Etomidate and midazolam are newly developed and used in clinical trials. Etmoidate, a carboxylated imidazole derivative, decreases systemic vascular resistance and increases the pulmonary artery pressure in vivo. Midazolam, a water soluble derivative of benzodiazepine, decreases pulmonary artery pressure and is useful for pulmonary hypertensive patients. This study was designed to investigate the direet effects of etomidate and midazolam on vascular tension of the rabbit abdominal aorta and the pulmonary artery in vitro. In the vascular preparations with or without endothelium, changes in tension were measured following cumulative administration of etomidate (10(-6)M, 10(-5) M, 5X10(-4) M) and midazolam (10(-6)M, 10(-5)M, 10(-4)M). Vascular effects of these drugs were also studied in the preparations pretreated with indomethacin, nitro(w)-L-arginine methyl ester (L-NAME) and methylene blue. The results wer as follows; 1) Etomidate and midazolam induced vasorelaxation and the degree of relaxation depended on the concentration. 2) After denudation of the endothelium, vasorelaxant effect of etomidate and midazolam was efficiently decreased in abdominal aorta but not in pulmonary artery. 3) Indomethacin reduced vasorelaxing effect of etomidate efficiently, but didn't affect vasorelaxing effect of midazolam. 4) Following pretreatment of vascular preparations respectively with L-NAME and methylene blue, the relaxing responses to etomidate (10(-5) and 5X10(-5) M) of both abdominal aorta and pulmonary artery were depressed. Also, depressed was the relaxing response of abdominal aorta to midazolam (10(-5) M). The results of present study suggest that etomidate and midazolam possess vasorelaxing effects in both rabbit aMominal aorta and pulmonary artery. The vascular effect of etomidate is mediated via the nitric oxide pathway and also in part, by PGI2, whereas part of the vascular effect of midazolam is associated with the nitric oxide pathway.
Aorta ; Aorta, Abdominal* ; Benzodiazepines ; Endothelium ; Epoprostenol ; Etomidate* ; Humans ; Indomethacin ; Methylene Blue ; Midazolam* ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Pulmonary Artery* ; Relaxation ; Vascular Resistance ; Vasodilation

Etomidate and midazolam are newly developed and used in clinical trials. Etmoidate, a carboxylated imidazole derivative, decreases systemic vascular resistance and increases the pulmonary artery pressure in vivo. Midazolam, a water soluble derivative of benzodiazepine, decreases pulmonary artery pressure and is useful for pulmonary hypertensive patients. This study was designed to investigate the direet effects of etomidate and midazolam on vascular tension of the rabbit abdominal aorta and the pulmonary artery in vitro. In the vascular preparations with or without endothelium, changes in tension were measured following cumulative administration of etomidate (10(-6)M, 10(-5) M, 5X10(-4) M) and midazolam (10(-6)M, 10(-5)M, 10(-4)M). Vascular effects of these drugs were also studied in the preparations pretreated with indomethacin, nitro(w)-L-arginine methyl ester (L-NAME) and methylene blue. The results wer as follows; 1) Etomidate and midazolam induced vasorelaxation and the degree of relaxation depended on the concentration. 2) After denudation of the endothelium, vasorelaxant effect of etomidate and midazolam was efficiently decreased in abdominal aorta but not in pulmonary artery. 3) Indomethacin reduced vasorelaxing effect of etomidate efficiently, but didn't affect vasorelaxing effect of midazolam. 4) Following pretreatment of vascular preparations respectively with L-NAME and methylene blue, the relaxing responses to etomidate (10(-5) and 5X10(-5) M) of both abdominal aorta and pulmonary artery were depressed. Also, depressed was the relaxing response of abdominal aorta to midazolam (10(-5) M). The results of present study suggest that etomidate and midazolam possess vasorelaxing effects in both rabbit aMominal aorta and pulmonary artery. The vascular effect of etomidate is mediated via the nitric oxide pathway and also in part, by PGI2, whereas part of the vascular effect of midazolam is associated with the nitric oxide pathway.
Aorta ; Aorta, Abdominal* ; Benzodiazepines ; Endothelium ; Epoprostenol ; Etomidate* ; Humans ; Indomethacin ; Methylene Blue ; Midazolam* ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Pulmonary Artery* ; Relaxation ; Vascular Resistance ; Vasodilation

