目的：探讨尤瑞克林（UK）对心脏骤停后综合征（PCAS）兔脑的保护作用及机制。 方法：将42只日本 大耳白兔随机分为假手术组（n=6）、PCAS组（n=12）、UK大剂量（UK-H）组（n=12）、UK小剂量（UK-L）组（n= 12）。采用窒息性心脏骤停法制备兔PCAS模型，假手术组不造成窒息。复苏成功后UK-H、UK-L组立即给 予UK 17.5×10- 3 PNAU/kg、3.5×10- 3 PNAU/kg，PCAS组注射等量生理盐水。分别于复苏前、复苏后6 h、24 h、 48 h检测血清神经元特异性烯醇化酶（NSE），并进行神经功能缺损评分。48 h后取兔脑组织，应用Western blot方法测定脑组织Caspase-3、Caspase-9表达。结果：与假手术组比，PCAS组、UK-H组、UK-L组血清NSE 水平在复苏后6 h、24 h、48 h均明显升高（P<0.01）。与PCAS组比，UK-H组、UK-L组血清NSE水平、神经功 能损伤评分在复苏后24 h、48 h明显减少，复苏后48 h Caspase-3、Caspase-9表达水平减低（P<0.05），且在复 苏后48 h UK-H组较UK-L组减低更为明显（P<0.05）。结论：UK能减少复苏后脑炎性因子表达，改善神经 功能，其机制可能与抑制细胞凋亡有关。

To investigate the brain protective effects and mechanism of urinary kallidinogenase (UK) in rabbits with post-cardiac arrest syndrome (PCAS). Methods: Japanese white rabbits were random divided into the sham group (n=6), PCAS group (n=12), UK high-dose group (UK-H group , n=12), and UK low-dose group (UK-L group, n=12). PCAS models were established by using asphyxia-induced cardiac arrest; the sham group was not subjected to asphyxia. Immediately after ROSC, UK-H and UK-L groups were given 17.5×10-3 PNAU/kg and 3.5×10-3 PNAU/kg doses of UK, and the PCAS group was injected with an equal amount of saline. Serum level of neuron specificity enolization enzyme (NSE) was examined before ROSC and 6 h, 24 h, and 48 h after ROSC respectively. Functional outcomes were measured by neurological deficit score. Rabbit brain tissue was collected after 48 h, and Western blot was performed to determine brain tissue Caspase-3 and Caspase-9 expression. Results: Compared to the sham group，serum level of NSE was significantly elevated in the PCAS group, UK-L group, and UK-H group 6 h, 24 h, and 48 h after ROSC (P<0.01). Compared to PCAS group，serum level of NSE and neurological deficit score was clearly decreased in the UK-L group and UK-H group 24 h and 48 h after ROSC; the expression level of Caspase-3 and Caspase-9 was significantly attenuated in the two groups 48 h after ROSC (P<0.05), with the UK-H group showing a greater reduction than the UK-L group (P<0.05). Conclusion: UK reduced brain inflammation and alleviated neurological deficit, and the mechanism may be related to inhibition of apoptosis