BACKGROUND: In order to understand the pathogenetic mechanism of sepsis-induced acute lung injury, inhibition of phospholipase A2 (PLA A2) was carried out in an endotoxin-induced septic lung model. METHODS: Sprague-Dawley rats were divided three groups; sham group, endotoxin group (instillation of E coli endotoxin, 100microgram/rat, type 017) and mepacrine group (the non-specific PLA2 inhibitor, 50 ml/kg intraperitoneal injection after endotoxin treatment). Five hours after endotoxin treatment, protein contents, neurophils counts, gamma-glutamyl transpeptidase (GGT) activity and surfactant concentrations in the bronchoalveolar fluid (BAL), meyloperoxidase (MPO) and PLA2 activity in the lung were measured. A morphological study for the effect of the endotoxin and mepacirne, and a cytochemical electron microscopy for detection of hydrogen peroxide in the lung were also performed. RESULTS: Endotoxin increased the concentrations of protein, the number of neutrophils, and GGT activity in the BAL fluid, MPO and PLA2 activity in the lung but mepacrine decreased these parameters (P < 0.001). The light density of surfactant was increased by the endotoxin (P < 0.001), but mepacrine diminished this pathological change. In the light microscopic findings, the endotoxin caused pulmonary accumulation of neutrophils, atelectasis and transudation of intravascular protein was observed. In contrast, mepacrine lessened these pathological findings. In ultrastructural findings, adhesion of neutrophils to endothelial cells, necroses of type II cells and endothelial cells, and the damage of lamellar bodies were observed after the endotoxin treatment, which recovered with mepacrine. In the cytochemical electron microscopy for detection of hydrogen peroxide in the lung, the deposits of cerrous perhydroxide were increased by the endotoxin but mepacrine decreased deposits of cerrous perhydroxide. CONCLUSIONS: Inhibition of PLA2 in an endotoxin induced acute lung leak showed protection against oxidative stress by a diminution of neutrophilic respiratory bursts and a decreased production of free radicals. It is suggested that PLA2 has a pivotal role in causing acute oxidative stress in endotoxin induced acute lung injury.
Acute Lung Injury* ; Endothelial Cells ; Escherichia coli* ; Free Radicals* ; gamma-Glutamyltransferase ; Hydrogen Peroxide ; Injections, Intraperitoneal ; Lung* ; Microscopy, Electron ; Necrosis ; Neutrophils ; Oxidative Stress ; Oxygen* ; Phospholipases A2* ; Phospholipases* ; Pulmonary Atelectasis ; Quinacrine ; Rats, Sprague-Dawley ; Respiratory Burst

BACKGROUND: There are many factors which cause postoperative hepatic dysfunction. Anesthetic agents are not the most common factor and there aremany other factors such as preoperative condition of the patients, site and duration of the operation, operation per se and so on. The purposeof this study is to evaluate postoperative liver function with respect to different types of surgery. METHOD: Fourty three patients were classified into three groups; 11 patients for tympanoplasty with mastoidectomy (Group 1), 16 patients for total abdominal hysterectomy (Group 2), 15 patients for subtotal gastrectomy (Group 3). All patients were anesthesized with about 2 vol% of enflurane combined with 50% nitrous oxide. Serum glutamic oxalacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT) and alkaline phosphatase (ALP) were measured before anesthesia, 1, 3 and 7 days after surgery in all group, respectively. RESULT: In Group 1 and 2, postoperative SGOT and SGPT levels were maintained with preoperative level during the 7days, but in Group 3, those levels were increased in the 1st day but below upper limit (p<0.05) and decreased thereafter. Alkaline phosphatase level was maintained within the normal range for all the group during the 7 days. CONCLUSION: We consider that postoperative liver functioin may be influenced by different types of surgery, and also may be influenced by anesthetic time.
Alanine Transaminase ; Alkaline Phosphatase ; Anesthesia ; Anesthesia, Inhalation* ; Anesthetics ; Aspartate Aminotransferases ; Enflurane* ; Gastrectomy ; Humans ; Hysterectomy ; Inhalation* ; Liver* ; Nitrous Oxide ; Reference Values ; Tympanoplasty

