Ischemia results when the decrease in tissue perfusion exceeds the tissues ability to increase an oxygen extraction from the blood. Brain edema has been defined as an abnormal accumulation of fluid within brain parenchyma associated with a volumetric enlargement of the brain tissue. In most instances, the labelling of edema as vasogenic or cytotoxic is only relative. For cerebral protection, there were many possible techniques which could increase or maintain cerebral perfusion and reduce cerebral metabolic demand for oxygen. This study was carried out the effect of mild
Brain Edema* ; Brain Ischemia* ; Brain* ; Edema ; Ischemia ; Oxygen ; Perfusion ; Tissues

Hyperglycemia has repeatedly been shown to exacerbate the neurologic injury produced by episodes of global cerebral ischemia. Under hypoxic conditions, glucose may be metabolized to glutamate, a known neurotoxin which has been implicated as a mediator of ischemic neumnal cell death. This study examined the effect of pre-existing hyperglycemia on the extracellular concentrations of glutamate and glycine in the rabbit hippocampus using in vivo microdialysis during brief episodes of transient global ischemia. Sixteen rabbits were anesthetized with halo- thane and mechanically ventilated with oxygen. Microdialysis probes were stereotacticly inserted into the dorsal hippocampus. Animals were randomized to receive an intravenous infusion of either saline or dextrose. The dextrose infusion rate was adjusted to produce a blood glucose level of approximately 40 mg/dl. Global cerebral ischemia (7.5 min duration) was then produced by the combination of neck tourniquet inflation and the induction of systemic hypotension. Dialystate was collected throughout the peri-ishemic period and analyzed by liquid chromato- graphy for glutamate, aspartate and glycine concentrations. There were no significant differences in physiologic variables among the groups with the exception of the intended increase in blood glucose concentrations in the dextrose-treated animals. Glutamate and glycine concentrations in the dialysate were similar between the three groups during the baseline period. Administration of dextmse had no effect on these levels. As anticipated, glutamate and glycine concentrations increased several fold during each of the ischemic periods when compared to baseline. However, hippocampal glutamate concentrations were lower in the dextrose treated groups during the peri-ischemic period (p=0,02). Glycine concentrations were higher during the reperfusion period in the dextrose-treated animals when compared with saline controls (p=0.03). Aspartate eoncentrations increased during the peri-ischemic period in the hyperglycemic group. However, there was not statistically significant. The results of this study suggest that hyperglycemia does not exert its detrimental effects by the enhanced release or production of glutamate. It may be that with this short duration of ischemia, pre-existing hyperglycemia is able to provide additional substrate for metabolism and cellular homeostasis thereby attenuating the synaptic release of glutamate. The increased concentration of extracellular glycine which was observed in the dextrose-treated animals may contribute to the neurologic injury which occurs during episodes of global ischemia.
Animals ; Aspartic Acid* ; Blood Glucose ; Brain Ischemia ; Cell Death ; Glucose ; Glutamic Acid* ; Glycine* ; Hippocampus* ; Homeostasis ; Hyperglycemia* ; Hypotension ; Inflation, Economic ; Infusions, Intravenous ; Ischemia ; Metabolism ; Microdialysis ; Neck ; Oxygen ; Rabbits ; Reperfusion ; Tourniquets

Acid-base balances in the CSF have been reported by a number of groups during the past 20 years. The CSF contains only neligilbe concentrations of buffer anions other than HCO3(-). Acid-base balances in the CSF depend mainly on arterial PCO2 because arterial CO2 diffuses easily into the blood-brain barrier to form H2CO2 in the CSF. This study was primarily undertaken to observe the changes of pH, CO2 and HCO3(-) values in the CSF in the acute stage of hyperventilation. We have studied relatively healthy patients who were scheduled for surgery for cerebral aneuryams. Prior to induction of anesthesia, the radial artery was cannulated for and arterial line and blood samples taken and lumbar tapping was performed at the level of L3-4 using at 14 gause long needle, then a 18 gauze catheter was inserted through the needle. Pre-operative samples for gases were taken, then the patient was anesthetized and his repiration was controlled and maintained at the PaCO2 of 30 torr. The samples in both blood and CSF for gases were obtained at intervals of 15, 30, 45 and 60 minutes and observed and compared. The results were as follows: The PCO2 in CSF decreased as rapidly as the arterial PCO2 decreased by hyperventilation. The data obtained after hyperventilation of 45 minutes showed a significant decrease of CO2 value in the CSF as compared to the control group. The pH in the CSF increased as rapidly as the pH of the arterial blood. The arterial HCO3(-) decreased significantly in the groups of 15, 30 and 45 minutes and it was highly significant in the 60 minutes group, despite this the HCO3(-) in the CSF showed no significant changes in any of the groups. In conclusion as a result of this study, no visible metabolic compensation in the CSF for respiratory alkalosis was observed in an acute stage of hyperventilation.
Alkalosis, Respiratory ; Anesthesia ; Anions ; Blood-Brain Barrier ; Catheters ; Compensation and Redress ; Gases ; Humans ; Hydrogen-Ion Concentration ; Hyperventilation* ; Needles ; Radial Artery ; Vascular Access Devices

