ABSTRACT
Objective: This study aimed to investigate age-related differences in the effects of dexamethasone pre-treatment on pain intensity and morphine consumption in patients undergoing laparoscopic cholecystectomy
Design: Randomized, prospective study
Setting: Operating room of a Wonkwang university hospital, South Korea
Subjects: Three hundred and eighty-eight patients undergoing laparoscopic cholecystectomy, 194 from a younger age group [18 - 45 years] and 194 from an older age group [ >/= 65 years]
Intervention: The patients within each group were randomly allocated into younger [normal saline/dexamethasone: 97/97] and older [97/97] groups. They received either intravenous dexamethasone 0.1 mg/kg or normal saline 1 hour before anaesthesia induction
Main outcome measures: The effect of dexamethasone on cumulative morphine-containing patient-controlled analgesia consumption, visual analogue scale scores for pain at 1, 2, 6, 12, and 24 hours after surgery, mean morphine consumption, and time to first rescue analgesia
Results: When dexamethasone was administered, both age groups had significantly less cumulative patient-controlled analgesia consumption, mean morphine consumption, and longer time to first rescue analgesia. These effects were of greater magnitude in the older than in the younger group. Visual analogue scales for pain at 1, 6, and 12 hours after surgery was significantly higher in the younger group
Conclusion: The effects of dexamethasone on clinically relevant pain were greater in the older group, who experienced less post-operative pain. Further investigation regarding this association is warranted
ABSTRACT
Objective: This study aimed to investigate the effect of preoperative administration of 5% dextrose on hyperalgesia induced by high-doses remifentanil
Design: Randomized, prospective
Setting: Operating room of a Wonkwang university hospital, South Korea
Subjects: One hundred and twenty-six patients undergoing laparoscopy-assisted distal gastrectomy
Intervention: Three groups received either 250 ml Hartmann's solution [HS] or 5% dextrose in HS for 1 hour before anesthesia and intraoperative remifentanil infusion. Group LHS received HS and 0.05 microg/kg/min remifentanil; group HHS received HS and 0.3 microg/kg/min remifentanil, and group HHD received 5% dextrose in HS and.3 microg/kg/min remifentanil
Main outcome measures: Mechanical hyperalgesia threshold at 1 hour after surgery, time to first postoperative analgesicrequirement, cumulative patient-controlled analgesia [PCA] volume containing morphine for 24 hours after surgery, and pain intensity using visual analog scale [VAS] for 24 hours after surgery were measured
Results: Mechanical hyperalgesia threshold of group HHS and HHD were significantly lower than that of LHS group. Cumulative PCA volume containing morphine for 24 hours after surgery and pain intensity for 12 hours after surgery of group LHS were significantly reduced than that of both HHS and HHD groups, both of which were not significant.Time to first postoperative analgesic requirement was longer in group LHS than in groups HHS and HHD, both of which were not significant
Conclusion: Preoperative intravenous administration of dextrose in patients undergoing laparoscopy-assisted distal gastrectomy didn't show any effects on hyperalgesia induced by high-doses remifentanil
ABSTRACT
BACKGROUND: Propofol is the extensively used general anesthetic-sedative agent.Although propofol is known to be involved in migration of various cells, migration response to it in vascular smooth muscle cells is not investigated. This study was carried out to determine the role of propofol in migration of rat aortic smooth muscle cells (RASMCs). METHODS: A7r5 RASMCs were used.Cell migration was examined by the analysis of 5 ng/ml of platelet-derived growth factor (PDGF)-induced RASMC response after treatment of cells with propofol (1-100micrometer) in the Boyden chamber.The activity of cofilin by propofol in RASMCs was measured by the Western blot analysis for the change of cofilin dephosphorylaton in cells treated with 10micrometer propofol for 5, 10, 15 and 20 min, for the effect of propofol (1, 10 and 100micrometer) on cofilin phosphorylation, and for the effects of ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetra acetic acid (2 mM; EGTA), Na3VO4 (200micrometer), and calyculin A (10 nM) on 10micrometer propofol-induced cofilin dephosphorylation. RESULTS: PDGF increased RASMC migration and this response was dose-dependently inhibited by treatment with propofol. Propofol attenuated the cofilin phosphorylation in RASMCs in a dose- and time-dependent manner.Propofol-induced dephosphorylation of cofilin in RASMCs was abolished by calyculin A, a protein phosphatase 2A inhibitor, but not by EGTA, a Ca2+ chelating agent, or Na3VO4, a protein tyrosine phosphatase inhibitor. CONCLUSIONS: The present results suggest that propofol induces the diminution of PDGF-stimulated RASMC migration and this response may be associated with dephosphorylation of cofilin mediated by the protein phosphatase 2A-dependent pathway.