TY - JOUR
AU - Matsuki, A
AB - Summary Schizophrenic patients are reported to have immunological dysfunction, however, the immune response to surgery in schizophrenic patients remains unclear. We measured plasma interleukin-6 (IL-6), interleukin-8 (IL-8) and tumour necrosis factor-α (TNF-α) before, during and after colectomy, hemicolectomy and sigmoidectomy in 25 chronic schizophrenic patients (Group S) and 25 control patients (Group C) using ELISA assays. We could find no significant difference in the baseline plasma concentrations of IL-6, IL-8 and TNF-α between Group S and Group C. Plasma IL-6 concentrations (32·1 (30·3) and 15·8 (9·6) pg/ml) in Group S at the end of the operation and 24 h after surgery were significantly lower than 76·9 (37·1) and 35·1 (21·5) pg/ml of Group C. Plasma IL-8 concentration (6·1 (2·8)) in Group S at the end of the operation was significantly lower than 8·7 (4·2) pg/ml of Group C. There were no significant changes in plasma TNF-α concentration throughout the study period in either group. Plasma cortisol concentrations of schizophrenic patients during surgery were significantly lower than those of control patients. The plasma IL-6 concentrations correlated with plasma cortisol concentrations in either group. We conclude that proinflammatory cytokine response to abdominal surgery is inhibited in schizophrenic patients. schizophrenia, abdominal surgery, interleukin-6, interleukin-8, tumour necrosis factor-α Introduction We previously reported that chronic schizophrenic patients have many complications during the postoperative course, including wound infection and pneumonia [1]. This may be associated with abnormalities in the immune system in chronic schizophrenic patients. The number of schizophrenic patients who have rheumatoid arthritis is lower than expected [2]. Elevated plasma of concentrations of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-8 (IL-8) have been found in schizophrenic patients [3,4]. Naudin et al. reported that increases of plasma IL-6 concentrations were related to the clinical status of schizophrenia [5]. On the other hand, neuroleptics have been reported to have immunosuppressive effects [6]. In addition, the endocrine system is also closely associated with the immune system [7], and we reported that chronic schizophrenic patients have depressed adrenocorticotrophic hormone (ACTH) and cortisol response to surgical stress [8]. Thus, several factors affect the immune system in chronic schizophrenic patients. Cytokines are peptides produced by cells of the immune system that act as mediators of both the immune response and the response of other tissues in the body to injury. IL-6, IL-8 and TNF-α are considered to be important mediators of the integrated host response. IL-6 is particularly important in stimulating the production of acute phase proteins by the liver [9]. IL-6 increases in response to the trauma of abdominal surgery [10] and may be associated with the development of postoperative complications [11]. C-reactive protein, which is one of the indicators of inflammatory response, is affected by IL-6 [12]. To our knowledge, proinflammatory cytokine responses in chronic schizophrenic patients to surgical stress have not been reported. The purpose of this study was to investigate the changes in IL-6, IL-8 and TNF-α in chronic schizophrenic patients during abdominal surgery. Patients and methods This study was done in Hakodate Watanabe Hospital. The protocol was approved by the institutional ethical committee of each hospital and informed consent was obtained from each patient. We studied 25 (19 males and 6 females) schizophrenic patients (Group S) ranging in age from 40 to 69 years who were on chronic phenothiazine derivatives for over 10 years, and 25 (18 males and 7 females) patients (Group C) ranging from 43 to 73 years in age as the control. All patients underwent lower abdominal surgery including either colectomy, hemicolectomy or sigmoidectomy for malignant tumours during the period from 1992 to 1997. The clinical status of malignancy in each