BACKGROUND: The studies related to induced hypotention using propofol were rare. So we studied the effectiveness of propofol as induced hypotensive agent in brain aneurysmal surgery. METHODS: The hemodynamic changes during induced hypotension with propofol (propofol-group) and isoflurane(isoflurane group) were observed in patients undergoing aneurysmal surgery. Twenty patients were allocated randomly to receive propofol induction and maintenance, or thiopental sodium induction and isoflurane maintenance for anesthesia. Both groups also received fentanyl, vecuronium, nitrous oxide and oxygen. These hypotensive effects were evaluated before, during and after induced hypotension. Hemodynamic changes were evaluated by measuring systemic arterial blood pressure, heart rate, central venous pressure, pulmonary capillary wedge pressure, cardiac output, systemic vascular resistance and pulmonary vascular resistance. We also compared the ventilatory effect of hypotensive anesthesia by blood gas analysis. RESULTS: There were no significant changes of heart rate, cardiac output, mean pulmonary arterial pressure, pulmonary capillary wedge pressure, central venous pressure and pulmonary vascular resistance before, during and after induced hypotension in both group. Mean arterial pressure and systemic vascular resistance were significantly decresed during induced hypotension (p<0.05). There were no significant changes of PO2, PCO2, HCO3 , base excess before, during and after induced hypotension in both group. CONCLUSION: Propofol is also an effective hypotensive agent comparable to isoflurane.
Anesthesia ; Anesthetics ; Aneurysm ; Arterial Pressure ; Blood Gas Analysis ; Cardiac Output ; Central Venous Pressure ; Fentanyl ; Heart Rate ; Hemodynamics* ; Humans ; Hypotension* ; Intracranial Aneurysm ; Isoflurane ; Nitrous Oxide ; Oxygen ; Propofol* ; Pulmonary Wedge Pressure ; Thiopental ; Vascular Resistance ; Vecuronium Bromide

BACKGROUND: During pediatric general anesthesia with Mapleson D-circuit, we used large amount of FGF(fresh gas flow) for avoidance of rebreathing of expired gas but low FGF are employed, the amount of anesthetic consumption and air contamination can be reduced. The aim of this study was to evaluate the fact that FGF of 220 ml/kg/min is clinically acceptable. METHODS: We selected sixty children weighing < or =20 kg who were scheduled for inguinal hernia repair under general anesthesia. The study was performed by 2 steps; In the step 1, the patients were divided into two groups according to weight(less than or greater than 8 kg) and end-tidal Pco2 were compared with simultaneous arterial Pco2 measurements. In the step 2, the patients were divided into two groups according to FGF(2MV or 220 ml/kg) and arterial Pco2, end tidal Pco2 and PminCO2(minimum inspired Pco2) were measured. RESULTS: In the step 1 study, arterial Pco2 was significantly higher than end-tidal Pco2 in the group 1 and there was slight difference in arterial Pco2 and end-tidal Pco2 in the group 2. In the step 2 study, PaCO2, PetCO2, PminCO2 were significantly increased in the group 3 than group 2 but there were no clinical hypoxemia in all patients. CONCLUSIONS: We consider that FGF of 220 ml/kg/min is appropriate during controlled ventilation with Mapleson D circuit in children weighing > or =8 kg because of economic and ecological advantages. Also, we consider FGF can be reduced in children weighing <8 kg under accurate respiratory gas monitoring.
Anesthesia, General* ; Anesthetics ; Anoxia ; Blood Pressure ; Child ; Heart Rate ; Hernia, Inguinal ; Humans ; Lidocaine ; Ventilation

