In the beginning of anesthetic training, one of the clinical practices that anesthetists have to learn is manually controlled ventilator techniques. The popularity of manually controlled ventilatory techniques has been gradually decreased with increased use for anesthetic ventilators. However it is important and basic for the anesthetists to master manually controlled ventilator techniques skillfully. Recently, we analyzed the arterial blood gas in 30 cases before and during general anesthesia, and studied the effects of the manually controlled ventilation on the pulmonary gas exchange. The results were as follow; 1) Mean value of PaCO₂ during the manually controlled ventilation, 29.9±2.0 mmHg was decreased statistically comparing with that of PaCO₂ before the anesthesia, 39.8±2.8 mmHg. 2) Mean values of pH and HCO₃⁻ during the manually controlled ventilation were 7.48±0.03, 22.2±2.4 mEq/1, respectively and values before the anesthesia were 7.41±0.02, 25.2±1.8 mEq/1, respectively. 3) Mean value of PaO₂ and O₂ saturation during the manually controlled ventilation were 270.0±28.8 mmHg, 99.6±0.2%, respectively and values before the anesthesia were 92.5±4.0 mmHg, 96.9±1.0%, respectively. These results indicates that manually controlled ventilation at our department of anesthesiology produced mild hyperventilatory state. However these were no significant changes in cerebral blood flow and other biochemical parameters.
Anesthesia ; Anesthesia, General* ; Anesthesiology ; Cerebrovascular Circulation ; Hydrogen-Ion Concentration ; Pulmonary Gas Exchange ; Ventilation* ; Ventilators, Mechanical

Before beginning the extracorporeal circulation, perfusionists should supply oxygen into the oxygenator and establish blood flow through the blood line of the heart-lung machine. But these manipulation can induce severe hypocarbic state of priming solutions due to wash out of CO2 gas in the solution. This study was carried out to examine the relationship of blood gas changes between hypocarbic priming solutions and body circulation in 15 patients undergoing open heart surgery with extracorporeal circulation. PaCO₂, pH, buffer base and PaO2 were measured from priming solutions before and 15 minutes after the extracorporeal circulation. The results were as follows; 1) Before the extracorporeal circulation, mean PaCO₂ level was 12.1±7.8 mmHg in the priming solution. However, 15 minutes after extracorporeal circulation, the PaCO₂ level was maintained at 35.7±5.7 mmHg. 2) pH in the priming solution was variable from 6.93 to 7.99 (mean 7.45±0.29), but after 15 minutes it was ranged from 7.28 to 7.42 (mean 7.35±0.05). 3) Mean buffer base level in the priming solution was 7.9±3.5 mmol/l. but after 15 minutes, it was 19.6±1.2 mmol/l. 4) Mean PaO₂ level in the priming solution was 667.1±45.6 mmHg, but after 15 minutes, it was 280.7±131.7 mmHg.
Extracorporeal Circulation* ; Heart* ; Heart-Lung Machine ; Humans ; Hydrogen-Ion Concentration ; Oxygen ; Oxygenators ; Thoracic Surgery*

A study was undertatken to determine whether the pressure preset ventilator such as the Bennett PR-1 or PR-2 that are used for respiratory care in the intensive care unit or in the recovery room after anesthesia could also be used as and anesthetic ventilator for pediatric anesthesia. Maintaining anesthesia with halothane(0.5~1.0%)-N2O(2.51/min)-O2(2.51/min)-pancuronium bromide(0.1mg/kg) and using the Jackson-Rees modified Ayre's T-piece, the reservoir bag was removed from that device and the reservoir tube was connected to the pressure present ventilator. The inspiratpry pressure of the ventilator was fixed at 15cm H2O and the respiratory frequency was controlled at 30/min in 15 patients under 10kg of body weight, and at 25/min in 15 patients weighing 11~17kg. Arterial blood gas tension was measured 30 minutes after ventilator use. The following results were obtained: 1) pH: 7.28~7.44(7.35+/-0.04) 2) PaCO2: 28.4~41.3mmHg(35.4+/-2.9mmHg). 3) PaO2: 184.9+/-289.0mmHg(242.7+/-30.5mmHg). 4) HCO2(-): 15.5~23.5mEq/L(19.8+/-1.9mEq/L). 5) B.E.: -10.0~-0.6mEq/L(-4.6+/-2.3mEq/L) The above values of arterial blood gas tension showed a normal ranges in all cases. Therefore, it could be assumed that replacing the reservoir bag of the Jackson-Rees modified Ayre's T-piece with the pressure present ventilator is an excellent device for pediatric anesthesia.
Anesthesia* ; Body Weight ; Humans ; Hydrogen-Ion Concentration ; Intensive Care Units ; Recovery Room ; Reference Values ; Ventilators, Mechanical*