patient was either stage I or II according to the pathology tumour node metastasis classification system. All patients with a history of anaemia (Hb < 10 g/dl), dysfunction of the immune system, marked cardiovascular disease, respiratory disease or endocrine disorders were excluded. Anaesthesia was induced with 1·5 mg/kg of intravenous propofol and 2 μg/kg fentanyl, and then tracheal intubation was facilitated by vecronium 0·1 mg/kg intravenously. Anaesthesia was maintained with an infusion of propofol at a starting rate of 10 mg/(kg h), which was reduced at intervals of 10 min each to 8 and 6 mg/(kg h) and then maintained at that rate until skin closure. The design of the propofol infusion was similar to the dose regimen used by Roberts et al. [13] aiming at a target blood concentration of 3 μg/ml. Six μg/kg fentanyl was administrated until the operation started and was followed by further increments according to the response of vital signs such as systolic blood pressure and heart rate, which were controlled within 20% of preoperative values. A 20-gauge arterial catheter was indwelt in the left radial artery to measure blood pressure and take arterial blood samples. The end-expiratory (Et) concentration of oxygen, carbon dioxide (CO2) and anaesthetics were monitored throughout the anaesthesia period using a 5250 RGM Analyser (Ohmeda, Madison, USA). The lungs were mechanically ventilated with 30% oxygen (O2) in air to maintain EtCO2at 35–45 mmHg. None of the patients required transfusion with packed red blood cells. The nasopharyngeal temperature was monitored continuously with an electric thermistor and was maintained at 36·0–37·0°C using a warming blanket and controlling temperature in operating room. Postoperatively, all patients were treated with continuous epidural administration of 2 ml/h of 1% lidocaine and 6 mg/day of morphine for pain relief. Blood samples of 5 ml were obtained from the arterial cannula before (T0) and at 15 min after the induction of anaesthesia (T1), at the end of surgery (T2) and at 24 h (T3) and 3 days after the operation (T4). The samples were immediately centrifuged and stored at − 80°C until analysis. Arterial plasma cytokine (IL-6, IL-8, TNF-α) concentrations were determined using enzyme-linked immunosorbent assay (ELISA) kits (Toray Fuji Bionics Inc., Tokyo, Japan). The minimal detectable values of IL-6, IL-8 and TNF-α by the ELISA kit were 2·5 pg/ml for IL-6, 3·0 pg/ml for IL-8 and 6 pg/ml for TNF-α. Intraassay and interassay coefficients of variation were all less than 10% in each determination. Plasma cortisol was determined with spectrometry. Interassay coefficients of variation were 1·5%. Plasma CRP was determined with turbidimetric immunoassay and coefficients of variation were all less than 5% in each determination. Data were expressed as mean (standard deviation). The data were log-transformed before carrying out anova analysis to avoid serious miscalculation of P-value. Comparisons between group means at each points (T2, T3, T4) were analysed by repeated-measures anova followed by using Bonferroni's correction. Comparisons between the baseline measurement (T0) and the other four measurements (T1, T2, T3, T4) were analysed by anova followed by using Dunnett's test. Spearman's test was used for calculating correlation coefficients. P-values less than 0·05 were considered significant. Results There was no significant difference between the groups in age, but average weight in Group S was significantly higher than that of Group C. There were no haemodynamic differences between the two groups in systolic and diastolic blood pressure and heart rate. There were no significant differences in the mean duration of anaesthesia and surgery and mean volume of blood loss between the two groups Table 1. Total fentanyl consumptions were 462·5 (23·7) µg for Group S and 457·0 (21·6) µg for Group C and there was no significant difference in total fentanyl consumption between both groups. There were no severe infectious complications in both groups. The numbers of patients with stage I and II