[Changes of fatty acid composition of brain synaptosomal phospholipids in isoflurane exposure rat].

We examined effects of inhalational anesthetic drug, isoflurane, on phospholipid and fatty acid in brain synaptosome. Wistar strain male rat was treated by inhalation of isoflurane. Rats were divided into 3 groups each 6 rats, one was 1 minimum alveolar concentration (MAC) exposure group, 1MAC group, and another was 2 times of MAC exposure group, 2MAC group, and the other was non exposure group, control group. The animals were kept in to box (0.343 m3) and the gas flow rate was set in 4 L/min by anesthetic instrument. After 60 minutes of exposure, rats were decapitated. Immediately, cerebrums were removed and fraction of synaptosome was sampled. In 2MAC group, C14:0 of phosphatidylcholine (PC) increased significantly as compared to the control group, but C16:1, C18:0, C18:2 and C20:3 decreased significantly. And also, C18:2 and C20:3 decreased significantly in 1MAC group. In terms of phosphatidylethanolamine(PE), C18:1 in 1MAC group, C14:0 and C16:1 in 2MAC group increased, but C20:3, C20:4 and C22:5 in 2MAC group decreased significantly as compared to the control group. Regarding phosphatidylserine + phosphatidylinositol, C14:0 in 2MAC group increased, but C22:5 decreased. In lysophosphatidylcholine, C12:0 and C14:0 in 2MAC group and C18:0, C20:4 in 1MAC group increased significantly, but C18:1 in 2MAC decreased. The changes of phospholipids and fatty acid in synaptosome were due to the metabolism of phospholipids of basic matrix and this was caused by effects of isoflurane on neural cellular membrane. The results indicated the suppression of membrane activity. Isoflurane has physiological activity on metabolism of phospholipid of cellular membrane. Thus, it has effects on neural cellular functions in brain.

[A new sedation technique with propofol during spinal anesthesia].

We compared our new sedation technique with propofol during spinal anesthesia (Group B, n = 50) with a previously described method by Mackenzie et al. (Group A, n = 20). In Group A, propofol was started at a rate of 6 mg.kg-1.h-1 for 10 minutes, followed by continuous infusion at a rate of 4 mg.kg-1.h-1 till the end of surgery. In Group B, propofol 0.4 mg.kg-1 was administered by a bolus injection at the beginning. One-hundred and fifty minutes after the first injection, propofol 0.2 mg.kg-1 was added. The third dose of 0.1 mg.kg-1 of propofol was given 150 seconds after the second dose, followed by continuous infusion at a rate of 4 mg.kg-1.h-1 till the end of surgery. When adequate sedation was not obtained in Group B, propofol 0.1 mg.kg-1 was added by bolus fashion occasionally. In Group A, it took 9 min. 29 sec. to complete adequate sedation assessed by Mackenzie and Grant's sedation score. On the other hand, in Group B, it was 7 min. 27 sec. (P < 0.05 compared with Group A). There was neither excitation nor movement during sedation in Group B, while 5 patients experienced such events in Group A. The blood concentrations of propofol in Group B was 0.946 +/- 0.076 microgram.ml-1 and 0.693 +/- 0.136 microgram.ml-1 at 5 minutes and 10 minutes after the beginning of propofol, respectively. These values were significantly lower than those reported by Kugimiya. Our newly developed method for sedation with propofol during spinal anesthesia would be safer and more effective than that previously described by Mackenzie et al.

[An abnormal hemoglobin which was found by chance at a health checkup].

A 68-year-old female visited our hospital because of low hemoglobin A1c content, which was found by chance at a health checkup. She did not have any symptom or sign except hypertension and low HbA1c. To determine the reason why HbA1c was so low in usual laboratory test, we carried out isoelectrofocusing (IEF) of the hemolysate, Hb instability test, and detection and isolation of the abnormal globin chain by urea CM-cellulose column chromatography. The abnormal beta-globin chain was digested with TPCK-trypsin, and the tryptic peptides were separated by HPLC on a reversed phase column. Finally the determination of amino acid composition and amino acid sequence of the abnormal peptide were performed. The Hb variant was identified as Hb Riyadh (beta 120Lys-->Asn). The detection and analysis of abnormal hemoglobin will be expected to increase in accordance with the increased opportunity of public health checkup.

[Concentrations of ethanol and ethanol metabolites and symptoms of acute alcohol-intoxicated patients].

Five patients who presented to an emergency room and did not have other injury and disease with acute alcohol intoxication were analyzed about blood and urine ethanol, acetaldehyde, acetate and acetone levels. The average concentrations of ethanol, acetaldehyde, acetate and acetone in blood were 37.0 mM (1.7 mg/ml), 18 microM, 1.00 mM and 18 microM, respectively and the concentrations in urine were 50.8 mM (2.3 mg/ml), 37 microM, 0.79 mM and 47 microM, respectively. Clinical symptoms were concerned with both ethanol concentration and concentrations of ethanol metabolites. Their symptoms of acute alcohol-intoxicated patients were caused by the ethanol concentrations which was less than the levels reported in early studies.

[Can ozone administration activate the tissue metabolism?--A study on brain metabolism during hypoxic hypoxia].

As it was thought that the tissue metabolism could be activated by administration of ozone, the influence of ozone on cerebral metabolism was studied under hypoxic condition. Ozone 1.5% was obtained from an ozonizer which separates the ozone from oxygen. Objects were 30 mature rabbits and they inhaled 3% oxygen in 97% nitrogen (PaO2 17-19 mmHg) by spontaneous respiration through a tracheostomy cannula. Objects were divided into three groups. Control rabbits inhaled only anoxic gases without ozone administration. Although the oxygen group also inhaled anoxic gases, pure oxygen was administered through an A-V shunt, previously made on femoral artery and vein, with an oxygenator, named Nichidai style (counter-current-exchange method). Similarly, the ozone group was given ozone with the oxygenator via A-V shunt. In each group, survival time as well as ATP, ADP, AMP and lactic acid lipo-peroxide in brain were examined. After the administration of ozone, survival time was prolonged significantly, compared with the control group (P < 0.005). Equally, ATP and energy charge in the brain were well maintained (P < 0.005) and the lactate production was inhibited significantly (P < 0.005). These results indicate that oxidizing effect of ozone will be beneficial to maintain energy charge in brain tissue during hypoxia. Further, ozone might activate the energy metabolism in animal tissues.

[Anesthetic management of a patient with diffuse pulmonary hamartoangiomyomatosis associated with spontaneous pneumothorax].

We reported successful anesthetic management of a 34 year-old woman with diffuse pulmonary hamartoangiomyomatosis associated with spontaneous pneumothorax. She had recurrent pneumothorax and chest X-ray film showed reticulo-granular shadow, and chest CT revealed multiple bullae. Induced by thiopental and succinylcholine, anesthesia was maintained safely with enflurane in oxygen. Nitrous oxide was used after thoracotomy. This disease accompanies multiple bullae in the lung and some patients have complications such as tuberous sclerosis or hemangioma of the kidney. Therefore, we have to pay attention to both bullae and other complications.