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1.
Acta Anaesthesiol Scand ; 61(8): 935-941, 2017 Sep.
Article in English | MEDLINE | ID: mdl-28707325

ABSTRACT

BACKGROUND: Pain is considered as being one cause of post-operative emergence agitation (EA) from sevoflurane anaesthesia. The purpose of this study was to investigate the pure effect of post-operative pain on EA after sevoflurane anaesthesia in preschool children undergoing excision of scalp nevi. METHODS: Forty-four children, 1-7 years old, undergoing scalp nevus excision were enrolled. Patients were randomly assigned to two groups: the remifentanil group received single intravenous injection of short-acting synthetic opioid, remifentanil 1 µg/kg just before the scalp incision, and the block group received scalp nerve block with 0.25% ropivacaine after intubation. The end-tidal sevoflurane concentration was maintained around 1.5 vol% unless the mean arterial pressure is out of ±20% range of preoperative values during surgery in both groups. Watcha behaviour scale for EA and face, legs, activity, cry, consolability (FLACC) scale scores for pain were recorded post-operatively. RESULTS: There was no difference in end-tidal sevoflurane concentration between the two groups during surgery and the emergence period. Agitation incidence and scores were not different between the two groups during the recovery period. FLACC scale was significantly lower in the block group than in the remifentanil group at post-anaesthesia care unit (PACU) arrival, at 10 and 20 min after PACU arrival, respectively. CONCLUSION: The scalp nerve block decreased the early post-operative pain after paediatric nevus excision, but it did not decrease the incidence of EA with sevoflurane anaesthesia.


Subject(s)
Nerve Block , Nevus/surgery , Pain, Postoperative/prevention & control , Psychomotor Agitation/prevention & control , Scalp/innervation , Scalp/surgery , Amides , Anesthetics, Inhalation , Anesthetics, Intravenous , Anesthetics, Local , Child , Child Behavior , Child, Preschool , Emergence Delirium , Female , Humans , Infant , Male , Methyl Ethers , Pain, Postoperative/epidemiology , Pain, Postoperative/psychology , Piperidines , Prospective Studies , Psychomotor Agitation/epidemiology , Psychomotor Agitation/psychology , Remifentanil , Ropivacaine , Sevoflurane , Single-Blind Method
2.
Int J Hyperthermia ; 19(4): 431-43, 2003.
Article in English | MEDLINE | ID: mdl-12850928

ABSTRACT

This paper investigated the induction of apoptosis and perturbation of cell cycle progression caused by carboplatin (CPt) and hyperthermia alone or combined in WERI human retinoblastoma cells in vitro. An incubation of the cells with 25 or 50 microm of CPt at 37 degrees C caused apoptosis, which progressively increased during the 24-72 h treatment. Hyperthermia at 42.5 degrees C for 1 h induced apoptosis, which became significant from 24 h after the heating. Heating the cells in the presence of CPt and subsequent incubation with CPt was far more effective than treating the cells with hyperthermia or CPt treatment alone in inducing apoptosis in the WERI cells, indicating that the combination of these two modalities is potentially useful for the treatment of retinoblastoma. It appeared that the apoptosis in WERI cells caused by hyperthermia and CPt occurs during G1 phase. An interesting observation was that caspase 9 activation preceded the release of cytochrome C from mitochondria during apoptosis in WERI cells, contrary to the general notion that caspase 9 is activated by cytochrome C.


Subject(s)
Antineoplastic Agents/pharmacology , Apoptosis , Carboplatin/pharmacology , Hyperthermia, Induced , Retinal Neoplasms/physiopathology , Retinal Neoplasms/therapy , Retinoblastoma/physiopathology , Retinoblastoma/therapy , Blotting, Western , Caspase 9 , Caspases/metabolism , Cell Cycle , Cell Line, Tumor , Cyclin-Dependent Kinase Inhibitor p21 , Cyclins/metabolism , Cytochromes c/metabolism , Humans , Poly(ADP-ribose) Polymerases/metabolism , Retinal Neoplasms/metabolism , Retinal Neoplasms/pathology , Retinoblastoma/metabolism , Retinoblastoma/pathology , Tumor Suppressor Protein p53/metabolism
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