This is a case of cervical cord injury which is a rare complication of endotracheal intubation. A 32 year old muscular male with a short neck had a laparotomy for panperitonitis. He was tranfered to the recovery room after surgery, and the anesthetic procedure wase completed uneventfully. Endotracheal intubation was attempted on several occations on an emergency basis because of unexpected cyanosis associated with hiccups and vomiting in the recovery room. Therefore, his respiration was controlled by the respirator, but he was not able to breath spontaneously for several days. The condition was due to a cervical cord injury with signs of paralysis of the respiratory muscles and upper extremities. The mechanism and process was described.
Adult ; Cyanosis ; Emergencies ; Hiccup ; Humans ; Intubation* ; Intubation, Intratracheal ; Laparotomy ; Male ; Neck ; Paralysis ; Recovery Room ; Respiration ; Respiratory Muscles ; Upper Extremity ; Ventilators, Mechanical ; Vomiting

Halothane is most easily blamed when a postoperative casef hepatitis occurs because it is most commonly used as an anesthetic agent and hepatitis has been intermittently reported for time. However, it is not easy to prove halothane induced the hepatitis clinically because there a long are many factors causing hepatitis. We had two cases of acute hepatitis developing following surgery. Case 1. A 49 year old male underwent surgery for femur fracture under halothane anesthesia. The preperative liver function tests were normal and the operation was uneventful. He developed epigastirc descomfor on the second postoperative day and jsundice with marked elevation of SGOT, SGPT, alkaline phosphatase and bilirubin on the 3rd day. Since the 7th postoperative day, the signs of acute renal failure with ascites became evident, therefore, dialysis was carried out. The died of acute respiratory and renal failure on the 20th postoperative day. We consider the nonA, nonB viral hepatitis infection as a possible cause in this case. Case 2. A 35 year old male had an operation for right femur fracture under repeated halothane anesthesia. On the 3rd day, he developed high fever of 39 degrees C. Liver function tests showed marked elevation of SGOT, SGPT, alkaline phosphatase and leukocytosis with eosinophilia, followed by gross jaundice. HBs Ag(-) and anti-HBs(+) were reported. He recovered gradually from the hepatitis and went home in good health on the 30th postoperative day. A possible cause of the hepatitis in this case was considered to be the halothane anesthetic.
Acute Kidney Injury ; Adult ; Alanine Transaminase ; Alkaline Phosphatase ; Anesthesia ; Ascites ; Aspartate Aminotransferases ; Bilirubin ; Dialysis ; Eosinophilia ; Femur ; Fever ; Halothane ; Hepatitis* ; Humans ; Jaundice ; Leukocytosis ; Liver Function Tests ; Male ; Middle Aged ; Renal Insufficiency

