Wang Qun-Li, Wang Gang, Wang Hua-Min, Pei Guo-Xian
Department of Orthopedics and Traumatology, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China.
Di Yi Jun Yi Da Xue Xue Bao. 2002 Jul;22(7):617-9.
To study the effect of ischemic preconditioning (PC) and pharmacological preconditioning with adenosine or diazoxide on ischemia-reperfusion (IR) injury in the limbs of rats.
According to different treatment received before ischemic-reperfusion injury, 66 SD rats were divided into 6 groups including a normal control and a ischemia-reperfusion control group, IP10 group in which the rats received 10-min ischemia followed by 10-min interval for reperfusion for 3 times before IR, IP5 group in which the rats were subjected to 5-min ischemia with 5-min reperfusion intervals for 3 times before IR, adenosine (Ade) pretreatment group and diazoxide (Dia) pretreatment group. Except the normal control group, which consisted of 6 rats, each group contained 12 rats, and IR injury was induced by blocking the blood flow in bilateral limbs for 4 h, followed by reperfusion for 2 or 24 h when twitch and spastic contractility of the tibialis anterior muscle and serum creatine phosphokinase (CPK) were measured.
In IP5 and Ade pretreatment group, the twitch tension of the tibialis anterior muscle of the rats was significantly enhanced after 2 and 24 h of reperfusion, achieving the level of the normal control. The twitch tension was also enhanced in rats of IP10 group at 24 h, but at 2 h, though with less effectiveness than that in IP5 and Ade group. Dia pretreatment reduced twitch and tetanic contraction forces of the tibialis anterior muscle after 2 h of reperfusion, but obviously improved twitch tension at 24 h. Improvement in the tetanic tension, however, was seen in none of the groups. Serum CPK of IP5, IP10 and Ade groups after 2 and 24 h while Dia at only 24 h of reperfusion was obviously lower than that of IR group.
Ischemic and Ade preconditioning can protect the limbs of rats from ischemia-reperfusion injury, and Dia has delayed protective effect. IP5 is superior than IP10 and Ade PC can produce similar effect to that of ischemic PC.
研究缺血预处理（PC）以及腺苷或二氮嗪药物预处理对大鼠肢体缺血再灌注（IR）损伤的影响。
根据缺血再灌注损伤前接受的不同处理，将66只SD大鼠分为6组，包括正常对照组和缺血再灌注对照组、IP10组（大鼠在IR前接受10分钟缺血，随后间隔10分钟再灌注，共3次）、IP5组（大鼠在IR前接受5分钟缺血，5分钟再灌注间隔，共3次）、腺苷（Ade）预处理组和二氮嗪（Dia）预处理组。除正常对照组（6只大鼠）外，每组12只大鼠，通过阻断双侧肢体血流4小时诱导IR损伤，随后再灌注2或24小时，同时测量胫前肌的抽搐和痉挛收缩力以及血清肌酸磷酸激酶（CPK）。
在IP5和Ade预处理组中，再灌注2和24小时后，大鼠胫前肌的抽搐张力显著增强，达到正常对照组水平。IP10组大鼠在24小时时抽搐张力也增强，但在2小时时，效果不如IP5和Ade组。Dia预处理在再灌注2小时后降低了胫前肌的抽搐和强直收缩力，但在24小时时明显改善了抽搐张力。然而，所有组均未观察到强直张力的改善。再灌注2和24小时后，IP5、IP10和Ade组的血清CPK以及Dia组仅在再灌注24小时时明显低于IR组。
缺血和Ade预处理可保护大鼠肢体免受缺血再灌注损伤，Dia具有延迟保护作用。IP5优于IP10，Ade预处理可产生与缺血预处理相似的效果。
