Katzav S, Shapiro J, Segal S, Feldman M
Isr J Med Sci. 1986 May;22(5):339-45.
Our previous studies indicated that anesthetic drugs cause acceleration of postoperative metastasis of mouse tumors. We tested whether this augmentation could be attributed to a decrease in natural killer (NK) activity. The results indicated that two of the anesthetic drugs used during excision of the Lewis lung carcinoma (3LL) tumor, halothane and ketamine, decreased NK activity, whereas the other two, thiopental sodium and N2O, had no effect on NK activity in in vitro assays. The observed decrease in NK cell activity was reversed following treatment with polyinosinic-polycytidylic acid (poly I:C), which is an NK cell potentiator. Treatment of mice with poly I:C abolished the accelerated growth of metastases following excision of the tumor under ketamine or halothane anesthesia. On the other hand, treatment with poly I:C seemed to have no effect on acceleration of postoperative metastasis in mice anesthetized with N2O or thiopental sodium.
我们之前的研究表明，麻醉药物会加速小鼠肿瘤术后转移。我们测试了这种增强是否可归因于自然杀伤（NK）活性的降低。结果表明，在Lewis肺癌（3LL）肿瘤切除术中使用的两种麻醉药物，氟烷和氯胺酮，降低了NK活性，而另外两种，硫喷妥钠和N2O，在体外试验中对NK活性没有影响。在用聚肌苷酸-聚胞苷酸（poly I:C）治疗后，观察到的NK细胞活性下降得到逆转，poly I:C是一种NK细胞增强剂。在用氯胺酮或氟烷麻醉下切除肿瘤后，用poly I:C治疗小鼠消除了转移瘤的加速生长。另一方面，用poly I:C治疗似乎对用N2O或硫喷妥钠麻醉的小鼠术后转移加速没有影响。