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

BACKGROUND: Reactive oxygen species (ROS) induce lipid peroxidation and tissue damage in the isolated rabbit thoracic aorta. The aim of this study was to explore the influence of the propofol and midazolam against ROS in the isolated rabbit thoracic aortic endothelium. METHODS: Eighteen white male rabbits (weighing 2.0-2.5 kg) were used. The thoracic aorta was dissected free and cut into rings (3-4 mm) and then suspended in a organ bath filled with 10 ml Krebs solution bubbled with 5% CO2 95% O2 at 37 degrees C. Aortic rings were then equilibrated for 90 min, and a resting tension of 1.5 g was applied. The Krebs solution was changed every 15 min. Isometric tension was recorded with transducer coupled to a data acqusition system (Biopac Inc. USA) on a PC. After precontraction with norepinephrine (NE, 10(-6)M), changes in tension were measured following the cumulative administration of acetylcholine (ACh 3x10(-7), 10(-6) and 3x10(-6)M) and nitroglycerin (NTG, 10(-5)M). Data are expressed as percentage of the 10 5 M NTG-induced relaxation (ACh/NTG). The ACh/NTG, before and after electrolysis were defined as the control and the experimental groups. The aortic rings were pretreated with propofol (3x10(-5), 10(-4), 3x10(-4) and 5.7x10(-4) M, n = 8, 10, 15, 13), midazolam (10(-4)M, n = 7), catalase (1,000 U/ml, n = 12), mannitol (3x10(-4)M, n = 5) or not pretreated group (Free, n = 6). After 30 minutes, the aortic rings were exposed to ROS generated by electrolysis (DC 9 V, 20 mA, aortic rings 1 cm away from electrode) in Krebs solution for 2 minutes, which was then changed for physiologic buffered salt solution. The aortic rings were precontracted with NE and vasorelaxation was induced with ACh and NTG at the above mentioned concentrations. RESULTS: Propofol produced vasorelaxation of NE-precontracted thoracic aorta in a dose-dependent fashion in all groups of propofol (3x10(-5), 10(-4), 3x10(-4) and 5.7x10(-4)M) even after ROS attack (P < 0.05 vs control value). Catalase produced vasorelaxation after ROS attack (P < 0.05 vs control value).On the other hand, ACh-induced significant endothelium-dependent vasorelaxation were not observed in the midazolam or mannitol pretreated group or the non-pretreated group (P <0.05 vs control group). CONCLUSIONS: These findings suggest that propofol and catalase preserve ACh induced endothelium-dependent vasorelaxation and that propofol has a concentration dependent ROS scavenging effect like catalase.
Acetylcholine ; Aorta, Thoracic ; Baths ; Catalase ; Electrolysis ; Endothelium ; Hand ; Humans ; Lipid Peroxidation ; Male ; Mannitol ; Midazolam ; Nitroglycerin ; Norepinephrine ; Propofol* ; Rabbits ; Reactive Oxygen Species* ; Relaxation ; Transducers ; Vasodilation

Ketamine hydrochloride is a phencyclidine derivatives and dissociative anesthetics. Ketamine induce the pulmonary vasoconetrietion in vivo. This study was designed to deter- mine the direct effect of the ketamine on the rabbit pulmonary artery in vitro. Isolated pulmonary artery was precontracted with norepinephrine (NE) 10-7M in the 20 ml organ bath. Concentration of ketamine was gradually increased 10-5M, 10 4M and 10-3M at 10 minutes intervals. I divided forty three experimental speeimens into 5 groups : pulmonary artery with and without endothelium, pretreated with indomethacin, nitrow-L-arginine methyl ester(L-NAME) and methylene blue. The results were as follows : 1. Norepinephrine precontracted pulmonary arterial tone wss significantly decreased by ketamine(10-3M), and the relaxing percent were 81.0 19.3, 60.6 55.4 (Mean S.D.) in unrubbed and rubbed endothelium, respectively (p<0.05). 2. The changes of vascular tone in denuding and intact groups were not significantly different. 3. Vasorelaxation induced by ketamine was not related with nitric oxide(NO) synthase, cyclooxygenase and soluble guanylate cyclase. Ketamine induce relaxation of the rabbit pulmonary artery, especially at 10-3 M concentra- tion. The relaxing effect was not related with endothelium presence, nitric oxide synthase, cyclooxygenase and soluble guanylate cyclase pathways. This data suggest that the relaxing effect of ketamine was not associated with endothelium, Nitric oxide, prostacyclin and cyclic guanosinemonophosphate.
Anesthetics, Dissociative ; Arteries ; Baths ; Endothelium ; Epoprostenol ; Guanylate Cyclase ; Indomethacin ; Ketamine* ; Methylene Blue ; NG-Nitroarginine Methyl Ester ; Nitric Oxide ; Nitric Oxide Synthase ; Norepinephrine ; Phencyclidine ; Prostaglandin-Endoperoxide Synthases ; Pulmonary Artery ; Relaxation ; Vasodilation