BACKGROUND: During adult general anesthesia, we used 3~5 L/min of fresh gas flow(FGF) but low FGF are employed, the amount of anesthetic consumption and air contamination can be reduced. The aim of this study was to determine the minimal appropriate inflow rate of oxygen and nitrous oxide during semiclosed circle technique. METHODS: We selected 40 patients, ASA group 1 or 2, scheduled for elective, nonabdominal surgery under general anesthesia with semiclosed circle system. Anesthesia was maintained with 50% oxygen, nitrous oxide and enflurane, controlled ventilation was used; rate of 10/min, tidal volume of 10 ml/kg. After induction and vital signs stabilized, FGF was changed to 4 L, 3 L, 2 L and 1L/min at interval of 30 minutes. We observed mean airway pressure and arterial blood gas tensions. RESULTS: The changes of mean airway pressure did not correlated with fresh gas inflow rate. In arterial blood gas analysis, PaO2 showed a decreasing tendency significantly according to decreasing fresh gas inflow rate(p<0.01) but there were no clinical hypoxemia in all patients. There were no significant changes in pH, PaCO2 and base excess. CONCLUSIONS: We consider that FGF of 1~2 L/min is appropriate during adult general anesthesia because of economic and ecological advantages. Also, we consider low flow technique with below 1L/min can be used safely and effectively under proper gas monitoring such as oxygen analyzer, capnometer.
Adult* ; Anesthesia ; Anesthesia, General* ; Anesthetics ; Anoxia ; Blood Gas Analysis ; Enflurane ; Humans ; Hydrogen-Ion Concentration ; Nitrous Oxide* ; Oxygen* ; Tidal Volume ; Ventilation ; Vital Signs

The vasoactive effecs of ketamine on aortic and pulmonary arteries have not heen clearly characterized. Nevertheless, it has been recommended to avoid ketamine in systemic and pulmonary hypertension because of its tendency to increase systemic and pulmonary vascular resistance. This study was designed to investigate and compare the direct effects of ketamine on isolated rat aortic and pulmonary arteries, with or without intact endothelium. The optimal resting tension (Lmax) of each ring was searched hased on contractile responses to 3.7X10(6)M norepinephrine. Once the Lmax was Obtained, the peak developed tension was recorded as the control. Thereafter, in the second part of the experiments, prior to ketamine exposure, the endothelium was denuded which was confirmed pharmacologically using norepinephrine(3.7X10-6M) and acetylcholine(10(-6)M). In groups with intact endothelium, .3X10(3)M ketamine relaxed aortic and pulmonary artery ring by -10.3+/-5.6%, -17.8+/-4.4%, respectively. In groups without intact endothelium, 3X10(3)M ketamine relaxed aortic and pulmonary artery ring by -9.9+/-3.6%, -14.2+/-3.8%, respectively. It was statistically significant. In groups with or without intact endothelium, 0.1X10(3) M ketamine relaxed aortic and pulmonary artery ring. Hut it was statistically insignificant. We conclude that ketamine is a powerful aortic and pulmonary artery dilator in vitro and that is endothelium independent.
Animals ; Aorta* ; Endothelium ; Hypertension, Pulmonary ; Ketamine* ; Norepinephrine ; Pulmonary Artery* ; Rats* ; Vascular Resistance

