Background: Surgical treatment for esophageal cancer is major invasive surgery. Recently, opioids have been implicated in the promotion of cancer recurrence and metastasis because of their immunosup-pressive effects. ...Background: Surgical treatment for esophageal cancer is major invasive surgery. Recently, opioids have been implicated in the promotion of cancer recurrence and metastasis because of their immunosup-pressive effects. However, it has not been fully evaluated whether the intraoperative use of opioids is directly correlated with postoperative prognosis in the clinical setting. Therefore, this study aimed to identify perioperative factors related to postoperative complications and 2-year survival in patients undergoing esophageal cancer surgery. Methods: We retrospectively reviewed 105 patients who underwent surgery for esophageal cancer at Kagoshima University Hospital from January 2013 to December 2017. Patient parameters were compared between survivors and non-survivors for 2 years after surgery. Results: The 2-year survival rate after esophageal cancer surgery was 76.2% (80 survivors vs. 25 non-survivors). The incidence of postoperative pneumonia within 7 days after surgery was significantly higher in non-survivors compared with survivors (36.0% vs. 16.3%;odds ratio, 2.90;95% confidence interval, 1.06 - 7.96, P P = 0.029). The intraoperative dosage of opioids calculated as fentanyl equivalents was not correlated with any postoperative complications or 2-year survival. The preoperative albumin level and neutrophil-lymphocyte ratio were associated with the incidence of postoperative pneumonia. Conclusions: Postoperative pneumonia may be a possible predictor of 2-year prognosis in patients after esophageal cancer surgery, and is not correlated with intraoperative use of opioids. Preoperative physical status including immune and nutrient states may be more important for postoperative prognosis after esophageal cancer surgery.展开更多
Background: General anesthesia using remifentanil may suppress the unwanted metabolic changes caused by surgical stress including hyperglycemia and ketogenesis. Surgery-related changes in catabolism can be attenuated ...Background: General anesthesia using remifentanil may suppress the unwanted metabolic changes caused by surgical stress including hyperglycemia and ketogenesis. Surgery-related changes in catabolism can be attenuated with low-dose glucose load, without causing hyperglycemia. However, the impact of glucose load in diabetic patients during surgery is unknown. In this study, we investigated the effect of glucose load on catabolism during remifentanil-based anesthesia in patients with diabetes mellitus. Methods: Twenty-nine patients with diabetes mellitus undergoing elective surgery were randomly assigned to receive a glucose load (1.5 mg/kg/min) or not. Plasma levels of glucose, insulin, cortisol, dopamine, adrenaline, noradrenaline, acetoacetic acid, free fatty acid, ketone bodies, 3-hydroxybutyric acid, and 3-methylhistidine/creatinine, a marker of protein catabolism were measured at the start of surgery and 3 h after the start of surgery. Results: Glucose and insulin levels were significantly higher in patients who received a glucose load than in those who did not. Cortisol levels decreased at 3 h after the start of surgery in both groups whereas the levels of catecholamines were unchanged. Acetoacetic acid and total ketone body levels were significantly lower in patients given a glucose load than in those who were not 3 h after the start of surgery. The difference in the 3 methylhistidine/creatinine ratio between the two groups was not significant. Conclusions: The infusion of glucose suppressed lipid catabolism in diabetic patients under remifentanil-based anesthesia during surgery. Our study also suggests that in patients with diabetes mellitus, protein sparing is inhibited by remifentanil-based anesthesia, regardless of the glucose load. Trial registration: the University Hospital Medical Information Network identifier: UMIN000010914.展开更多
Background: Perioperative exacerbation of hyperglycemia and insulin resistance is associated with increased complications in patients with diabetes mellitus. We recently reported that glucose load during anesthesia wi...Background: Perioperative exacerbation of hyperglycemia and insulin resistance is associated with increased complications in patients with diabetes mellitus. We recently reported that glucose load during anesthesia with sevoflurane suppressed lipid catabolism in diabetic patients. In contrast to inhaled anesthetics, propofol solution contains triglycerides, which can be an energy source during surgery. However, the clinical relevance of glucose load under propofol-based anesthesia in diabetic patients is unknown. Therefore, we investigated the effect of intraoperative glucose load on catabolism during propofol-based anesthesia in patients with diabetes mellitus. Methods: Twenty-three patients with diabetes mellitus undergoing elective surgery with propofol-remifentanil-based