No abstract available.
Lung*

Purpose: The extraction conditions for bioactive components from peanut shells, which is a byproduct of peanut processing, were optimized to enhance the total phenolic content (TPC, Y1 ), total flavonoid content (TFC, Y2 ), and 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity (RSA, Y3). In addition, this study evaluated the anti-obesity effect of peanut shell extract. Methods: Optimization of ultrasonic‐assisted extraction (UAE) was performed using a response surface methodology. The independent variables applied for extraction were time (X1 : 5.0–55.0), temperature (X2 : 26.0–94.0), and ethanol concentration (X3 : 0.0%–99.5%). Quadratic regression models were derived based on the results of 17 experimental sets, and an analysis of the variance was performed to verify its accuracy and precision of the regression equations. Results: When evaluating the effects of independent variables on responses using statistically-based optimization, the independent variable with the most significant effect on the TPC, TFC, and RSA was the ethanol concentration (p = 0.0008). The optimal extraction conditions to satisfy all three responses were 35.8 minutes, 82.7°C, and 96.0% ethanol. Under these conditions, the inhibitory activities of α-glucosidase and pancreatic lipase by the extract were 86.4% and 78.5%, respectively. Conclusion In this study, UAE showed superior extraction efficiency compared to conventional hot-water extraction in the extraction of polyphenols and bioactive materials. In addition, α-glucosidase and pancreatic lipase inhibitory effects were identified, suggesting that peanut shells can be used as effective antioxidants and anti-obesity agents in functional foods and medicines.

No abstract available.
Communicable Diseases* ; Emigrants and Immigrants* ; Humans ; Korea ; Vaccination*

BACKGROUND: The reperfusion following ischemia produces reactive oxygen species (ROS). We studied the influences of methylprednisolone (MPD) and hydrocortisone (CRT) on ROS effects using the endothelium of rabbit abdominal aorta. METHODS: Isolated rabbit aortic rings were suspended in an organ bath filled with Krebs-Henseleit (K-H) solution. After precontraction with norepinephrine, changes in arterial tension were recorded following the cumulative administration of acetylcholine (ACh). The percentages of ACh-induced relaxation of aortic rings before and after exposure to ROS, generated by electrolysis of K-H solution, were used as the control and experimental values, respectively. The aortic rings were pretreated with MPD or CRT at the same concentrations, and the effects of these agents were compared with the effects of ROS scavenger inhibitors: superoxide dismutase inhibitor, diethylthiocarbamate (DETCA), and the catalase inhibitor, 3-amino-1,2,4-triazole (3AT). RESULTS: Both MPD and CRT maintained endothelium-dependent relaxation induced by ACh in a dose-related manner in spite of ROS attack. The restored ACh-induced relaxation of MPD and CRT group was not attenuated by pretreatment of 3AT and DETCA. CONCLUSIONS: MPD and CRT preserve the endothelium-dependent vasorelaxation against the attack of ROS, in a dose-related manner. Endothelial protection mechanisms of MPD and CRT may be not associated with hydrogen peroxide and superoxide scavenging.
Acetylcholine ; Amitrole ; Antioxidants ; Aorta, Abdominal ; Arterial Pressure ; Baths ; Catalase ; Electrolysis ; Endothelium ; Hydrocortisone ; Hydrogen Peroxide ; Ischemia ; Methylprednisolone ; Norepinephrine ; Reactive Oxygen Species ; Relaxation ; Reperfusion ; Superoxide Dismutase ; Superoxides ; Vasodilation

