results indicate that estrogen activation of its receptors promotes mesenteric lymphatic contractility through suppression of HS-induced ERS Lymphatic circulation is crucial for regulation of body uid homeostasis (26). During HS, abnormal intestinal lymphatic contractility is an important cause for microcirculation dysfunction (27). HS-induced hypoxia and ischemia causes vascular hyper-permeability and tissue edema (28, 29), which leads to refractory shock and even death.…”

Section: Discussionmentioning

confidence: 99%

Estrogen activates its receptors to improve lymphatic contractility through suppression of endoplasmic reticulum stress induced by hemorrhagic shock

Zhao

2023

Preprint

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Lymphatic contractility dysfunction is associated with the deterioration of hemorrhagic shock (HS). Endoplasmic reticulum stress (ERS) has been demonstrated to be involved in HS-induced organ injury, while estrogen alleviates HS-induced ERS and organ injury. However, whether estrogen improves lymphatic contraction through inhibition of HS-induced ERS remains unclear. We hypothesized that estrogen activation of its receptors (ERs) promoted mesenteric lymphatic contractility through suppression of HS-induced ERS in lymphatic smooth muscle cells (LSMCs). In a rodent model of HS, 17β-estradiol (E2) administration abrogated HS-induced upregulation of GRP78 in lymphatic tissues. Either E2 or ERS inhibitor 4-phenylbutyric acid (4-PBA) promoted the survival HS rats in the first 72 hours after resuscitation. E2, ER-α agonist PPT, ER-β agonist DPN, GPR30-selective agonist G-1, 4-PBA significantly enhanced the contractility of mesenteric lymphatics following HS in vivo and in vitro. In contrast, ICI 182,780 (ERα and ERβ selective inhibitor) and G-15 (GPR30-selective inhibitor) partly abolished the beneficial effects of E2. Furthermore, ERS agonist XCT-790 abolished the beneficial effects of E2, PPT, DPN, and G-1 on lymphatic contractility. Additionally, E2, PPT, DPN, and G-1 inhibited ERS, and thus ameliorate ERS agonist tunicamycin-induced hypo-contractility in primary LSMCs. Taken together, the data indicates that E2 promotes the lymphatic contractility after HS by inhibiting ERS and estrogen receptor activation mediates the beneficial effect of E2.

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Section: Discussionmentioning

confidence: 99%