BACKGROUND: Laryngoscopy and endotracheal intubation cause hemodynamic changes such as hypertension and tachycardia. Adjuvant fentanyl administration have been used to reduce the hemodynamic changes. Remifentanil, a newly developed ultra short acting opioid, has recently been used to reduce the hemodynamic changes. This study investigated the effects of fentanyl and remifentanil on hemodynamic responses to laryngoscopy and endotracheal intubation. METHODS: Sixth ASA class I or II patients who scheduled for elective surgery were divided randomly into 3 groups. Each patient received normal saline, fentanyl 1.5microgram/kg or remifentanil 1.5microgram/kg, respectively. Predetermined drugs for each group were administered over 30 seconds after induction of anesthesia with TCI of propofol effect site target concentration 4.0microgram/ml and rocuronium 1.0 mg/kg. Laryngoscopy and endotracheal intubation was carried out and systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and heart rate (HR) were measured baseline (initial), before intubation (BI) and during 5 minutes after intubation (I1 to I5). RESULTS: In the fentanyl group, I1 HR value was significantly higher than baseline. In the remifentanil group, SBP and MAP were significantly lower than baseline during post-intubation period. Fentanyl and remifentanil groups show lesser hemodynamic changes than those in the control group. There were no significant differences of hemodynamic changes between fentanyl and remifentanil group. CONCLUSIONS: Fentanyl and remifentanil can attenuate hemodynamic responses after laryngoscopy and endotracheal intubation.
Anesthesia* ; Arterial Pressure ; Blood Pressure ; Fentanyl* ; Heart Rate ; Hemodynamics* ; Humans ; Hypertension ; Intubation ; Intubation, Intratracheal* ; Laryngoscopy ; Propofol* ; Tachycardia

BACKGROUND: Mitochondrial trans-2-enoyl-CoA reductase (MECR) is involved in mitochondrial synthesis of fatty acids and is highly expressed in mitochondria. MECR is also known as nuclear receptor binding factor-1, which was originally reported with yeast two-hybrid screening as a binding protein of the nuclear hormone receptor peroxisome proliferator-activated receptor alpha (PPARalpha). However, MECR and PPARalpha are localized at different compartment, mitochondria, and the nucleus, respectively. Therefore, the presence of a cytosolic or nuclear isoform of MECR is necessary for functional interaction between MECR and PPARalpha. METHODS: To identify the expression pattern of MECR and the cytosolic form of MECR (cMECR), we performed reverse transcription polymerase chain reaction (RT-PCR) with various tissue samples from Sprague-Dawley rats. To confirm the interaction between cMECR and PPARalpha, we performed several binding assays such as yeast two-hybrid, coimmunoprecipitation, and bimolecular fluorescence complementation. To observe subcellular localization of these proteins, immunocytochemistry was performed. A luciferase assay was used to measure PPARalpha activity. RESULTS: We provide evidence of an alternatively spliced variant of the rat MECR gene that yields cMECR. The cMECR lacks the N-terminal 76 amino acids of MECR and shows uniform distribution in the cytoplasm and nucleus of HeLa cells. cMECR directly bound PPARalpha in the nucleus and increased PPARalpha-dependent luciferase activity in HeLa cells. CONCLUSION: We found the cytosolic form of MECR (cMECR) was expressed in the cytosolic and/or nuclear region, directly binds with PPARalpha, and enhances PPARalpha activity.
Alternative Splicing ; Amino Acids ; Animals ; Carrier Proteins ; Complement System Proteins ; Cytoplasm ; Cytosol* ; Fatty Acids ; Fluorescence ; HeLa Cells ; Humans ; Immunohistochemistry ; Luciferases ; Mass Screening ; Mitochondria ; Oxidoreductases* ; Polymerase Chain Reaction ; PPAR alpha* ; Rats ; Rats, Sprague-Dawley ; Reverse Transcription ; Yeasts