BACKGROUND: The purpose of the present study was to determine the effect of positive end-expiratory pressure on intraocular pressure under general anesthesia. METHODS: Contact tonometer HA-1 (Kowa, Japan) was used to measure the intraocular pressures of 22 subjects at zero end-expiratory pressure and positive end-expiratory pressure of 15 cmH2O under general anesthesia. The data were statistically analyzed by paired t-test. RESULTS: There is no statistically significant difference between intraocular pressure of zero end-expiratory pressure and positive end-expiratory pressure of 15 cmH2O in a population with normal basal ocular tonometry. CONCLUSIONS: Mechanical ventilation with positive end-expiratory pressure of 15 cmH2O under general anesthesia dose not present a clinically important significant risk for intraocular pressure increase in a population with normal basal ocular tonometry.
Anesthesia, General* ; Intraocular Pressure* ; Positive-Pressure Respiration* ; Respiration, Artificial* ; Tonometry, Ocular

PURPOSE: Hepatocellular carcinoma (HCC) patients are asymptomatic and the tumor remains in an unresectable state until the tumor progresses. Recently much efforts for elucidation of the early hepatocarcinogenesis have been made, and for this purpose it is very crucial to investigate the genetic abnormalities. We evaluated microsatellite alterations of five markers from chromosome 9, 13, 16 and investigated the relationships with the clinicopathological parameters in HCC. METHODS: The microsatellite alteration analysis was performed using polymerase chain reaction with five polymorphic microsatellite markers (D9S171, D9S1747, D13S156, D16S419, D16S3106) in 40 surgically resected HCCs and their respective non-tumorous counterparts. RESULTS: D9S171, D9S1747, D13S156, D16S419, D16S3106 abnormalities were detected in 20.0%, 14.3%, 50.0%, 32.4% and 22.6%, respectively. Loss of heterozygosity (LOH) of D9S171 correlated well with higher tumor histologic grade and LOH of D13S156, D16S419 and D16S3106 correlated well with increased tumor size. Microsatellite instability (MSI) was found in two markers, D13S156, D16S419. CONCLUSION: As a result, we concluded that alterations in microsatellites of various chromosomes may contribute to the hepatocarcinogenesis and tumor progression. Especially LOH of chromosome 13 and 16 are considered to correlate with tumor progression.
Carcinoma, Hepatocellular* ; Chromosomes, Human, Pair 13 ; Chromosomes, Human, Pair 9 ; Humans ; Loss of Heterozygosity ; Microsatellite Instability ; Microsatellite Repeats* ; Polymerase Chain Reaction