were 10 and 15 in Group S, 8 and 17 in Group C. Table 1 Profile of patients, clinical and haemodynamic data during anaesthesia in this study Group S Group C Number of patients 25 25 Age (year) 53·4 (9·0) 55·1 (8·3) Weight (kg) 60·6 (11·3)* 54·2 (9·7) Duration of surgery (min) 143·4 (41·7) 132·1 (30·8) Duration of anaesthesia (min) 186·0 (47·8) 174·5 (42·0) Blood loss (g) 291·4 (120·6) 261·2 (132·7) Duration of neuroleptics 17·5 (9·4) none Systolic blood pressure (mmHg)  Before induction 137·4 (18·3) 138·8 (12·2)  15 min after skin incision 133·0 (16·6) 132·9 (14·3)  60 min after induction 147·2 (17·1) 144·8 (16.1)  24 h after end of surgery 135·6 (19·0) 131·5 (18·9) Diastolic blood pressure (mmHg)  Before induction 69·7 (9·3) 68·1 (10·4)  15 min after skin incision 67·4 (9·0) 67·0 (9·2)  60 min after induction 72·3 (9·6) 70·7 (13·8)  24 h after end of surgery 67·5 (10·3) 66·7 (11·3) Heart rate (bpm)  Before induction 70·0 (12·5) 68·2 (14·6)  15 min after skin incision 70·8 (13·1) 68·1 (11·7)  60 min after induction 73·3 (14·9) 73·8 (13·0)  24 h after end of surgery 71·6 (14·4) 69·3 (11·8) Group S Group C Number of patients 25 25 Age (year) 53·4 (9·0) 55·1 (8·3) Weight (kg) 60·6 (11·3)* 54·2 (9·7) Duration of surgery (min) 143·4 (41·7) 132·1 (30·8) Duration of anaesthesia (min) 186·0 (47·8) 174·5 (42·0) Blood loss (g) 291·4 (120·6) 261·2 (132·7) Duration of neuroleptics 17·5 (9·4) none Systolic blood pressure (mmHg)  Before induction 137·4 (18·3) 138·8 (12·2)  15 min after skin incision 133·0 (16·6) 132·9 (14·3)  60 min after induction 147·2 (17·1) 144·8 (16.1)  24 h after end of surgery 135·6 (19·0) 131·5 (18·9) Diastolic blood pressure (mmHg)  Before induction 69·7 (9·3) 68·1 (10·4)  15 min after skin incision 67·4 (9·0) 67·0 (9·2)  60 min after induction 72·3 (9·6) 70·7 (13·8)  24 h after end of surgery 67·5 (10·3) 66·7 (11·3) Heart rate (bpm)  Before induction 70·0 (12·5) 68·2 (14·6)  15 min after skin incision 70·8 (13·1) 68·1 (11·7)  60 min after induction 73·3 (14·9) 73·8 (13·0)  24 h after end of surgery 71·6 (14·4) 69·3 (11·8) * P < 0·05, between groups. Open in new tab Table 1 Profile of patients, clinical and haemodynamic data during anaesthesia in this study Group S Group C Number of patients 25 25 Age (year) 53·4 (9·0) 55·1 (8·3) Weight (kg) 60·6 (11·3)* 54·2 (9·7) Duration of surgery (min) 143·4 (41·7) 132·1 (30·8) Duration of anaesthesia (min) 186·0 (47·8) 174·5 (42·0) Blood loss (g) 291·4 (120·6) 261·2 (132·7) Duration of neuroleptics 17·5 (9·4) none Systolic blood pressure (mmHg)  Before induction 137·4 (18·3) 138·8 (12·2)  15 min after skin incision 133·0 (16·6) 132·9 (14·3)  60 min after induction 147·2 (17·1) 144·8 (16.1)  24 h after end of surgery 135·6 (19·0) 131·5 (18·9) Diastolic blood pressure (mmHg)  Before induction 69·7 (9·3) 68·1 (10·4)  15 min after skin incision 67·4 (9·0) 67·0 (9·2)  60 min after induction 72·3 (9·6) 70·7 (13·8)  24 h after end of surgery 67·5 (10·3) 66·7 (11·3) Heart rate (bpm)  Before induction 70·0 (12·5) 68·2 (14·6)  15 min after skin incision 70·8 (13·1) 68·1 (11·7)  60 min after induction 73·3 (14·9) 73·8 (13·0)  24 h after end of surgery 71·6 (14·4) 69·3 (11·8) Group S Group C Number of patients 25 25 Age (year) 53·4 (9·0) 55·1 (8·3) Weight (kg) 60·6 (11·3)* 54·2 (9·7) Duration of surgery (min) 143·4 (41·7) 132·1 (30·8) Duration of anaesthesia (min) 186·0 (47·8) 174·5 (42·0) Blood loss (g) 291·4 (120·6) 261·2 (132·7) Duration of neuroleptics 17·5 (9·4) none Systolic blood pressure (mmHg)  Before induction 137·4 (18·3) 138·8 (12·2)  15 min after skin incision 133·0 (16·6) 132·9 (14·3)  60 min after induction 147·2 (17·1) 144·8 (16.1)  24 h after end of surgery 135·6 (19·0) 131·5 (18·9) Diastolic blood pressure (mmHg)  Before induction 69·7 (9·3) 68·1 (10·4)  15 min after skin incision 67·4 (9·0) 67·0 (9·2)  60 min after induction 72·3 (9·6) 70·7 (13·8)  24 h after end of surgery 67·5 (10·3) 66·7 (11·3) Heart rate (bpm)  Before induction 70·0 (12·5) 68·2 (14·6)  15 min after skin incision 70·8 (13·1) 68·1 (11·7)  60 min after induction 73·3 (14·9) 73·8 (13·0)  24 