Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin-6 (IL-6) and monocyte chemotactic and activating factor/monocyte chemoattractant protein-1 (MCAF/MCP-1) play pivotal roles in systemic inflammation, immune response, and tissue damage after cardiopulmonary bypass (CPB). Previous reports have described transient rises in IL-6 and MCAF after CPB, but the data seem to vary according to the different surgical procedures used. To evaluate the influence of the different surgical procedures on the proinflammatory cytokine responses, we compared perioperative serum IL-6 and MCAF release in coronary artery bypass grafting (CABG) and valvular surgery cases. Eighteen CABG (CABG group) and 7 single valvular cardiac surgery patients (valve group) were included in this study. Blood samples were taken to measure the serum concentrations of IL-6 at the induction of anesthesia, at the removal of the aortic cross-clamp, at the end of CPB, at the end of surgery, and 24 h after the termination of surgery. Serum IL-6 and MCAF were assayed by ELISA. Serum IL-6 increased immediately after aortic declamping and reached its peak at the end of surgery in both groups. Serum IL-6 concentrations at the end of surgery and 24 h after surgery were significantly higher in the valve group than in the CABG group (123.9 +/- 21.7 pg/ml vs. 79.7 +/- 10.4 pg/ml, p = 0.049; 113.6 +/- 25.0 pg/ml vs. 39.9 +/- 11.5 pg/ml, p = 0.006, respectively). Serum MCAF increased immediately after aortic declamping, and the MCAF level at the end of surgery was significantly higher in the valve group than in the CABG group (1118.4 +/- 353.9 pg/ml vs. 241.0 +/- 71.2 pg/ml, p = 0.002, respectively). IL-6 and MCAF may play important roles in the pathophysiology of surgical damage with CPB, and the different surgical procedures appear to affect the proinflammatory cytokine release after cardiac surgery differently.
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PMID:Influence of surgical procedures on interleukin-6 and monocyte chemotactic and activating factor responses: CABG vs. valvular surgery. 1067 Jun 46

Several studies suggest that anesthetics modulate the immune response. The aim of this study was to investigate the effect of halothane and thiopental on the lung inflammatory response. Rats submitted or not to intratracheal (IT) instillation of lipopolysaccharides (LPS) were anesthetized with either halothane (0. 5, 1, or 1.5%) or thiopental (60 mg. kg(-1)) and mechanically ventilated for 4 h. Control rats were treated or not by LPS without anesthesia. Lung inflammation was assessed by total and differential cell counts in bronchoalveolar lavage fluids (BALF) and by cytokine measurements (tumor necrosis factor-alpha [TNF-alpha], interleukin-6 [IL-6], macrophage inflammatory protein-2 [MIP-2], and monocyte chemoattractant protein-1 [MCP-1]) in BALF and lung homogenates. In the absence of LPS treatment, neither halothane nor thiopental modified the moderate inflammatory response induced by tracheotomy or mechanical ventilation. Cell recruitment and cytokine concentrations were increased in all groups receiving IT LPS. However, in halothane-anesthetized rats (halothane > or = 1%), but not in thiopental-anesthetized rats, the LPS-induced lung inflammation was altered in a dose-dependent manner. Indeed, when using 1% halothane, polymorphonuclear leukocyte (PMN) recruitment was decreased by 55% (p < 0.001) and TNF-alpha, IL-6, and MIP-2 concentrations in BALF and lung homogenates were decreased by more than 60% (p < 0.001) whereas total protein and MCP-1 concentrations remained unchanged. The decrease of MIP-2 (observed at the protein and messenger RNA [mRNA] level) was strongly correlated to the decrease of PMN recruitment (r = 0.73, p < 0.05). This halothane-reduced lung inflammatory response was transient and was reversed 20 h after the end of the anesthesia. Our study shows that halothane > or = 1%, delivered during 4 h by mechanical ventilation, but not mechanical ventilation per se, alters the early LPS-induced lung inflammation in the rat, suggesting a specific effect of halothane on this response.
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PMID:Halothane reduces the early lipopolysaccharide-induced lung inflammation in mechanically ventilated rats. 1111 52

