Premium
Depression of Monocytes and Lymphocytes by Stress‐Related Humoral Factors and Anaesthetic‐Related Drugs
Author(s) -
Hole A.
Publication year - 1984
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1984.tb02061.x
Subject(s) - monocyte , medicine , prostaglandin e2 , endocrinology , cytolysis , endocrine system , lymphocyte , prostaglandin e , prostaglandin , serotonin , in vitro , pharmacology , receptor , chemistry , cytotoxicity , biochemistry , hormone
The in vitro effects of six anaesthesia‐related drugs and five stress‐related serum factors on monocyte‐mediated cytolysis and thymidine uptake in mitogen‐(PHA)‐stimulated lymphocytes have been studied. Thiopentone depressed both the monocyte and lymphocyte function in a dose‐dependent way. However, at thiopentone concentrations which may be present in the serum after a single intravenous anaesthesia induction dose, the monocyte depression was moderate and depression of the lymphocytes was not observed. The other drugs tested, fentanyl, morphine, pancuronium, diazepam and bupivacaine, did not alter the cellular functions significantly. Prostaglandin‐E2 in concentrations of 10 ‐6 and 10 ‐7 M markedly depressed monocyte‐mediated cytolysis. Cortisol, catecholamines and serotonin did not alter this function. However, a synergistic depressive effect of the combination of prostaglandin^ and Cortisol was observed. The proliferative response of PHA‐stimulated lymphocytes was depressed by Cortisol in concentrations of 2200 nmol/1 and 1100 nmol/ I. Again, there was a marked synergistic effect of the combination of Cortisol and prostag!andin‐E2, while prostaglandin‐E2 alone, catecholamines and serotonin did not influence the PHA‐response. A possible explanation for the depression of monocyte‐mediated cytolysis and lymphocyte‐thymidine uptake during and after surgery under general anaesthesia may be the combined effect of endocrine and local stress factors.