h after end of surgery 71·6 (14·4) 69·3 (11·8) * P < 0·05, between groups. Open in new tab Plasma IL-6 concentration There was no significant difference in plasma IL-6 concentration before anaesthesia between Group C and Group S. Plasma IL-6 concentrations achieved the maximal values at the end of the operation in both Group C and Group S (76·9 (37·1) pg/ml for Group C and 32·1 (30·3) pg/ml for Group S). Plasma IL-6 concentrations remained elevated even 24 h after surgery in both Group C and Group S (35·1 (21·5) pg/ml for Group C and 15·8 (9·6) pg/ml for Group S). Plasma IL-6 concentrations in Group S at the end of the operation and 24 h after surgery were significantly lower than those of Group C. We investigated the relationships between plasma IL-6 concentrations at the end of the operation and duration of illness (plasma IL-6 concentrations versus duration of illness; r = 0·21, P = 0·31). However, we could not find a significant relationship Table 2. Table 2 Change in mean plasma IL-6, IL-8 and TNF-α concentrations before (T0) and at 15 min after the induction of anaesthesia (T1), the end of surgery (T2), 24 h (T3) and 3 days after the operation (T4) Plasma IL-6 concentrations (pg/ml) Plasma IL-8 concentrations (pg/ml) Plasma TNF-α concentrations (pg/ml) Group C Group S Group C Group S Group C Group S T0 5·5 (1·6) 4·7 (1·6) 0 0 10·8 (6·8) 10·5 (5·5) T1 6·4 (4·9) 5·1 (2·0) 0 0 13·8 (7·1) 12·6 (4·8) T2 76·9 (37·1)§ 32·1 (30·3)§ ** 8·7 (4·2)§ 6·1 (2·8)§* 12·1 (5·2) 12·8 (4·2) T3 35·1 (21·5)§ 15·8 (9·6)§* 3·8 (1·5)§ 2·6 (1·0)§* 12·7 (5·4) 12·0 (4·3) T4 18·6 (10·6) 9·7 (2·7) 0 0 12·0 (5·5) 12·6 (5·2) Plasma IL-6 concentrations (pg/ml) Plasma IL-8 concentrations (pg/ml) Plasma TNF-α concentrations (pg/ml) Group C Group S Group C Group S Group C Group S T0 5·5 (1·6) 4·7 (1·6) 0 0 10·8 (6·8) 10·5 (5·5) T1 6·4 (4·9) 5·1 (2·0) 0 0 13·8 (7·1) 12·6 (4·8) T2 76·9 (37·1)§ 32·1 (30·3)§ ** 8·7 (4·2)§ 6·1 (2·8)§* 12·1 (5·2) 12·8 (4·2) T3 35·1 (21·5)§ 15·8 (9·6)§* 3·8 (1·5)§ 2·6 (1·0)§* 12·7 (5·4) 12·0 (4·3) T4 18·6 (10·6) 9·7 (2·7) 0 0 12·0 (5·5) 12·6 (5·2) All values were expressed as mean (standard deviation). § P < 0·01 § P < 0·001 versus before induction of anaesthesia. * P < 0·05 ** P < 0·01 versus Group S. Open in new tab Table 2 Change in mean plasma IL-6, IL-8 and TNF-α concentrations before (T0) and at 15 min after the induction of anaesthesia (T1), the end of surgery (T2), 24 h (T3) and 3 days after the operation (T4) Plasma IL-6 concentrations (pg/ml) Plasma IL-8 concentrations (pg/ml) Plasma TNF-α concentrations (pg/ml) Group C Group S Group C Group S Group C Group S T0 5·5 (1·6) 4·7 (1·6) 0 0 10·8 (6·8) 10·5 (5·5) T1 6·4 (4·9) 5·1 (2·0) 0 0 13·8 (7·1) 12·6 (4·8) T2 76·9 (37·1)§ 32·1 (30·3)§ ** 8·7 (4·2)§ 6·1 (2·8)§* 12·1 (5·2) 12·8 (4·2) T3 35·1 (21·5)§ 15·8 (9·6)§* 3·8 (1·5)§ 2·6 (1·0)§* 12·7 (5·4) 12·0 (4·3) T4 18·6 (10·6) 9·7 (2·7) 0 0 12·0 (5·5) 12·6 (5·2) Plasma IL-6 concentrations (pg/ml) Plasma IL-8 concentrations (pg/ml) Plasma TNF-α concentrations (pg/ml) Group C Group S Group C Group S Group C Group S T0 5·5 (1·6) 4·7 (1·6) 0 0 10·8 (6·8) 10·5 (5·5) T1 6·4 (4·9) 5·1 (2·0) 0 0 13·8 (7·1) 12·6 (4·8) T2 76·9 (37·1)§ 32·1 (30·3)§ ** 8·7 (4·2)§ 6·1 (2·8)§* 12·1 (5·2) 12·8 (4·2) T3 35·1 (21·5)§ 15·8 (9·6)§* 3·8 (1·5)§ 2·6 (1·0)§* 12·7 (5·4) 12·0 (4·3) T4 18·6 (10·6) 9·7 (2·7) 0 0 12·0 (5·5) 12·6 (5·2) All values were expressed as mean (standard deviation). § P < 0·01 § P < 0·001 versus before induction of anaesthesia. * P < 0·05 ** P < 0·01 versus Group S. Open in new tab Plasma IL-8 concentration Plasma IL-8 concentration (6·1 (2·8) pg/ml) in Group S at the end of the operation was significantly (P < 0·05) lower than 8·7 ± 4·2 pg/ml of Group C. There were no significant differences in plasma IL-8 concentrations between Group C and Group S at the other sampling points Table 2. Plasma TNF-α concentration Plasma TNF-α concentrations of Group S were 10·5 (5·5) pg/ml prior to anaesthesia and 12·8 (4·2) pg/ml at the end of the operation. Plasma TNF-α concentrations of Group C were 10·8 (6·8) pg/ml prior to anaesthesia