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

Hypoxic pulmonary vasoconstriction(HPV) plays an important role in matching ventilation and perfusion, and in a homeostatic compensatory mechanism for maintaining arterial blood oxygen tension. The purpose of this study was to explore effect of hypoxia on the vascular tension and to elucidate mechanism underlying hypoxic pulmonary vasoconstriction. The ring segments of the pulmonary artery were taken from forty rabbits(2~2.5 kg, male). Each ring was attached to an isometric force transducer(Grass FT-03) and suspended in a tissue bath(37degrees C) filled with 5 ml Krebs solution, aerated with 95% O2 + 5% CO2(pH 7.4) gas mixture. During 90 minutes of equilibrium period, the Krebs solution was changed every 15 minutes and the last resting tension was adjusted to 2 gm. After precontraction of the preparations with K(+) 40 mM, the aerating gas mixture was replaced by hypoxic gas(95% N2 + 5% CO2) and changes in vascular tension of isolated pulmonary artery with(n=36) and without endothelium(n=14) were recorded for 60 minutes. HPV induced biphasic vasoactive effects. To determine the mechanism of the vasorelaxing response, the pulmonary arterial rings were pretreated with indomethacin(n=8), L-nitro(w) arginine methyl ester(L-NAME, n=l0), tetra ethyl ammonium(TEA, n=12), glybenclamide(n=l1). And also to elucidate the mechanism of the hypoxic vasoconstricting response, effects of Ca free solution and pretreatment of ryanodine on the HPV were examined. The results obtained were as follows: 1) Transient phase 1 contraction followed by long lasting(about 30 minutes) relaxation and sustained phase 2 contraction were induced by hypoxic gas(95% N2+5% CO2) in rabbit pulmonary artery. 2) In endothelium removed pulmonary artery, transient phase 1 contraction was not apparent. 3) Vasorelaxation was partially blocked by K' channel blockers(TEA, glybenclamide). 4) Indomethacin and L-NAME pretreatments did not affect on the vasorelaxing response of the HPV to hypoxia. 5) Sustained phase 2 contraction was blocked by calcium free Krebs solution. 6) Indomethacin and ryanodine pretreatments did not change the phase 1 and phase 2 vasocontsricting reponses. The results of present study suggest that hypoxia-induced phase 1 contractile response is endothelium dependent, while phase 2 contractile response is dependent on calcium influx, and that the vasorelaxant response is partially mediated by K(+) channel.
Anoxia ; Arginine ; Calcium ; Characidae ; Endothelins ; Endothelium ; Indomethacin ; NG-Nitroarginine Methyl Ester ; Oxygen ; Perfusion ; Pulmonary Artery* ; Relaxation ; Ryanodine ; Vasoconstriction* ; Vasodilation ; Ventilation

Doxapram is a peripheral and central respiratory stimulant, producing an increase in tidal volume and a slight increase in respiratory rate. It can temporarily overcome drug-induced respiratory and central nervous system depression, including that seen immediately postoperatively. However, it can also cause side effects, including laryngospasm and vomiting postoperatively. Doxapram-induced laryngospasm causes the increased respiratory efforts to induce more negative pleural pressure, thus causing a negative-pressure pulmonary edema.Therefore, doxapram should not be used if signs of upper airway obstruction are present.
Airway Obstruction ; Central Nervous System ; Depression ; Doxapram ; Laryngismus ; Pulmonary Edema ; Respiratory Rate ; Tidal Volume ; Vomiting

BACKGROUND: The purpose of this study was to determine the incidence of side effects, rate of recovery, and maintenance of anesthesia when using a mixture of propofol and thiopentone as compared with propofol alone. METHODS: Fifty ASA Physical Status I or II patients aged between 12 and 60 years scheduled for minor surgical procedures were randomly allocated to group P (propofol) or group PT (propofol mix with thiopentone) in which a loading dose of propofol 2 mg/kg (group P) or propofol 1 mg/kg and thiopentone 2.5 mg/kg (group PT) was applied. At induction of anesthesia, an independent anesthesiologist graded the incidence and severity of pain. After administering the induction dosage, he also checked spontaneous movements. The duration of operation time and the duration of anesthesia were also noted. RESULTS: There was a significant decrease of the incidence of pain on injection and spontaneous movements in group PT compared with group P (P < 0.05). The propofol maintenance dose was also significantly decreased (P < 0.05). There were no significant differences in recovery indexes between the two groups except delay in time to eye opening. CONCLUSIONS: Our data indicate that a propofol-thiopentone mixture for induction, maintenance and recovery are satisfactory during anesthesia undergoing minor surgery. In addition, there were significant reductions in pain on injection, spontaneous movement, and cost-effectiveness.
Anesthesia ; Humans ; Incidence ; Propofol* ; Surgical Procedures, Minor ; Thiopental

