Hunter James P, Hosgood Sarah A, Patel Meeta, Furness Peter, Sayers Robert D, Nicholson Michael L
Department of Infection, Immunity and Inflammation, University of Leicester, Leicester General Hospital, Leicester, UK.
Department of Infection, Immunity and Inflammation, University of Leicester, Leicester General Hospital, Leicester, UK.
Ann Vasc Surg. 2015 Feb;29(2):353-60. doi: 10.1016/j.avsg.2014.11.002. Epub 2014 Nov 26.
Remote renal ischemia-reperfusion injury (IRI) following infra-renal aortic occlusion leads to acute kidney injury and systemic inflammation. Hydrogen sulfide is a mediator of IRI and can ameliorate tissue injury in many organ systems. Its role in vascular surgery has yet to be established. We assessed the role of hydrogen sulfide in a rodent model of aortic occlusion.
Wistar rats were divided into sham, control, and treatment groups (n = 6). Inflammation was assessed using a nonrecovery protocol. The infra-renal aorta was cross-clamped for 60 min and animals were reperfused for 120 min. Ten minutes before clamp release, treatment animals received hydrogen sulfide (10, 30, or 50 μg/kg) and control animals received 0.9% saline injected into the retroperitoneum. Renal injury and histology were assessed by a recovery protocol. The procedure was identical to the nonrecovery arm but with a single dose of hydrogen sulfide (30 μg/kg) and animals were recovered for 7 days.
There was no difference in animal weight between the groups (P = 0.337). In the nonrecovery arm, there was a reduction in serum levels of tumor necrosis factor alpha in sulfide-treated animals compared with controls (909 ± 98 vs. 607 ± 159 pg/mL; P = 0.0038). There was also a reduction in myeloperoxidase-positive cells in renal tissue in the sulfide-treated animals compared with controls (8 ± 4 vs. 17 ± 9; P = 0.03). There was no difference in histological injury score or endothelin-1 levels. In the recovery arm, there was no difference in renal function, Kidney Injury Molecule-1 levels, or histological injury scores.
Hydrogen sulfide has systemic and renal anti-inflammatory effects in remote IRI following aortic occlusion in rats.
肾下主动脉闭塞后的远程肾缺血再灌注损伤（IRI）可导致急性肾损伤和全身炎症。硫化氢是IRI的一种介质，可改善许多器官系统的组织损伤。其在血管手术中的作用尚未确定。我们评估了硫化氢在主动脉闭塞的啮齿动物模型中的作用。
将Wistar大鼠分为假手术组、对照组和治疗组（n = 6）。使用非恢复方案评估炎症。肾下主动脉夹闭60分钟，动物再灌注120分钟。在松开夹子前10分钟，治疗组动物接受硫化氢（10、30或50μg/kg），对照组动物接受注入腹膜后的0.9%生理盐水。通过恢复方案评估肾损伤和组织学。该过程与非恢复组相同，但使用单剂量硫化氢（30μg/kg），动物恢复7天。
各组动物体重无差异（P = 0.337）。在非恢复组中，与对照组相比，硫化物治疗动物的血清肿瘤坏死因子α水平降低（909±98 vs. 607±159 pg/mL；P = 0.0038）。与对照组相比，硫化物治疗动物肾组织中髓过氧化物酶阳性细胞也减少（8±4 vs. 17±9；P = 0.03）。组织学损伤评分或内皮素-1水平无差异。在恢复组中，肾功能、肾损伤分子-1水平或组织学损伤评分无差异。
硫化氢对大鼠主动脉闭塞后的远程IRI具有全身和肾脏抗炎作用。