anesthesia were randomly assigned to receive a glucose load (1.5 mg/kg/ min) or not. Plasma levels of glucose, insulin, cortisol, catecholamines, acetoacetic acid, free fatty acids, ketone bodies, 3-hydroxybutyric acid, and 3-methylhistidine/creatinine, used as a marker for protein catabolism, were measured at the start of surgery and 3 h later. Results: Glucose and insulin levels were significantly higher in patients who received a glucose load than in those who did not. Nonetheless, the levels of cortisol and catecholamines were unchanged during surgery. Similarly, the difference in the levels of markers for lipid as well as protein catabolism was not significant between the groups at 3 h after the start of surgery. Conclusions: Changes in lipid as well as protein catabolism were not altered by glucose load in diabetic patients under propofol-based anesthesia with remifentanil. Our study suggested that continuous infusion of propofol at a clinical dose is sufficient to reduce the requirement for glucose infusion during surgery in patients with diabetes.展开更多
Background: Transient receptor potential ankyrin (TRPA) 1 is known as a peripheral initiator of acute inflammation and hyperalgesia. However, its role in the facilitation of innate immune responses followed by resolut...Background: Transient receptor potential ankyrin (TRPA) 1 is known as a peripheral initiator of acute inflammation and hyperalgesia. However, its role in the facilitation of innate immune responses followed by resolution of the inflammation triggered by a surgical incision has not been fully investigated. Therefore, we evaluated the mechanism by which TRPA1 regulates the inflammatory responses mainly facilitated by neutrophils and macrophages in the early course of wound repair after an incision. Methods: Plantar incision was performed in wild-type and TRPA1-/- mice. The infiltration of polymorphonuclear neutrophils, macrophage phenotype, and induction of inflammatory mediators were assessed for 7 days postoperatively. Results: TRPA1-/-?mice exhibited decreased infiltration of polymorphonuclear neutrophilscompared with wild-type mice on day 1. Consistently, the influx of F4/80+ iNOS+ proinflammatory M1 macrophages to incised sites was markedly decreased on day 2. Similarly, F4/80+ CD206+M2 macrophages, which regulate the resolution of inflammation and promote wound healing in the later phase of acute inflammation, were significantly decreased in TRPA1-/- compared with those in wild-type mice on day 7. In addition, the induction of heme oxygenase-1, which promotes wound healing by switching phenotype of macrophages, was decreased in the early phase of acute inflammation, whereas the expression of proinflammatory mediators such as tumor necrosis factor and cyclooxygenase-2, and 15-lipoxygenase, which are involved in the resolution of inflammation was increased in the late phase in TRPA1-/- mice. Conclusions: Early innate immune responses including neutrophil infiltration and macrophage polarization at incised sites were inhibited in TRPA1-/- mice, associated with increased pro-inflammatory mediators in later phase. Peripheral TRPA1 may facilitate the acute inflammatory process, leading to the promotion of macrophage-mediated resolution of inflammation and wound repair after a surgical incision.展开更多
文摘Background: Surgical treatment for esophageal cancer is major invasive surgery. Recently, opioids have been implicated in the promotion of cancer recurrence and metastasis because of their immunosup-pressive effects. However, it has not been fully evaluated whether the intraoperative use of opioids is directly correlated with postoperative prognosis in the clinical setting. Therefore, this study aimed to identify perioperative factors related to postoperative complications and 2-year survival in patients undergoing esophageal cancer surgery. Methods: We retrospectively reviewed 105 patients who underwent surgery for esophageal cancer at Kagoshima University Hospital from January 2013 to December 2017. Patient parameters were compared between survivors and non-survivors for 2 years after surgery. Results: The 2-year survival rate after esophageal cancer surgery was 76.2% (80 survivors vs. 25 non-survivors). The incidence of postoperative pneumonia within 7 days after surgery was significantly higher in non-survivors compared with survivors (36.0% vs. 16.3%;odds ratio, 2.90;95% confidence interval, 1.06 - 7.96, P P = 0.029). The intraoperative dosage of opioids calculated as fentanyl equivalents was not correlated with any postoperative complications or 2-year survival. The preoperative albumin level and neutrophil-lymphocyte ratio were associated with the incidence of postoperative pneumonia. Conclusions: Postoperative pneumonia may be a possible predictor of 2-year prognosis in patients after esophageal cancer surgery, and is not correlated with intraoperative use of opioids. Preoperative physical status including immune and nutrient states may be more important for postoperative prognosis after esophageal cancer surgery.