Metastatic tumors to the heart are far more frequent than primary tumors of the heart. Cardiac metastasis may be detected up to 30 percent of patients with fatal lung cancers. Metastatic cancer to the heart is difficult to suspect. Where cardiac metastasis is diagnosed ante-mortem, signs and symptoms of the primary cancer are usually the presenting features and the presence of cardiac involvement is often incidentally detected. We experienced a case of 35-year-old woman with metastatic lung cancer invading the left atrium via pulmonary vein, which was not proved pathologically. She presented with hemoptysis and chest pain. Transthoracic echocardiography demonstrated massive cardiac infiltration with tumor and decreased cardiac wall motion, correlating with the chest CT findings, which were also remarkable for the presence of intracardiac mass and direct invasion to adherent pericardium, pulmonary vein and left atrium. We suggest that careful examination of 2D echocardiography can be noninvasive and valuable tool for diagnosis of metastatic cancer to the heart.
Adult ; Carcinoma, Large Cell* ; Chest Pain ; Diagnosis ; Echocardiography ; Female ; Heart ; Heart Atria* ; Hemoptysis ; Humans ; Lung Neoplasms ; Lung* ; Neoplasm Metastasis* ; Pericardium ; Pulmonary Veins ; Tomography, X-Ray Computed

Thrombospondin-1 (TSP-1) level is tightly regulated at the transcriptional level. To determine the detailed molecular mechanisms of TSP-1 expression, nine serial 5'-deletion constructs of the human genomic tsp-1 promoter (nucleotides -2,220 to +756) were prepared, inserted into luciferase reporter plasmids, and transiently transfected into the Hep3B human hepatocarcinoma cell. Among the nine 5'-deletion constructs, pTSP-Luc-4 (-767~+756) had consistently decreased luciferase activity with or without PMA stimulation, whereas a further truncated construct [pTSP-Luc-4' (-407~+756)] had increased levels of expression. By searching the nucleotides from -767 to -407, a consensus binding sequence (5'-CCATTTT-3') for the repressor Yin Yang-1 (YY-1) at nucleotide -440 was identified. The suppression induced by this site was weakened in the presence of the region upstream of nucleotide -767 (pTSP-Luc-1 and -2). Nuclear protein directly bound to an oligonucleotide containing the repressive YY-1 sequence but the binding capacity of the sequence was decreased by the increased c-Jun levels. Moreover, proteins immunoprecipitated with anti-YY-1 revealed an interaction between c-Jun and YY-1 factor. These data suggest that the repressive YY-1 site of the tsp-1 promoter could not be functional via activating positive cis-elements on the upstream from this site and weakened via c-Jun/YY-1 interactions.
Binding Sites/genetics ; Cell Line, Tumor ; DNA-Binding Proteins/*metabolism ; Down-Regulation/genetics ; Electrophoretic Mobility Shift Assay ; Genes, Reporter/genetics ; Humans ; Luciferases/analysis/genetics ; Promoter Regions (Genetics)/*genetics ; Proto-Oncogene Proteins c-jun/genetics/*metabolism ; Repressor Proteins/*metabolism ; Research Support, Non-U.S. Gov't ; Sequence Deletion/genetics ; Thrombospondin 1/*genetics/metabolism ; Transcription Factor AP-1/metabolism ; Transcription Factors/*metabolism

Among exocrine pancreatic tumors, adenosquamous carcinoma is a rare, aggressive subtype with a poor prognosis and a high potential for metastases compared with its more conventional glandular counterpart, adenocarcinoma of the pancreas. We herein describe the imaging findings of pancreatic adenosquamous cell carcinoma with solitary liver metastasis showing different imaging features and also review the previous literature to recognize characteristic imaging features of pancreatic adenosquamous cell carcinoma.
Adenocarcinoma ; Carcinoma, Adenosquamous ; Liver* ; Neoplasm Metastasis* ; Pancreas ; Prognosis

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

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