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*

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

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

The characteristics of an ideal intravenous anesthetic agent include stability in solution, rapid onset of action, minimal effect on the cardiovascular and respiratory systems, short elimination half life, and minimal side effects. Using this criteria, the ultra-short acting barbiturate, thiopental has long been considered the gold standard of intravenous agents used for induction of anesthesia. In normovolemic subjects, thiopental produces a transient decrease in blood pressure, and increase in heart rate. In practice, thiopental is administered high dose(30 mg/kg IV) for brain protection, rarely. We tried to confirm the direct vascular effects of thiopental and its mechanism on the rabbit abdominal aorta in vitro. The rabbit abdominal aorta were precontracted with norepinephrine(10(-7) M) in 5 ml tissue bath and 10(-5), 10(-4), and 10(-3) M thiopental was administrated in cumulative manner. Ten minutes later, changes of the vascular tones were obtained. For confirming the relaxing mechanism induced by thiopental, experiment was performed by indomethacin, methylene blue and LNAME pretreatment, and endothelium removed, respectively. The results were as follows 1) Thiopental at 10(-5), and 10(-4) M produced no signifcant changes, and at 10(-3) M produced signifcant relaxation. 2) There were no significalnt difference in their vascular tones between intact and denuded endothelium group. 3) The vascular tones were not affected by LNAME, methylene blue, and indomethacin pretreatment. These results suggest that thiopental induce vasorelaxation in rabbit abdominal aorta at high concentration(10(-3) M). The vasorelaxation mechanism is not correlated with NO, cyclic GMP, prostacyclin and endothelium.
Anesthesia ; Aorta, Abdominal* ; Baths ; Blood Pressure ; Brain ; Cyclic GMP ; Endothelium ; Epoprostenol ; Half-Life ; Heart Rate ; Indomethacin ; Methylene Blue ; Relaxation ; Respiratory System ; Thiopental* ; Vasodilation

BACKGROUND: Reactive oxygen species (ROS) are free radicals that induce lipid peroxidation and cause tissue damage. ROS are frequently produced by ischemia and subsequent reperfusion in clinical situation and like coronary artery bypass graft surgery and transplantation. More over, some anesthetics are known to act as an antioxidants and free radical scavenger and, the aim of this study was to explore the scavenging effects of thiopental and ketamine against ROS induced by isolated rabbit thoracic aortic endothelial damage. METHODS: Twenty white male rabbits (weighing 2.0-2.5 kg) were used. Thoracic aorta and were dissected free, cut into rings (3-4 mm), and suspended in an organ bath filled with 10 ml Krebs solution bubbled with 5% CO2 and 95% O2 at 37oC. The rings were equilibrated for 90 min and the solution changed every 15 min, and then a resting tension of 1.5 g was applied to the rings. Isometric tensions were recorded using a transducer connected to a data acqusition system (Biopac Inc. USA). Aortic rings were precontracted with norepinephrine (NE, 10-6 M), and changes in tension were measured after the cumulative administration of acetylcholine (ACh 3 x 10-7, 10-6 and 3 x 10-6 M) and nitroglycerin (NTG 10-5 M). Data are expressed as percentages of the 10-5 M NTG-induced relaxation (ACh/NTG). Percentages of ACh/NTG, before and after ROS exposure by electrolysis were noted for control and experimental groups. Aortic rings were pretreated with thiopental (3 x 10-5, 10-4 and 3 x 10-4 M, n = 9, 13, 17), ketamine (10-4 M, n = 8), catalase (1000 U/ml, n = 12), mannitol (3 x 10-4 M, n = 5) or not pretreated (free, n = 6). After 30 minutes, with the rings were exposed to ROS by electrolysis (DC 9 V, 20 mA, aortic rings 1 cm removed from the anode) in Krebs solution for 2 minutes. After electrolysis, the organ bath fluid was replaced with fresh Krebs solution, and the aortic rings were precontracted with NE and was vasorelaxation with ACh and NTG as above mentioned concentrations. RESULTS: Endothelium-dependent vasorelaxation was induced in all concentrations of thiopental groups in a dose-dependent fashion (P <0.05 vs control value) even with ROS attack. The catalase group produced vasorelaxation after ROS attack (P <0.05 vs control value). On the other hand, no ACh-induced significant endothelium-dependent vasorelaxation after ROS exposure was observed in the ketamine and mannitol pretreated group, or in the free group (P <0.05 vs control group). CONCLUSIONS: These findings suggest that thiopental and catalase preserve ACh induced endothelium-dependent vasorelaxation and that thiopental has a dose-dependent ROS scavenging effect like catalase.
Acetylcholine ; Anesthetics ; Antioxidants ; Aorta ; Aorta, Thoracic* ; Baths ; Catalase ; Coronary Artery Bypass ; Electrolysis ; Free Radicals ; Hand ; Humans ; Ischemia ; Ketamine* ; Lipid Peroxidation ; Male ; Mannitol ; Nitroglycerin ; Norepinephrine ; Rabbits ; Reactive Oxygen Species* ; Relaxation* ; Reperfusion ; Thiopental* ; Transducers ; Transplants ; 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