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: 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

The incidence of cardiac arrhythmias during anesthesia in a total 5,845 surgical patients who were admitted to Hanyang university hospital from Janury 1 to December 31, 1988 was investigated using on-line continuous EKG monitoring. The results were as follows: 1) Among study patients, 111 patients (1.9%) had pre-existing cardiac arrhythmias before anesthesia and showed significantly higher incidence of arrhythmias (49.5%) than that of patients without pre-existisng arrhythmias before anesthesia (2.9%). 2) Among arrhythmias found during anesthesia, most types of arrhythmias were ventricular premature contractions (77.4% in the patients with pre-existing cardiac arrhythmias and 43.6% in the patients without pre-existing cardiac arrhythmias) except sinus bradycardia and tachycardia. 3) Although the incidence of arrhythmias during the induction of anesthesia was similar to that during anesthesia maintenance, it was somewhat greater on the basis of incidence per unit time. 4) The incidence of arrhythmias was increased with age. 5) The incidence of arrhythmias when anesthesia was induced with halothane (3.7%) was greater than that when anesthesia was induced with enflurane (2.1%). 6) Most of the arrhythmias were controlled with sufficient ventilation and oxygen supply, adjusting concentration of inhaled anesthetics or changing anesthetics, and occasionally, intravenous admininstration of 1% lidocaine (1.0-1.5 mg/kg). Considering the above results, it may be an appropriate conclusion that the continuous on-line EKG monitoring during the induction and maintenance of anesthesia is a noninvasive and simple method for detecting early signs of cardiac arrhythmias and hemodynamic changes during anesthesia, and consequently, improving the overall efficiency of patient care. Therefore, we are impressed with an idea that the continuous EKG monitoring should be mandatory for all surgical patients to be anesthetized.
Anesthesia* ; Anesthetics ; Arrhythmias, Cardiac* ; Bradycardia ; Electrocardiography ; Enflurane ; Halothane ; Hemodynamics ; Humans ; Incidence* ; Lidocaine ; Oxygen ; Patient Care ; Tachycardia ; Ventilation

After the hemodynamic comparison of venous air volume in 32 rabbits, the following conclusions were derived. 1) The precordial doppler ultrasonography was most sensitive and end titdal CO2 pressure was statistically decreased at 0.1 ml/kg of air. 2) The mean arterial pressure was suddenly decreased at 1 minute after injection of more than 0.25 ml/kg of air, and was furether reduced according to the time. 3) The arterial PCO2 was continuously increased and statistically different from 0.25 ml/kg of air, and the arterial PO2 was suddenly decreased to about 1/3 of the control data. 4) The pulse rate was statistically decreased at more than 0.5 ml/kg of air and shown peaked p wave, arrhythmias, ST depression and premature ventricular contraction on the EKG. There 4 dead rabbits at 1.0 ml/kg of air, so we could conclucle that the fatal dose of rabbits was more decreased than that of the dogs in venous air embolism.
Animals ; Arrhythmias, Cardiac ; Arterial Pressure ; Depression ; Dogs ; Electrocardiography* ; Embolism, Air* ; Heart Rate ; Hemodynamics ; Rabbits* ; Ultrasonography, Doppler ; Ventricular Premature Complexes

BACKGROUND: This study was performed to assess the effect of fentanyl and ketorolac in intravenous patient-controlled analgesia (IV-PCA) on postoperative nausea and vomiting and the antiemetic effect of prophylactic ondansetron after a total abdominal hysterectomy. METHODS: Of 115 women having general anesthesia for a total abdominal hysterectomy, a non-PCA group (n = 52) didn't receive IV-PCA and a PCA group (n = 39) and ondansetron group (n = 24) received IV fentanyl 1 - 1.5 microgram/kg and IM ketorolac 30 mg as a loading dose and IV-PCA with a mixture of 60 ml with fentanyl 25 - 30 microgram/kg and ketorolac 4 - 5 mg/kg. In addition, the ondansetron group received IV ondansetron 4 mg before an IV-PCA was started. We assessed nausea, vomiting and the need for rescue antiemetics during the first 24 hours postoperation. RESULTS: During the first 24 hours postoperation, there were no significant differences in the incidence of nausea, vomiting and the need for rescue antiemetics among the groups. CONCLUSIONS: Intravenous patient-controlled analgesia with fentanyl and ketorolac didn't increase postoperative nausea, vomiting and the need for rescue antiemetics during the first 24 hours postoperation. Also, prophylactic ondansetron didn't significantly reduce the chance of postoperative nausea, vomiting and rescue antiementics.
Analgesia, Patient-Controlled* ; Anesthesia, General ; Antiemetics ; Female ; Fentanyl* ; Humans ; Hysterectomy ; Incidence ; Ketorolac* ; Nausea ; Ondansetron* ; Passive Cutaneous Anaphylaxis ; Postoperative Nausea and Vomiting* ; Vomiting

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