重症中暑对大鼠心肌肾素-血管紧张素系统的影响

目的：探讨重症中暑对大鼠心肌肾素-血管紧张素系统的影响。方法选用雄性Wistar大鼠24只，应用随机数表法将大鼠分为正常对照组、热打击后2 h组、热打击后24 h组，每组8只。采用放射免疫法测定大鼠血浆和心肌肾素及血管紧张素Ⅱ活性，采用免疫组化法测定心肌血管紧张素Ⅱ-1、2型受体(AT1R、AT2R)蛋白表达水平。结果大鼠热打击后60 min左右肛温达到42℃，77 min左右平均动脉压下降25 mmHg，此时即重症中暑造模成功。热打击后2 h及24 h组大鼠血浆和心肌肾素-血管紧张素系统显著激活血浆RA：(2237.0±173.2)、(1498.0±172.3) vs (785.4±43.2)，P<0.05；血浆AngⅡ：(143.4±19.8)、(76.8±21.6) vs (42.8±8.6)，P<0.05；心肌RA：(10.63±0.59)、(8.49±0.92) vs (1.66±0.38) P<0.05；心肌AngⅡ：(279.9±11.3)、（212.5±10.1) vs (39.6±6.3) P<0.05]；热打击后24 h组大鼠血浆和心肌肾素-血管紧张素系统仍处于激活水平，但较热打击后2 h组明显下降血浆RA：(2237.0±173.2) vs (1498.0±172.3)，P<0.05；血浆AngⅡ：(143.4±19.8) vs (76.8±21.6)，P<0.05；心肌RA：(10.63±0.59) vs (8.49±0.92)，P<0.05；心肌AngⅡ：(79.9±11.3) vs (212.5±10.1)，P<0.05]。热打击后2 h及24 h组心肌AT1R蛋白表达明显上调(49.8±14.1)、(52.6±15.8) vs (13.0±5.0)，P<0.05]；热打击对AT2R蛋白表达无影响(14.1±6.2)、(16.8±7.3) vs (9.8±4.5)，P>0.05]。结论重症中暑早期能够导致大鼠心肌肾素-血管紧张素系统显著激活。

Effect of severe heatstroke on local cardiac renin angiotensin system in rats

Objective To investigate the effects of severe heatstroke on rat cardiac renin angiotensin system (RAS). Methods A total of 24 male Wistar rats were randomly divided into control group, 2 hours after severe heat-stroke group and 24 hours after severe heatstroke group, with 8 rats in each group. Renin activity (RA) and angiotensinⅡ(AngⅡ) in plasma and myocardium were determined with radioimmunoassay. Cardiac angiotensinⅡtype 1, 2 recep-tor (AT1R, AT2R) protein levels were examined by immunohistochemical method. Results After 60 minutes of heat-stroke, rectal core temperature of rats reached 42℃or above, and mean arterial pressure decreased to 25 mmHg after 77 minutes. When these conditions meet the requirements, the severe heatstroke model was successfully established. Com-pared with control group, 2 and 24 hours after heat stroke groups had significantly higher RA and AngⅡin plasma and myocardium plasma RA:(2237.0±173.2), (1498.0±172.3) vs (785.4±43.2), P<0.05;plasma AngⅡ:(143.4±19.8), (76.8± 21.6) vs (42.8 ± 8.6), P<0.05;myocardium RA:(10.63 ± 0.59), (8.49 ± 0.92) vs (1.66 ± 0.38), P<0.05;myocardium AngⅡ:(279.9 ± 11.3), (212.5 ± 10.1) vs (39.6 ± 6.3) P<0.05];Compared with 2 hours after heat stroke groups, 24 hours after heat stroke groups had significantly lower RA and AngⅡin plasma and myocardium plasma RA:(2 237.0±173.2) vs (1 498.0± 172.3), P<0.05;plasma AngⅡ:(143.4±19.8) vs (76.8±21.6), P<0.05;myocardium RA:(10.63±0.59) vs (8.49±0.92), P<0.05;myocardium AngⅡ:(279.9±11.3) vs (212.5±10.1), P<0.05]. Compared with control group, AT1R protein levels no-tably increased in 2 and 24 hours after heat stroke groups (49.8±14.1), (52.6±15.8) vs (13.0±5.0), P<0.05]. No apparent changes were observed in AT2R protein level (14.1 ± 6.2), (16.8 ± 7.3) vs (9.8 ± 4.5), P>0.05]. Conclusion Heat stroke can significantly activate renin angiotensin system in both plasma and myocardium in rats in the early stage.