文摘Background: General anesthesia using remifentanil may suppress the unwanted metabolic changes caused by surgical stress including hyperglycemia and ketogenesis. Surgery-related changes in catabolism can be attenuated with low-dose glucose load, without causing hyperglycemia. However, the impact of glucose load in diabetic patients during surgery is unknown. In this study, we investigated the effect of glucose load on catabolism during remifentanil-based anesthesia in patients with diabetes mellitus. Methods: Twenty-nine patients with diabetes mellitus undergoing elective surgery were randomly assigned to receive a glucose load (1.5 mg/kg/min) or not. Plasma levels of glucose, insulin, cortisol, dopamine, adrenaline, noradrenaline, acetoacetic acid, free fatty acid, ketone bodies, 3-hydroxybutyric acid, and 3-methylhistidine/creatinine, a marker of protein catabolism were measured at the start of surgery and 3 h after the start of surgery. Results: Glucose and insulin levels were significantly higher in patients who received a glucose load than in those who did not. Cortisol levels decreased at 3 h after the start of surgery in both groups whereas the levels of catecholamines were unchanged. Acetoacetic acid and total ketone body levels were significantly lower in patients given a glucose load than in those who were not 3 h after the start of surgery. The difference in the 3 methylhistidine/creatinine ratio between the two groups was not significant. Conclusions: The infusion of glucose suppressed lipid catabolism in diabetic patients under remifentanil-based anesthesia during surgery. Our study also suggests that in patients with diabetes mellitus, protein sparing is inhibited by remifentanil-based anesthesia, regardless of the glucose load. Trial registration: the University Hospital Medical Information Network identifier: UMIN000010914.
文摘Background: Perioperative exacerbation of hyperglycemia and insulin resistance is associated with increased complications in patients with diabetes mellitus. We recently reported that glucose load during anesthesia with sevoflurane suppressed lipid catabolism in diabetic patients. In contrast to inhaled anesthetics, propofol solution contains triglycerides, which can be an energy source during surgery. However, the clinical relevance of glucose load under propofol-based anesthesia in diabetic patients is unknown. Therefore, we investigated the effect of intraoperative glucose load on catabolism during propofol-based anesthesia in patients with diabetes mellitus. Methods: Twenty-three patients with diabetes mellitus undergoing elective surgery with propofol-remifentanil-based anesthesia were randomly assigned to receive a glucose load (1.5 mg/kg/ min) or not. Plasma levels of glucose, insulin, cortisol, catecholamines, acetoacetic acid, free fatty acids, ketone bodies, 3-hydroxybutyric acid, and 3-methylhistidine/creatinine, used as a marker for protein catabolism, were measured at the start of surgery and 3 h later. Results: Glucose and insulin levels were significantly higher in patients who received a glucose load than in those who did not. Nonetheless, the levels of cortisol and catecholamines were unchanged during surgery. Similarly, the difference in the levels of markers for lipid as well as protein catabolism was not significant between the groups at 3 h after the start of surgery. Conclusions: Changes in lipid as well as protein catabolism were not altered by glucose load in diabetic patients under propofol-based anesthesia with remifentanil. Our study suggested that continuous infusion of propofol at a clinical dose is sufficient to reduce the requirement for glucose infusion during surgery in patients with diabetes.
文摘Background: Transient receptor potential ankyrin (TRPA) 1 is known as a peripheral initiator of acute inflammation and hyperalgesia. However, its role in the facilitation of innate immune responses followed by resolution of the inflammation triggered by a surgical incision has not been fully investigated. Therefore, we evaluated the mechanism by which TRPA1 regulates the inflammatory responses mainly facilitated by neutrophils and macrophages in the early course of wound repair after an incision. Methods: Plantar incision was performed in wild-type and TRPA1-/- mice. The infiltration of polymorphonuclear neutrophils, macrophage phenotype, and induction of inflammatory mediators were assessed for 7 days postoperatively. Results: TRPA1-/-?mice exhibited decreased infiltration of polymorphonuclear neutrophilscompared with wild-type mice on day 1. Consistently, the influx of F4/80+ iNOS+ proinflammatory M1 macrophages to incised sites was markedly decreased on day 2. Similarly, F4/80+ CD206+M2 macrophages, which regulate the resolution of inflammation and promote wound healing in the later phase of acute inflammation, were significantly decreased in TRPA1-/- compared with those in wild-type mice on day 7. In addition, the induction of heme oxygenase-1, which promotes wound healing by switching phenotype of macrophages, was decreased in the early phase of acute inflammation, whereas the expression of proinflammatory mediators such as tumor necrosis factor and cyclooxygenase-2, and 15-lipoxygenase, which are involved in the resolution of inflammation was increased in the late phase in TRPA1-/- mice. Conclusions: Early innate immune responses including neutrophil infiltration and macrophage polarization at incised sites were inhibited in TRPA1-/- mice, associated with increased pro-inflammatory mediators in later phase. Peripheral TRPA1 may facilitate the acute inflammatory process, leading to the promotion of macrophage-mediated resolution of inflammation and wound repair after a surgical incision.
