Neder Meyer Tufi, Lázaro Da Silva Alcino
INCIS (Health Sciences Institute), Vale do Rio Verde University (UNINCOR), Rua Desembargador Alberto Luz 129, 37410-000 Três Corações, MG, Brazil.
Burns. 2004 Aug;30(5):425-30. doi: 10.1016/j.burns.2004.01.006.
Ketamine can provide protective effects, through its anti-inflammatory properties, as shown in animal models of septic shock and endotoxemia, and has elicited the heat-shock response (HSR) in experimental studies. The HSR has reduced the mortality after severe burns in rats. This study has tested the hypothesis that ketamine could be protective in experimental burns and that it could generate the HSR. One hundred and twenty adult male Fischer rats were randomly divided into five groups. Rats in the first group (n = 20) were sham-anesthetized. In the second group (n = 20), rats were anesthetized with ketamine and shaved. In the third group (n = 20) rats were anesthetized with midazolam plus fentanyl and shaved. In the fourth group (n = 30), rats were anesthetized with ketamine, shaved and submitted to 29% body surface third-degree burns using a brass bar. In the fifth group (n = 30), rats were anesthetized with midazolam plus fentanyl, shaved and submitted to 29% body surface third-degree burns using a brass bar. Mortality rates were measured at 1, 2, 3, 5, 7, 10, 15 and 25 days. Liver and lung samples were collected from all groups for heat-shock protein 70 (HSP70) detection. No animals died in the first, second or third group. Animals anesthetized with ketamine showed significantly decreased mortality, as compared to those anesthetized with midazolam plus fentanyl, from day 2 to day 10 (P < 0.01, Fischer's exact test) and from day 10 to day 25 (P < 0.05). HSP70 was positive in the lungs of animals from all groups, without any differences among them, and was found in none of the liver samples. In conclusion, the mortality was significantly lesser in ketamine-anesthetized burnt rats than in burnt animals anesthetized with midazolam plus fentanyl. Ketamine has not elicited the HSR in this model of experimental burns and, therefore, its protective effects were not shown to be mediated through this mechanism.
氯胺酮具有抗炎特性,在脓毒性休克和内毒素血症的动物模型中已显示出其具有保护作用,并且在实验研究中引发了热休克反应(HSR)。热休克反应降低了大鼠严重烧伤后的死亡率。本研究检验了以下假设:氯胺酮在实验性烧伤中具有保护作用,并且它可以引发热休克反应。120只成年雄性Fischer大鼠被随机分为五组。第一组(n = 20)大鼠接受假麻醉。第二组(n = 20)大鼠用氯胺酮麻醉并剃毛。第三组(n = 20)大鼠用咪达唑仑加芬太尼麻醉并剃毛。第四组(n = 30)大鼠用氯胺酮麻醉、剃毛,并用铜棒造成29%体表面积的三度烧伤。第五组(n = 30)大鼠用咪达唑仑加芬太尼麻醉、剃毛,并用铜棒造成29%体表面积的三度烧伤。在第1、2、3、5、7、10、15和25天测量死亡率。从所有组中采集肝脏和肺组织样本用于检测热休克蛋白70(HSP70)。第一、二或三组中无动物死亡。与用咪达唑仑加芬太尼麻醉的动物相比,用氯胺酮麻醉的动物从第2天到第10天(P < 0.01,Fisher精确检验)以及从第10天到第25天(P < 0.05)死亡率显著降低。所有组动物的肺中HSP70均为阳性,各组之间无差异,并且肝脏样本中均未发现HSP70。总之,氯胺酮麻醉的烧伤大鼠的死亡率显著低于用咪达唑仑加芬太尼麻醉的烧伤动物。在该实验性烧伤模型中,氯胺酮未引发热休克反应,因此,其保护作用并非通过该机制介导。