Seung Woo Ku

Protective effect of isoflurane anesthesia on noise-induced hearing loss in mice.

Hypothesis/Objectives: To examine the protective effect of general anesthesia with isoflurane against noise‐induced hearing loss in mice.

Comparison of the effects of propofol and pentobarbital on hydrogen peroxide-stimulated hepatic SNU761 cells

Background Propofol and barbiturates are both known to protect cells of several organs against ischemia/reperfusion injury, but there are few reports on any possible protective effects on human hepatocytes. We investigated the activities of both agents on human hepatic SNU761 cells under hydrogen peroxide (H2O2)-induced oxidative stress. Methods To determine whether propofol and pentobarbital protect hepatocytes from H2O2-induced toxicity, we used SNU761 cells, a human hepatocellular carcinoma (HCC) cell line. Cells were pretreated with different dosages (1, 10, 50 µM) of propofol or pentobarbital (1, 10, 50, 100, 400 µM) 30 min before H2O2 application. Lactate dehydrogenase (LDH) was measured to assess and quantify cell death. To determine the nature of cell death, treated hepatocytes were doubly stained with fluorescein isothiocyanate (FITC)-labeled Annexin V and propidium iodide (PI), and analyzed by flow cytometry. Results Pretreatment with propofol, but not pentobarbital, suppressed H2O2-induced LDH release. In Annexin V-FITC/PI binding analysis, propofol decreased the number of necrotic and late apoptotic cells, but no significant decreases in such cell numbers were seen when pentobarbital was used. Conclusions Unlike pentobarbital, propofol, at clinical concentrations, protected SNU-761 HCC cells against oxidative stress.

The effects of sevoflurane with propofol and remifentanil on tracheal intubation conditions without neuromuscular blocking agents.

Background Propofol and remifentanil are used for tracheal intubation in the absence of neuromuscular blocking agents. We hypothesized that the addition of sevoflurane to propofol and remifentanil would improve intubation conditions and provide hemodynamic stability. Methods Seventy-six patients scheduled for elective surgery were randomly allocated to be ventilated with either 4% (group I) or 7% sevoflurane (group II) after propofol injection (2 mg/kg). All patients received remifentanil (1 µg/kg) 30 seconds after administration of propofol. Ninety seconds after remifentanil was given, laryngoscopy and tracheal intubation were performed. Intubation conditions and hemodynamic changes were evaluated. Results The overall incidence of clinically acceptable intubation conditions was significantly higher in group II (92%) than group I (58%) (P = 0.001). Scores for vocal cord position, coughing, and limb movement were significantly better in group II (P < 0.05). Mean blood pressure remained significantly lower than the pre-induction level throughout the investigation in both groups (P < 0.001), but there was no incidence of bradycardia or hypotension requiring treatment. Conclusions Tracheal intubation without neuromuscular blocking agents can be achieved safely and reliably by adding 7% sevoflurane to propofol (2 mg/kg) and remifentanil (1 µg/kg).

Cardiovascular collapse due to right heart failure following ethanol sclerotherapy: a case report.

Ethanol sclerotherapy for the treatment of low-flow vascular malformations can cause catastrophic cardiopulmonary complications, including pulmonary embolism and pulmonary hypertension, that can result in right heart failure and fatal arrhythmias, leading to death. We here report a case of abrupt cardiovascular collapse that developed immediately following ethanol sclerotherapy in 31-year-old female patient who had a large arteriovenous malformation in her leg. Anesthesiologists should be aware of the fatal cardiopulmonary complications that are associated with ethanol sclerotherapy and consider the use of invasive hemodynamic monitoring, such as pulmonary artery pressure monitoring, when large doses of ethanol are required.

Effects of propofol and etomidate on hydrogen peroxide-induced oxidative damage in hepatocyte

BACKGROUND The present investigation was undertaken to evaluate the protective effect of propofol and etomidate against hydrogen peroxide (H2O2) induced oxidative damage in human hepatic SNU761 cells by measuring lactate dehydrogenase (LDH). METHODS The cell line of human hepatocellular carcinoma was grown for 24 hours in dissociated cell culture. They were divided into eight groups: negative control (NC) group with no drug administration, positive control (PC) group with H2O2 250 micrometer and other groups pretreated with propofol (P; 1, 10, 50 micrometer) or etomidate (ET; 1, 10, 50 micrometer) followed H2O2 administration. After 7 hours, cell death was assessed by morphology under the light microscope and quantified by measuring the LDH in the culture media. RESULTS In the light microscopic findings, the intact cells were increased in all three propofol groups compared to group PC. H2O2-induced LDH production was also significantly suppressed in all three propofol groups compared to group PC (P < 0.001). There were no significant differences in the microscopic findings and LDH production between the etomidate groups and group PC. CONCLUSIONS These results suggest that the propofol has protective effect on the hepatocyte against H2O2-induced oxidative stress.