Surgical tissue damage induces dual phenomenon of peripheral and central sensitization. Postoperative pain could be partially explained by neuronal hyperexcitability. As a postoperative pain model, formalin test, subcutaneous injection of formalin in the rat hind paw, results in initial vigorous flinching(phase 1), depends on acute chemical stimulation, followed by cessation of activity, and then resumption of flinching(phase 2), which depends on central sensitization. Pre-emptive analgesia, given before the onset of a painful stimuli, reduces or ptevents postoperative pain by preventing this central sensitization. This study was performed to evaluate the effect of local infiltration of lidocaine as a pre-emptive analgesia in the formalin test. Forty experimental rats were divided four groups; CONTROL group(without any treatment), POST group(0.04 mL of 1% lidocaine injection 5 min after formalin injection), PRE group(0.04mL of 1% lidocaine 5 min before formalin injection), and SHAM group(injection of normal saline 5 min before formalin injection). All animals received inhalation anesthesia for 15 min before and 5 min after formalin injection. Under halothane inhalation anesthesia, all were injected subcutaneously 0.04 mL of 5% formalin in the distal plantar area of right hind paw. After recovery of anesthesia, the formalin-induced flinching behavior was observed during only the phase 2 period(10-60 min) after formalin injection. The time to first flinching, the mean number of flinches per min, and the mean number of total flinches during phase 2 expressed as a percent of the values of the CONTROL group were compared between the groups with an t-test or an ANOVA. The first flinching was appeared before recovery of anesthesia in CONTROL and SHAM groups. The time to first flinching after formalin injection was 21.2+/-3.4, 16.6+/-3.1 min respectively in PRE and POST groups. It was significantly longer in PRE group than in POST group(P<0.05), despite of 10 min earlier injeetion of lidocaine in PRE group. The mean number of flinches per min was significantly lower in PRE and POST groups(P<0.05) until 25 min after formalin injection, and after that time the difference between PRE group and POST group was significant(P<0.05). The means of the total number of flinches during phase 2, expressed as a percent of the values of the CONTROL poup, were 100+/-17.2%, 31.8+/-13.1%, 76.9+/-14.5% respectively in SHAM, PRE and POST groups. Those in PRE and POST groups were significantly lower than that of CONTROL group(P<0.001), and the difference between PRE group and POST group was significant(P<0.05). In summary, pre-emptive infiltration of lidocaine on formalin test prolongs the duration of analgesia and reduces the severity of formalin pain in rat. Therefore, the infiltration of lidocaine before formalin test is really provided pre-emptive analgesia.
Analgesia ; Anesthesia ; Anesthesia, Inhalation ; Animals ; Central Nervous System Sensitization ; Formaldehyde* ; Halothane ; Injections, Subcutaneous ; Lidocaine* ; Neurons ; Pain Measurement ; Pain, Postoperative ; Rats* ; Stimulation, Chemical

The induction agents produce various effects to cardiovascular system. Among these, thio- pental, propofol, and etomidate produce reduction in cardiac output and peripheral vascular resistance. As a result severe systemic arterial hypotension is evoked. This phenomenon results from combined effects of CNS, cardiovascular and peripheral vascular systems. The purpose of this study was to obeserve direct effects of thiopental, propofol, etomidate in isolated rat aorta and pulmonary artery. Isometric tension was recorded in rat aortic and pulmonary artery ring preparation contracted by norepinephrine(1.8x10-6) . Thereafter thiopental, etomidate, propofol was added to organ bath. And the contractile or relaxing response was observed. Thiopental relaxed aortic ring by 3.6+/-1.3%(low dose), 3.9+/-1.4%(high dose), etomidate relaxed aortic ring by 2.0+/-0.7%(low dose), 5.4+/-2.8% (high dose), respectively. It was statistically insignificant. However, propofol relaxed aortic ring by 12.7+/-3.8%(low dose), 14.7+/-2.7%(high dose), respectively(p <0.05). Thiopental relaxed pulmonary artery ring by 4.8+/-1.1%(low dose), 5.1+/-2.3%(high dose), etomidate relaxed pulmonary artery ring by 4.8+/-1.1%(low dose), 5.1+/-2.3%(high dose), respectively. It was statistically insignificant. However, propofol relaxed pulmonary artery ring by 8.4+/-2.4%(low dose), 10.4+/-3.6(high dose), respectively( p<0.05). The results suggest that hypotension after propofol administration was due to direct vascular smooth muscle relaxation.
Animals ; Aorta* ; Baths ; Cardiac Output ; Cardiovascular System ; Etomidate* ; Hypotension ; Muscle, Smooth, Vascular ; Propofol* ; Pulmonary Artery* ; Rats* ; Relaxation ; Thiopental* ; Vascular Resistance

