General anesthesia during excision of a mouse tumor accelerates postsurgical growth of metastases by suppression of natural killer cell activity.

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.