and 12·1 (5·2) pg/ml at the end of the operation. There were no significant differences in plasma TNF-α concentrations between Group S and Group C throughout the study period Table 2. Plasma cortisol concentration Plasma cortisol concentration (19·5 (10·9) µg/dl) of Group S at the end of surgery was significantly lower than 29·1(12·0) µg/dl of Group C. We found that plasma IL-6 concentrations correlated with plasma cortisol concentrations (r = 0·71, P < 0·001 for schizophrenic patients and r = 0·79, P < 0·001 for control patients). In schizophrenic patients, for each 10 pg/ml increase in plasma IL-6 concentration there was a mean increase of 2·6 μg/dl in plasma cortisol Fig. 1. Fig. 1 Open in new tabDownload slide Relationship between plasma IL-6 concentrations and plasma cortisol concentrations at the end of surgery for (a) schizophrenic patients and (b) control patients. Plasma IL-6 concentrations correlated with plasma cortisol concentrations with a regression line of y = 0·26 x + 11·3 for schizophrenic patients and y = 0·25 x + 9·64 for control patients. Fig. 1 Open in new tabDownload slide Relationship between plasma IL-6 concentrations and plasma cortisol concentrations at the end of surgery for (a) schizophrenic patients and (b) control patients. Plasma IL-6 concentrations correlated with plasma cortisol concentrations with a regression line of y = 0·26 x + 11·3 for schizophrenic patients and y = 0·25 x + 9·64 for control patients. C-reactive protein (CRP) concentration CRP concentrations in Group S were 3·58 (1·69) mg/dl at 24 h after the end of surgery and 0·47 (0·03) mg/dl 3 days after the surgery. The plasma CRP concentrations of Group S at 24 h after the end of surgery was significantly lower than 5·11 (1·39) mg/dl of Group C. CRP concentrations at 24 h after the end of surgery correlated (r = 0·65, P < 0·001) with plasma IL-6 concentrations. In schizophrenic patients, for each 10 pg/ml increase in plasma CRP there was a mean increase of 0·4 μg/dl in plasma IL-6 concentration Fig. 2. Fig. 2 Open in new tabDownload slide Relationship between plasma IL-6 concentrations and CRP concentrations in schizophrenic patients at 24 h after the end of surgery. Plasma IL-6 concentrations correlated with CRP concentrations with a regression line of y = 0·04 x + 2·42 for schizophrenic patients. Fig. 2 Open in new tabDownload slide Relationship between plasma IL-6 concentrations and CRP concentrations in schizophrenic patients at 24 h after the end of surgery. Plasma IL-6 concentrations correlated with CRP concentrations with a regression line of y = 0·04 x + 2·42 for schizophrenic patients. Discussion The present study showed that elevation of plasma IL-6 and IL-8 concentrations by surgery was lower in schizophrenic patients than in control patients. IL-6 and IL-8 concentrations have been shown to correlate with the extent of the surgical trauma, duration of surgery and amount of blood loss [12]. The present study showed no significant differences in the duration of surgery and the amount of blood loss between schizophrenic patients and control patients. Suggesting these did not significantly influence the findings. The immunosuppressive response to surgical damage appears to be associated with schizophrenia itself or neuroleptics. Interaction between the hypothalamus–pituitary–adrenal (HPA) axis and the immune system has been demonstrated by Imura et al. [7]. The inflammatory cytokines released by surgery stimulate the hypothalamus and pituitary, resulting in release of corticotropin-releasing hormone (CRH), adrenocorticotrophic hormone (ACTH) and cortisol. Human lymphocytes and monocytes have CRH binding sites [14]. CRH increases release of IL-6 from peripheral blood mononuclear cells, suggesting a role of CRH as a mediator of immune cells [15]. We previously reported that chronic schizophrenic patients have depressed ACTH and cortisol response to surgical stress [8]. We demonstrated that down-regulation of ACTH and cortisol secretion during surgery in chronic schizophrenic patients seems to result from inhibition