BACKGROUND: Amrinone is a noncatecholamine, nonglycoside compound, which is known to possess both cardiac inotropic and vasodilatory actions. This drugs has been increasingly used in clinical practice for the management of low cardiac output syndrome during anesthesia, particularly for patients associated with right heart failure and pulmonary hypertension. The aim of this study was to explore the direct vasoactive effect of amrinone and its action mechanisms in the isolated rabbit pulmonary artery. METHODS: The rabbits' pulmonary arteries were dissected free and cut into rings (3 4 mm) and mounted for isometric tension in a tissue chamber. The effects of amrinone (5 10 6 5 10 4 M) on the vascular tension were assessed in the by KCl (40 mM)- or norepinephrine (NE, 10 6 M)- precontracted pulmonary arterial rings with or without endothelium. Also effects of K channel blockers (tetraethyl ammonium 20 mM, glybenclamide 2.5 10 5 M, 4-aminopyridine (4-AP) 5 10 4 M), protein kinase A & G inhibitor (H8), L-NAME, methylene blue and indomethacin on the amrinone- induced vascular responses were investigated. Also studied was effects of amrinone on the Ca2 influx through voltage operated channel (VOC) and receptor operated channel (ROC) of the vascular cells. RESULTS: Amrinone produced vasorelaxation of KCl- or NE-precontracted pulmonary artery in a dose-dependent fashion. The amrinone-induced vasorelaxation was not affected by the denudation of the endothelium. Pretreatment with L-NAME and methylene blue did not affect the vasodilatory effect of amrinone, suggesting that nitric oxide is not involved. Following pretreatment with indomethacin (a cyclooxygenase inhibitor) or K channel blockers, the amrinone-induced vasorelaxation was not altered. After exposure to Ca2 free solution, amrinone attenuated the KCl- or NE-induced contraction even in the presence of Ca2 , implying that VOC and ROC are blocked by amrinone. On the other hand, protein kinase A blocker (H8) completely abolished the amrinone-induced relaxation in the KCl-precontracted pulmonary artery. CONCLUSIONS: These findings suggest that the amrinone-induced vasorelaxations result from inhibition of VOC and ROC as well as from the activation of protein kinase A in the isolated rabbit pulmonary artery.
4-Aminopyridine ; Ammonium Compounds ; Amrinone* ; Anesthesia ; Cardiac Output, Low ; Cyclic AMP-Dependent Protein Kinases ; Endothelium ; Glyburide ; Hand ; Heart Failure ; Humans ; Hypertension, Pulmonary ; Indomethacin ; Methylene Blue ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Norepinephrine ; Prostaglandin-Endoperoxide Synthases ; Pulmonary Artery* ; Relaxation ; Vasodilation

BACKGROUND: Ketamine produces increasing in heart rate and arterial blood pressure, in vivo. However, the direct effects of ketamine itself on the porcine coronary arteries are not well determined. In this study, the direct effects of ketamine on the porcine coronary artery responses to vasoactive agents that operate through Ca2+ channel, K+ channels and endothelium related mechanisms were investigated, in vitro. METHODS: Adult porcine hearts(n=12) were obtained from a slaughter house. Coronary arteries were perfused and dissected with 4oC Krebs solution, and were cut into vessel rings and prepared with and without the endothelium(3~4mm in length). The ring segments were suspended in tissue bath(5ml) filled with Krebs solution at 37oC and bubbled with 95% O2-5% CO2 gas mixture. The effect of ketamine(5 10 5, 10 4, 2 10 4M) on vascular smooth muscle tone caused by Ca2+[voltage operated channel(VOC), receptor operated channel(ROC)] and K+channels(Ca2+activated K+ currents, ATP-sensitive K+ currents) regulation were studied with Ca2+ free solution and K+channel blocker. RESULTS: Ketamine induced vasorelaxation of porcine coronary rings that were precontracted by KCl(50 mM) or acetylcholine(3 10 7M). The changes of vascular tone in endothelium intact and removed group did not show statistical significance. In ketamine pretreated group(Ca2+ free solution), after ketamine pretreatment, the last vascular tone was same as that relaxed by ketamine. The other group that without pretreatment of ketamine, the last vascular tone was same as that precontracted with KCl or acetylcholine. In the TEA pretreated group, the porcine coronary artery relaxation was reversed. However, pretreatment with glybenclamide, the porcine coronary artery relaxation was not reversed. CONCLUSIONS: Ketamine induced vasorelaxation of the porcine coronary artery as concentration relating manner, in vitro. The vasorelaxation induced by ketamine was not associated with endothelium. Furthermore, an antagonism of Ca2+ channels(VOC, ROC) and activation of Ca2+ activated K+ channels may be responsible for the porcine coronary arterial relaxing effect of ketamine.
Acetylcholine ; Adult ; Anesthetics ; Arterial Pressure ; Arteries ; Coronary Vessels* ; Endothelium ; Glyburide ; Heart Rate ; Humans ; Ion Channels ; Ketamine* ; Muscle, Smooth, Vascular ; Pharmacology ; Potassium Channels, Calcium-Activated ; Relaxation ; Tea ; Vasodilation