Both propofol and midazolam are known to inhibit immune function. The aim of this study was to investigate cytokine production in critically ill surgical patients as early markers of immune response to prolonged infusion of propofol and midazolam. The study enrolled 40 elective patients who were to receive long-term sedation for more than 2 days. Patients were randomly allocated to one of two equally sized groups. Central venous blood samples for measurement of interleukin-1beta (IL-1beta), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) were drawn prior to the start and after 48 h of infusion. After 48 h, propofol caused significant increases in IL-1beta (24%), IL-6 (23%) and TNF-alpha (4.8 times) levels, while midazolam caused significant decreases in IL-1beta (21%), IL-6 (21%) and TNF-alpha (19%). Both agents caused significant decreases in IL-8 levels (propofol: 30%, midazolam: 48%, p < 0.05). Propofol caused significant decreases in IL-2 levels (68%, p < 0.001) but increases in IFN-gamma (30%, p < 0.05), whereas there was no significant change with midazolam compared with the pre-infusion level. In conclusion, during 48 h of continuous infusion, propofol stimulated, while midazolam suppressed, the production of the pro-inflammatory cytokines IL-1beta, IL-6 and TNF-alpha, and both caused suppression of IL-8 production. Propofol inhibited IL-2 production and stimulated IFN-gamma production, whereas midazolam failed to do so. Therefore, sedative agents may have clinical implications in high-risk and immunocompromised patients.
Anaesthesia 2001 Jan
PMID:The immunomodulatory effects of prolonged intravenous infusion of propofol versus midazolam in critically ill surgical patients. 1116 28

It is well known that, subsequent to cardiopulmonary bypass, and particularly in children, an inflammatory response within the body can often result in a characteristic syndrome. Recently, it has been suggested that this phenomenon is due to a systemic inflammatory response, with significant involvement of cytokines. With this in mind, we investigated the behavior of tumour necrosis factor-alpha and interleukin-6 during the operative and in the immediate postoperative period in a group of children submitted to open heart surgery. We investigated any possible relation between the levels of these cytokines in the serum and the length of cardiopulmonary bypass, with the serum levels of lactate, and with the extent of use of inotropic drugs in postoperative period. The cytokines were measured in samples withdrawn after induction of anesthesia, after 10 minutes of cardiopulmonary bypass, after re-establishment of circulation, and then 2 and 24 hours after the end of cardiopulmonary bypass. The levels of tumour necrosis factor-alpha and interleukin-6 increased between the beginning and at two hours of the end of cardiopulmonary bypass. There was no correlation between the levels of these cytokines in the serum and the length of cardiopulmonary bypass, although there was a positive relation between levels of interleukin-6 and lactate in samples withdrawn at two hours of the end of bypass, and the measured levels of the cytokines correlated with the extent of inotropic drugs employed in the postoperative period.
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PMID:Cytokines and pediatric open heart surgery with cardiopulmonary bypass. 1123 96

The aim of this clinical study was to investigate the time sequence between intraoperative and postoperative endotoxemia, changes in intramucosal pH(I), mediator release, and acute phase proteins and their relationship to postoperative infections. In 60 patients (median age 61 [33-72] years, male/female: 50/10) plasma levels of endotoxin, endotoxin neutralizing capacity (ENC), leukotriene-C4 (LTC4), 6-ketoprostaglandin-F-1alpha (PGF), thromboxane-B2 (TxB2), interleukin-6 (IL-6), and C-reactive protein (CRP) were measured before, during, and after cardiac surgery. The intraluminal pH(I) of the stomach was assessed as a marker of splanchnic blood circulation. Patients were divided in one group with postoperative infections (group A, n = 8) and another groups without infections (group B, n = 52). Among all measured parameters, endotoxin plasma levels showed the most rapid changes. A significant increase of endotoxin plasma levels and a decrease in ENC appeared after the induction of anesthesia, culminating in a peak after reperfusion. Endotoxin showed a significantly higher increase in group A (14fold) compared to group B (sixfold, p<0.001), whereas ENC decreased by eightfold in both groups. The parameters of the arachidonic cascade increased and pH(I) decreased, however, there were no significant differences between both groups. The latest increase was observed for the acute phase proteins IL-6 and CRP. IL-6 levels peaked 6 hours postoperatively with a 20fold (group B) and 30fold (group A) increase (p < 0.001 vs baseline; no differences between groups), whereas CRP rose at the first postoperative day with a 21 fold (group B) and 25fold (group A) increase at day 2 (p<0.001 vs baseline, no difference between groups). Differences between both groups appeared at the second postoperative day for IL-6 (median values group A/B: 421/219 pg/mL; p <0.05) and at the fifth postoperative day for CRP (median values group A/B: 321/81 mg/L; p < 0.05). In conclusion, endotoxin seems to be the earliest trigger of the mediator cascade in acute phase response and may indicate infections in the postoperative course.
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PMID:Changes of gut barrier function during anesthesia and cardiac surgery. 1151 87