of release of CRH [8]. The present study showed that the plasma cortisol response to surgical stress was lower than that of control patients, and that there was a correlation between IL-6 and cortisol concentrations. Thus, the depressed cytokine response appears to be related to hypothalamus–pituitary–adrenal dysfunction in chronic schizophrenic patients. Neuroleptics have been reported to have immunosuppressive effects. Maes et al. [6] reported that plasma IL-6 concentrations in schizophrenic patients were significantly lower after treatment with neuroleptics than before treatment. Haloperidol increases lipopolysaccharide (LPS)-stimulated production of IL-1 receptor antagonist [16]. Thus, decreased plasma IL-6 response to surgical trauma appears to be partly caused by immunosuppressive effects of neuroleptics. In schizophrenic patients in remission, the mean concentration of IL-6 did not significantly differ from control patients [17]. In this study, as the schizophrenic patients were in remission, we could find no significant difference in baseline plasma concentration of IL-6 between chronic schizophrenic patients and control patients. The CRP response to surgical trauma in chronic schizophrenic patients was lower than in control patients and the CRP concentrations correlated with plasma IL-6 concentrations. CRP is one of the acute-phase proteins and its level increases in plasma during an acute inflammatory response, thereby maximizing immune responsiveness and stimulating repair of damaged tissues. Ohzatoet al. reported that plasma IL-6 concentrations correlate with CRP response [12]. IL-6 is a potent stimulator of the hepatic acute-phase protein synthesis [18]. Maximal CRP synthesis in vitro has been shown to occur 20–30 h after hepatocytes have been stimulated with IL-6 [19]. Thus, the CRP response to surgical trauma depends on IL-6 and the decreased CRP response to surgical trauma may underestimate the acute inflammatory response in chronic schizophrenic patients. We could observe no significant differences in plasma concentrations of TNF-α between chronic schizophrenic patients and control patients through the perioperative course, during which the concentrations remained low in both groups. Chlorpromazine inhibits LPS-stimulated TNF-α production [20]. Thus, hypothalamic suppression by neuroleptics may at least in part result in low concentrations of TNF-α in chronic schizophrenic patients. On the other hand, Gilliland et al. also reported that TNF-α did not change from low baseline levels throughout the perioperative period in abdominal surgery of nonpsychotic patients [21]. The low concentration of plasma TNF-α may indicate a regulatory role in the production of the other inflammatory cytokines [22]. Anaesthetic technique influences the perioperative cytokine response. In this study, the intravenous anaesthetics with fentanyl and propofol were used for all patients. Intravenous anaesthetics are reported to induce proinflammatory cytokine production. Propofol increases proinflammatory cytokine TNF-α[23] and has minimal effect on anti-inflammatory cytokine IL-4 [24]. Gilliland et al. reported that inhaled anaesthetics resulted in lower postoperative levels of IL-10 than an intravenous anaesthetic technique [21]. Opiates contribute to immunosuppression. Fentanyl stimulates IL-1 receptor antagonist response and attenuates IL-1β release [25]. Thus, anaesthetics may affect the balance of perioperative cytokine response. In conclusion, plasma IL-6 and IL-8 responses to surgical trauma were inhibited in chronic schizophrenic patients. Plasma IL-6 concentration correlates with plasma cortisol concentration. 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TI - Plasma cytokine response to surgical stress in schizophrenic patients
JO - Clinical & Experimental Immunology
DO - 10.1046/j.1365-2249.2001.01581.x
DA - 2001-12-20
UR - https://www.deepdyve.com/lp/oxford-university-press/plasma-cytokine-response-to-surgical-stress-in-schizophrenic-patients-dHbgrckP0O
SP - 89
EP - 93
VL - 125
IS - 1
DP - DeepDyve
ER -