Halothane is a popular inhalation anesthetics in practice, which has been reported to cause a vasodilation through a direct depressant action on vascular smooth muscle, or by an indirect attenuation of vasoconstrictor activity. The membrane potential of the vascular smooth muscle cell is mainly regulated by the flow of Ca2+ and K+ ions through specialized channels. The purpose of this study was to determine whether blockade of the K+ channel alter the response to halothane vasodilating action. This study was done with rat thoracic aorta in tissue bath. Isometric tension of the ring (3~4 mm in length) was recorded. In halothane alone group (n=15), after precontraction with norepinephrine (10(-7) M), ring was exposed with halothane 0.7%, 1.5%, 2.1% concentration for 15 minutes, sequentially. The procedure of calcium activated K+ channel blocker pretreated group (n=12) was same manner as halothane alone group after tetraethylammonium (TEA 20 mM) pretreatment. The result of this study was shown to followings; 1) Vasodilation correlate with halothane concentration (p<0.05). 2) Vasodilation in tetraethylammonium (TEA) pretreated group also augmented 'significantly (p<0.05). 3) Especially, in the halothane 1.5%, 2.1%, the presence of TEA significantly potentiate vasodilating effect: halothane alone group, -35%, -53%: TEA group, -47%, -71%(p<0.05). These result demonstrate that: 1) halothane induce relaxation of rat aorta. 2) K+ charinel blokade potentiate the vasodilating effect of halothane.
Anesthetics, Inhalation ; Animals ; Aorta ; Aorta, Thoracic ; Baths ; Calcium ; Halothane* ; Ions ; Membrane Potentials ; Muscle, Smooth, Vascular ; Norepinephrine ; Rats ; Relaxation ; Tea ; Tetraethylammonium ; Vasodilation*

To assess the difference in analgesic effect of peridural demerol and morphine, we performed caudal anesthesia in patients under going hemorrhoidectomy. The patients were divided into three groups. As a control group, group l, was injected with 1.5% lidocaine alone for caudal anesthesia in 37 patients. in group ll(demerol group) 31 patients were injected with 1.5% lidocaine mixed with demerol 10mg and in group lll (morphine group) 82 patients were injected with 1.5% lidocaine mixed with morphine lung in to the caudal peridural space. The duration of the postoperative analgesic effect, frequency of analgetic injection and incidence of side reactions were checked and compared. The results of This study were as follos: 1) The analgesic effect in caudal peridural demerol and morphine groups were superior to the those of the control group and the morphine group were significantly prolonged analgesic effect compared to the demerol group (p<0.005). 2) The frequencty of analgetic injection was lowest in the morphine group. The 67 patients (81.7%) in the morphine group did not need and analgetic injection. 3) Urinary retention in the narcotic group was more frequent than in the control group. 4) Other side reactions of this study were minimal or any signs of CNS depression and respiratory depression were not observed.
Analgesia* ; Anesthesia, Caudal ; Depression ; Hemorrhoidectomy ; Humans ; Incidence ; Lidocaine ; Lung ; Meperidine* ; Morphine* ; Respiratory Insufficiency ; Urinary Retention

The ryanodine receptor/channel (RyR) mediates the release of calcium from the sarcoplasmic reticulum (SR) in both skeletal and cardiac muscle cells. There are three isoforms of the RyR: RyR1, RyR2, and RyR3. RyR1 is specifically expressed in skeletal muscles and RyR2 in cardiac muscles. RyR3 is yet another isoform found in non-muscle cells such as neuronal cells. Single channel recordings of RyR1 and RyR2 reconstituted in artificial lipid bilayer show that the characteristics of two isoforms are very distinct. RyR1 has a shorter mean open time and is activated at a higher concentration of Ca2+ than RyR2. In this study, we isolated the heavy SR membranes from canine latissimus dorsi muscles and investigated the single channel activities from the heavy SR membrane fraction using Cs+ as a charge carrier. Two different types of activities were observed. The fast-gating type (FG) with the mean open time of 0.9 ms was more frequently recorded (n = 12) than the slow-gating type (SG) with the mean open time of 269.2 ms. From the I-V relation, the slope conductance of the FG was calculated to be 514.7 pS and the SG, to 625.6 pS. The activity of the fast gating type increased by raising the concentration of Ca2+ in the cis-solution up to 100 microM. The appearance of the SG in the canine heavy SR membrane fraction suggests a possibility that two types of RyR isoform are co-expressed in mammalian skeletal muscle as well as in avian, amphibian and piscine fast twitch muscles.
Animal ; Calcium Channels/*metabolism ; Dogs ; *Ion Channel Gating ; Lipid Bilayers ; Microsomes/metabolism ; Muscle Proteins/*metabolism ; Muscle, Skeletal/*metabolism ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum/*metabolism ; Support, Non-U.S. Gov't ; Thorax ; Time Factors