It has been suggested that the incidence of early graft occlusion after arterial reconstructive surgery to the leg may be decreased by epidural analgesia. This effect may be mediated by the suppression of the usual cortisol response to surgery, which results in increased circulating plasminogen activator inhibitor-1 with consequent adverse effects on fibrinolysis. To investigate this and other potential mechanisms, 30 patients undergoing arterial reconstructive surgery to the leg were randomized to receive either general anaesthesia or general anaesthesia plus epidural analgesia. Post-operative analgesia was provided by morphine infusion or epidural analgesia, respectively. Blood samples were collected at 0, 2, 4, 6, 12 and 24 h, and 2, 3 and 5 days and analysed for cortisol, plasminogen activator inhibitor-1 antigen, interleukin-6 and beta thromboglobulin. The incidence of graft-related and systemic complications was recorded for 30 days. Only one patient developed early graft occlusion that required embolectomy and eventually amputation. There were no significant changes from control values in either group of patients in circulating cortisol, plasminogen activator inhibitor-1 and beta thrombogobulin (a marker for platelet degranulation). Interleukin-6 values increased significantly in both groups after 4 h and remained elevated until day 3. There were no significant differences between the groups in any variable measured. We conclude that any effect of epidural analgesia on early graft patency is unlikely to be mediated by fibrinolysis or platetlet degranulation.
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PMID:Epidural analgesia and arterial reconstructive surgery to the leg: effects on fibrinolysis and platelet degranulation. 1157 65

Several studies have been demonstrated that endotoxin is a potent stimulus of the acute inflammatory response following traumatic injury. Although numerous studies have indicated that the extent of surgical intervention correlates well with the inflammatory response, the potential role of endotoxin as a trigger under those conditions still remains unknown. Therefore, the aim of this study was to elucidate whether or not the up-regulated inflammatory mediators are paralleled by increased endotoxin plasma levels during and following surgery, and whether the extent of surgical intervention represents a crucial factor under those conditions. To study this, plasma was collected at various time points during and after surgery from 52 patients subjected to abdominal surgery (i.e., major surgery) and 25 patients subjected to thyroid surgery (i.e., minor surgery). Plasma was assessed for endotoxin, endotoxin neutralizing capacity (ENC), and inflammatory mediators (leucotriene-C4 [LTC4]-, 6-keto-prostaglandin-F-1-alpha [PGF]-, thromboxane-B2 [TxB2], interleukin-6 [IL-6], and C-reactive protein [CRP]). Furthermore, splanchnic blood circulation was measured by determination of the intraluminal pH of the stomach and sigma (pHi) by intraluminal tonometry. Mesenteric lymph nodes were also collected at the time point of organ mobilization in the major surgery group and were assessed for bacterial translocation. Among all parameters investigated, endotoxin showed the most rapid changes. A significant increase in plasma levels of endotoxin and a decrease of ENC were found in the major surgery groups following induction of anesthesia and in the minor surgery groups after skin incision. Moreover, the incidence of elevated endotoxin levels was significantly higher (89% with elevated endotoxin levels) than the incidence of bacterial translocation (35% with gram-negative bacteria) in mesenterial lymph nodes of the major surgery group. pHi decreased significantly in both groups after skin incision, but no difference was observed between the major and minor surgery groups. Plasma mediators of the arachidonic acid cascade (LTC4, PGF, and TxB2) were only elevated in individual patients during and following surgery in both groups. Conversely, the post-operative increase in the acute phase mediators was significantly different in the major and minor surgery groups. IL-6 plasma levels peaked higher and earlier after major surgery than after minor surgery and the delayed increase of CRP was significantly greater in the major surgery group. In conclusion, the results indicate that plasma levels of endotoxin significantly correlate with the severity of the surgical intervention and may play an important role in inducing mediators of the acute phase reaction under such conditions.
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PMID:Inflammatory response during abdominal and thyroid surgery: a prospective clinical trial on mediator release. 1169 69