To evaluate the regulation of and in the CSF during respiratory acidosis, the changes in cisternal CSF and arterial plasma acid-base status were asaessed in anesthetized, paralyzed, mechanically ventilated dogs rendered hypercapneic (PaCO2 of 60~70 mmHg) by hypoventilation. The electrochemical potential difference (u) between the CSF and blood for H+ and HCO2- was calculated from values for and in CSF and arterial plasma, and CSF/plasma DC potential difference was calculated. Simultaneously arterial blood and the CSF samples were drawn at 0, 1, 2, 3, 4, 6, 8 hours after hypercapnia. After 8 hours of respiratory acidosis, the arterial pH declined 0.09 units to 7.26 whereas the CSF pH fell by 0.07 units to 7.29. The CSF rose to 34 mEq/L whereas arterial plasma increased to 29 mEq/L. Therefore, increase of the CSF was almost 11 mEq/L, while the arterial plasma HCO, had increased 7 mE/L. So, much increase in CSF bicarbonate maintained the spinal fluid significantly less acidic than the blood during sustained hypercapnia. CSF/plasma PD was not only increased during acute respiratory acidosis, but also remained high as long as the plasma pH was acid. Values of p for H+ and HCO at 8 hours had returned to +1.1 and -0.1 mV of the control value. The attainment of steady-state values for u close to the control value may be compatible with passive distribution of these ions between the CSF and blood. But active mechanism can not be ruled out, because CSF/plasma PD remained high during the study.
Acidosis, Respiratory ; Animals ; Dogs ; Hydrogen-Ion Concentration ; Hypercapnia ; Hypoventilation* ; Ions ; Plasma

Caudal anesthesia appears to be a safe and reliable techniuqe for surgical anesthesia as well as an alternative to narcotics for postoperative analgesia for procedures below the umbilicus. The caudal anesthesia might be particularly helpful in infants and children to avoid repetitive injections of narcotics to control postoperative pain. Advantages of caudal anesthesia for pediatric surgery i.e. clearly defined anatomic landmarks, a simplicity of the technique and high success rate have been reported. However, it has not been popular in clinical practice due to several reasons. First of all, small children do not cooperate with technical procedures. Therfore, an additional measure to provide a cooperative state is needed, such as pentothal or ketamine injection, or general anesthesia induced beforehand. Secondly, there is no clear determination or unanimity in anesthetic dosage according to the patient's age or body weight. Lastly, clinical experience and reports have not been enough for clinical practice. The aim of this study was to determine whether commonly accepted dosages used in infants produce blood levels within a safe range. This study was undertaken to measure changes of plasma concentration of lidocaine in patients with pediatric caudal anesthesia, and to check pain and motor scores and analgesic level at the recovery room. The time courses of the plasma concentration were observed in 29 healthty children(0.5-13 yr) to whom were caudally injected with 1% lidocaine mixed 1: 200,000 epinephrine(10 mg/kg). The plasma concentrations were measured by immunofluoresence assay at the intervals of l5, 30, 45, and 60 minutes. The values of plasma concnetration were 1.67+/-0.41, 1.85+/-0.61, 1.73+/-0.46, 1.75+/-0.29mcg/ml(MEAN+/-SD). The peak plasma concentration was 1.85+/-0.61mcg/ml at 30 minutes. However, there no significant differences during the first hour. No data exceeded 5 mcg/ml which is plasma toxic level of lidocaine, nor children had an experience of toxic complications. When the pain and motor scores were checked in the recovery room, most children had no pain and were not ahle to stand but movalble. Sensory levels were checked up to T9 which were suitable for lower abdominal and perineal surgery. These results indicate that the injection of l% lidocaine 10 mg/kg with epinephrine in children is considered to be safe because plasma concentration dose not exceed the toxic levels.
Analgesia ; Anatomic Landmarks ; Anesthesia ; Anesthesia, Caudal* ; Anesthesia, General ; Body Weight ; Child ; Epinephrine ; Humans ; Infant ; Ketamine ; Lidocaine* ; Narcotics ; Pain, Postoperative ; Plasma* ; Recovery Room ; Thiopental ; Umbilicus