Laryngotracheal injury following endotracheal intubation has been extensively described in the literature, but most discussion has centered around the sequela of prolonged intubation. Little however, has been reported regarding the lesions from short-term endotracheal intubation to ensure the safe practice of anesthesia. In this regard, 72 healthy, male patients undergoing general anesthesia for surgical procedures were randomly assigned to have an endotracheal tube of 7.0, 8.0, or 9.0 mm in internal diameter and were evaluated for the upper airway symptoms by questionnaire within 4-8 hours following extubation. The larynx and trachea were examined and scored for extent and severity of lary- ngotracheal damage by fiberoptic laryngotracheoscopy, and risk factors causing laryngotracheal injury were studied. The results were as follows; The incidence of upper airway symptoms were 13 of 72 (18.1%), of which 10 (13.9%) were throat discomfort and 3 (4.2%) were sore throat. The incidence of laryngeal and tracheal injury was 52 of 72 (72.2%) and 20 of 72 (27.8%), respectively. 20 patients (27.8%) did not reveal any lesion in the laryngotracheal system. The common sites of intubation injury were vocal cords (65.3%, all erythema) and arytenoids (44.4%, erythema 37.5%, edema 6.9%). No correlation could be drawn between the injured and uninjured groups with respect to smoking and length of intubation. However, bucking was associated with severity and extent of laryngeal damage (p<0.05), and with the extent of tracheal damage only (p<0.05). Also, the increase in internal diameter of the tube used was associated with severity and extent of laryngeal damage (p<0.05), but not with tracheal damage.
Anesthesia ; Anesthesia, General ; Edema ; Erythema ; Humans ; Incidence ; Intubation ; Intubation, Intratracheal* ; Larynx ; Male ; Pharyngitis ; Pharynx ; Surveys and Questionnaires ; Risk Factors ; Smoke ; Smoking ; Trachea ; Vocal Cords

Isometric tension was recorded in uterine arterial ring preparation contracted by potassium (60 mM) and norepinephrine(1.8 X 10(-7) M). With pretreatment of various concentrations of nifedipine(2.9 x 10(-9) ~2.9 X10(-7) M) and verapamil(2.2 X 10(-7) -2.2 X 10(-5) M), the relaxation was dose-dependent and inhibitory effects of both agents were more marked on the potassium than norepinephrine-evoked contraction. After immersion of the arterial preparation in calcium-free solution, the potassium-evoked contraction was decreased to 21+/-4.1%(mean+/-SEM) of the response in normal Krebs solution and norepinephrine-evoked contraction to 26+/-3.8%. The responses to both agents were completely restored when the calcium concentration was increased to 4.0 mM. Pretreated nifedipine(2.9 x 10(-7) M) in calcium-free solution depressed the potassium-evoked contraction to 7.3+/-1.6% and norepinephrine-evoked contraction to 12+/-3.7%. In addition of calcium(0-4.0mM), the potassium-evoked contraction increased to 30+/-4.6% and that by norepinephrine to 45+/-5.4%. Pretreated verapamil(2.2 X 10(-5) M) in calcium-free solution depressed the potassium-evoked contraction to 14+/-3.6% and norepinephrine-evoked contraction to 18+/-3.3%. In addition of calcium(0-4.0mM), the potassium-evoked contraction increased to 41+/-4.2% and that by norepinephrine to 57+/-4.7%. It was concluded that nifedipine and verapamil relaxed KC1 contracted ring in the presence of external calcium and relaxed norepinephrine contracted ring in both the presence and absence of external calcium. These findings suggest that calcium antagonists interfere with the release of calcium from intracellular sites as well as with the slow inward current of calcium.
Calcium ; Humans* ; Immersion ; Nifedipine* ; Norepinephrine ; Potassium ; Relaxation ; Uterine Artery* ; Verapamil*