Plasma osteocalcin, a marker of osteoblastic activity, decreases after major abdominal and gynaecological surgery. Increased cortisol secretion and other hormonal and inflammatory components of the peri-operative stress response may play a role in mediating this response. We assessed the effects of three different anaesthetic techniques on peri-operative osteocalcin concentrations. Thirty-six female patients undergoing elective total hip replacement were randomly assigned to receive propofol, propofol plus 'three-in-one' block or etomidate as part of a general anaesthetic technique. We measured plasma osteocalcin and serum cortisol, bone specific alkaline phosphatase, interleukin-6, plasma epinephrine, norepinephrine, plasma glucose and cystatin C concentrations for up to 3 days after surgery. Etomidate successfully inhibited the cortisol response to surgery but plasma osteocalcin declined in all patients. This was accompanied by increased plasma catecholamines, interleukin-6 and glucose concentrations, and decreased cystatin C-values. Inhibition of the cortisol response to surgery failed to prevent a decrease in plasma osteocalcin concentrations after surgery, suggesting that other factors such as cytokines or catecholamines may play a significant role.
Anaesthesia 2002 Apr
PMID:Osteocalcin and the hormonal, inflammatory and metabolic response to major orthopaedic surgery. 1193 88

Perioperative stroke occurs in 2-3% of adult cardiac surgery patients, and significant cognitive dysfunction is experienced by 40-60% of patients in the first postoperative week. Perioperative neurocognitive abnormalities are associated with a greatly increased risk of perioperative mortality, lengthy intensive care and hospital stay, and more intensive rehabilitative care. Long-term cognitive dysfunction, ranging from months to years, occurs in 25-40% of adult cardiac surgery patients, resulting in a decreased quality of life. Cerebral emboli are an important cause of perioperative neurocognitive abnormalities. Aortic cannulation, clamping, and manipulation during surgery may dislodge atheromatous materials into the cerebral circulation, leading to perioperative or postoperative stroke. Nevertheless, acute and chronic neurocognitive dysfunction frequently occurs in non-cardiac surgery patients as well, suggesting that some element of surgery and/or anesthesia itself causes or contributes to this phenomenon. One possible cause may be central nervous system (CNS) responses to peripheral tissue injury or inflammation. The CNS is sensitive to systemic pro-inflammatory mediators such as endotoxin and the cytokines interleukin-6 and interleukin- 8, which are activated by surgical trauma. This article discusses the behavior and effects of these inflammatory agents and their intensification in combination with postoperative hyperthermia. The potential beneficial role of pharmacological agents such as heparin, lidocaine, and aprotinin is also examined.
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PMID:Emboli, inflammation, and CNS impairment: an overview. 1253 40

Hemodynamic instability is frequent after coronary surgery. The present study tested the hypothesis that inflammation, as determined by circulating cytokine levels, may contribute to the difficulty of controlling arterial blood pressure after coronary artery bypass grafting. A group of 44 male patients undergoing elective coronary artery bypass grafting with cardiopulmonary bypass were studied. Plasma levels of tumor necrosis factor-alpha, interleukin-6 (IL-6), IL-8, and IL-10 were measured before anesthesia induction, 5 minutes and 1 hour after reperfusion to the myocardium, and 2 and 18 hours after arriving in the intensive care unit (ICU). The 29 patients who did not need a vasopressor (norepinephrine) during their ICU stay were designated group I. They were compared to group II, which consisted of 15 patients who required a pressor agent in the ICU. Although no significant differences between groups were found regarding their hemodynamic variables, IL-6 and IL-8 levels were higher in the patients who used a pressor agent in the ICU. The norepinephrine dosage used in the ICU correlated with plasma IL-8 levels 2 hours after arriving in the ICU (r = 0.56, p = 0.031). Circulating IL-6 levels in group II were significantly higher than those in group I 2 hours after arriving in the ICU (126.5 +/- 90.5 vs. 66.5 +/- 48.2 pg/ml; p < 0.05). The mean IL-8 levels were higher in group II at 5 minutes (34.9 +/- 25.7 vs. 17.3 +/- 11.3 pg/ml) and 1 hour (38.6 +/- 30.5 vs. 22.4 +/- 16.7 pg/ml) after reperfusion, and 2 hours (33.0 +/- 21.6 vs. 22.8 +/- 16.7 pg/ml) after arriving in the ICU (p = 0.036). Postoperative vasodilation was associated with increased circulating IL-8 levels. Strategies that modulate cytokine responses may improve hemodynamic stability after coronary artery bypass grafting.
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PMID:Relation of cytokines to vasodilation after coronary artery bypass grafting. 1292 2


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