Preoxygenation is a standard anesthetic technique for preventing a significant hypoxemia during the induction of anesthesia. Complete denitrogenation is especially important in clinical situations of difficult intubation or in patients with decreased functional residual capacity, and in situations where oxygen saturation is critical. Oxygen consumption in pregnancy is markedly increased at term as compaired to the nonpregnant stage. It is important to evaluate how long parturient women can withstand apneic hypoxemia during induction of general anesthesia. This study was carried out to measure the duration of time required to decrease the SaO2 to 90% After written informed consent was obtained from six healthy parturients who were to under go elective Cesarean section and six healthy non-pregnant women who were to have total abdominal hysterectomies. All subjects had a tight fitting anesthesia mask applied and breathed 100% oxygen, and a single isolated apnea was carried out. Arterial oxygen saturation and gas tensions were measured at a time SaO2 decreased to 90%, also blood gas data of 4 minutes after apnea in the non-pregnant women were obtained. From these, arterial oxyhemoglobin content was calculated, and mean desaturation rate from denitrogenation to the time SaO2 decreased to 90% was calculated. The mean time to obtain 90% saturation was 7.5+/-0.9 minutes in the nonpregnant women and 3.6+/-0.8 minutes in the parturient group. The mean slope of desaturation was steeper in the paturient(-3.336) than the nonpregnant (-1.52). The PaO2 inereased over 400mmHg in both the groups after denitrogenatio. After 4 minutes of apnea, the mean PaO2 decreased to 200mmHg in the non-pregnant women. The rate of rise of alveolar PCO2 during apnea were alower in the non-pregnant women(2.8+/-1.2mmHg/minute) than in the parturient women(6.8+/-1.8mmHg/minute). This study demonstrates that the rate of oxygen desaturation is faster in the parturients than the nonpregnant women. It is suggested that those results came out because of pregnancy-in-duced increase of oxygen consumption rate and decrease in FRC. The results of this study show the induction for term parturients should be speeded up with caution after full oxygenation in comparison with non-pregnant patients.
Anesthesia ; Anesthesia, General ; Anoxia ; Apnea* ; Cesarean Section ; Female ; Functional Residual Capacity ; Humans ; Hysterectomy ; Informed Consent ; Intubation ; Masks ; Oxygen Consumption ; Oxygen* ; Oxyhemoglobins ; Pregnancy

The use of hyperventilation technique to reduce intracranial pressure for surgical intervention of cerebral aneurysm has been well documented and most common in general practice. The decrease of blood flow with hyperventilation may aggravate pre-existing ischemic region. On this occasion it was suggested that cerebral intracellular metabolic acidosis may be accentuated so that its metabolic status could be measured from the analysis of cerebrospinal fluid gases. Hyperventilation can cause an increase in PH of cerebrospinal fluid due to the decrease of PCO but if hyperventilation is induced chronically, an elevated PH returns gradually to its previous normal value by loss of HCO, from the cerebrospinal fluid. Anesthesia was maintained with hyperventilation throughout the cerebral aneurysm surgery then cerebrospinal fluid and arterial blood gases were measured at regular intervals. PH in cerebrospinal fluid at 1 hour after hyperventilation revealed severe metabolic acidosis and arterial blood gases showed respiratory alkalosis. At 6 hours after hyperventilation the PH in cerebrospinal fluid in-creased markedly but the changes of HCO2were not significant from its control value and accord-ingly metabolic acidosis in cerebrospinal fluid was improved. It was suggested that compensatory mechanism for PH of cerebrospinal fluid to return to its low value by decreasing HCO2was shown. If such mechaniwm does not exist cerebrospinal fluid HCO2must he increased theoretically.
Acidosis ; Alkalosis, Respiratory ; Anesthesia ; Cerebrospinal Fluid ; Gases ; General Practice ; Hydrogen-Ion Concentration ; Hyperventilation* ; Intracranial Aneurysm* ; Intracranial Pressure ; Reference Values

T-cain has been used for spinal anesthesia as a substitute agent for tetracaine for many years in Korea. However, no clinical study has been made since its use was started in 1971. This study was primarily undertaken to assess the clinical effects of T-cain and to compare its effects with tetracaine and lidocaine. T-cain is directly derived from tetracaine by substituting a diethyl group for a dimethyl group in tetracaine and its clinical effects are known to be similar to the tetracaine except for the duration of action of the drug that is 1 and 1/2 times longer than tetracaine. We had 52 cases of spinal anesthesia using T-cain in various doses for various surgeries. The time from the injection of the drug to the complete motor recovery was measured by Bromage scale. The level of sensory blockade checked in the recovery room was variable and unpredictable, and the motor blockade was below the knee joint level in all the cases in spite of variable dosages. As larger doses were given, the longer the duration of the motor blockade was noticed. The use of T-cain for ordinary surgery seems to be inconvenient because of its longer duration of motor paralysis with patients discomfort in the recovery room.
Anesthesia, Spinal* ; Humans ; Knee Joint ; Korea ; Lidocaine ; Paralysis ; Recovery Room ; Tetracaine