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A Matsuki

Publications and source records attributed to A Matsuki.

At least 73 records · Page 4Linked to original sources
PubMed2000

Acute myeloid leukaemia with trilineage myelodysplasia complicated by masked diabetes insipidus.

We describe a rare case of acute myeloid leukaemia with trilineage myelodysplasia complicated by central diabetes insipidus. In the present case, diabetes insipidus was masked by corticosteroid deficiency due to hypopituitarism and clinical symptoms presented after administering methylprednisolone. Although the remission of leukaemia was not achieved by chemotherapy, excessive urinary output was well-controlled by nasal administration of 1-desamino-8-D-arginine vasopressin (DDAVP) during the course.

Acute Disease↗
PubMed2000

Current perception thresholds of epileptic patients treated with valproate.

We investigated the current perception threshold (CPT) of epileptic patients treated with valproate. The CPTs at frequencies of 5 Hz, 250 Hz and 2000 Hz in the control group of patients were 198.9 +/- 15.8, 62.0 +/- 18.9 and 35.3 +/- 15.8, respectively. The CPTs at 5 Hz, 250 Hz and 2000 Hz in the epileptic group of patients were 350.6 +/- 61.3, 338.6 +/- 64.3 and 193.2 +/- 21.1, respectively. The CPTs at 5 Hz, 250 Hz and 2000 Hz in the epileptic group were significantly higher than those of the control group. We measured the CPTs for 6 months after the administration of valproate in three patients with traumatic epilepsy. Their CPTs were higher than that of the epileptic group. The CPTs at 5 Hz, 250 Hz and 2000 Hz reached a maximum 4 weeks after the administration of valproate for two of these patients and in 6 weeks for the other patient. When the administration of valproate to a patient was stopped, CPTs decreased.

Adolescent↗
PubMed2000

Spasmolytic effects of prostaglandin E1 on serotonin-induced bronchoconstriction and pulmonary hypertension in dogs.

In this study, we simultaneously evaluated the spasmolytic effects of prostaglandin E1 (PGE1) on serotonin-induced bronchoconstriction and pulmonary hypertension. Eleven mongrel dogs (8-12 kg) anaesthetized with pentobarbital were assigned to two groups: saline (n = 4) and PGE1 (n = 7). Bronchoconstriction and pulmonary hypertension were elicited with serotonin 10 micrograms kg-1 + 1 mg kg-1 h-1 and assessed as the percentage change in bronchial cross-sectional area (BCA) measured by bronchoscopy and pulmonary vascular resistance (PVR), respectively. Thirty minutes after starting the serotonin infusion, saline or PGE1 0 (saline), 0.01, 0.1, 1.0 or 10 micrograms kg-1 i.v. was given. %BCA and %PVR (basal = 100%) were assessed before and 30 min after serotonin, and 30 and 60 min after saline (saline group) or 5 min after each dose of PGE1 (PGE1 group). In the saline group, pulmonary hypertension and bronchoconstriction were stable. In the PGE1 group, PGE1 at > or = 0.1 microgram kg-1 significantly decreased %BCA and 10 micrograms kg-1 almost fully reversed the constriction (from mean (SEM) 56.2% (4.9%) to 94.4% (3.7%)). %PVR was significantly decreased at 10 micrograms kg-1 (from 230% (24%) to 176% (11%)) only. We suggest that PGE1 may produce bronchodilation rather than pulmonary vasodilation.

Alprostadil↗
PubMed2000

Inhibitory effects of intravenous anaesthetic agents on K+-evoked norepinephrine and dopamine release from rat striatal slices: possible involvement of P/Q-type voltage-sensitive Ca2+ channels.

The role of the voltage-sensitive Ca2+ channel (VSCC) as a target for anaesthetic action remains controversial. In this study we characterized the VSCC subtypes involved in K+-evoked norepinephrine and dopamine release from rat striatal slices and used this model system to examine the effects of a range of i.v. anaesthetics on release. Nifedipine (L-channel-selective), omega-conotoxin GVI(A) (N-channel-selective), omega-agatoxin IV(A) (P-channel-selective), omega-conotoxin MVIIc (P/Q-channel-selective) and Cd2+ (non-selective), along with alphaxalone, propofol and ketamine, were used in various combinations. Omega-Agatoxin IV(A), omega-conotoxin MVIIc and Cd2+ fully (100%) inhibited norepinephrine and dopamine release. Clinically achievable concentrations of alphaxalone inhibited norepinephrine and dopamine release, with concentrations producing 25 and 50% inhibition (IC25 and IC50) of the maximum of 2.1 and 7.8 microM respectively for norepinephrine and 2.9 and 7.2 microM for dopamine. The effects of propofol were observed at the top of the clinical range and those of ketamine exceeded this range. In addition, IC50 values for alphaxalone in the presence and absence of nifedipine and omega-conotoxin GVI(A) did not differ from the control. Our data suggest that clinically achievable concentrations of alphaxalone and propofol inhibit norepinephrine and dopamine release, which is mediated predominantly through P/Q-type VSCCs, suggesting a role for these channels in anaesthetic action.

Anesthetics, Intravenous↗
PubMed2000

Milrinone attenuates serotonin-induced pulmonary hypertension and bronchoconstriction in dogs.

UNLABELLED: We determined whether milrinone, a phosphodiesterase III inhibitor, attenuates serotonin-induced (5-hydroxytryptamine [5HT]) pulmonary hypertension (PH) and bronchoconstriction. Dogs were anesthetized with pentobarbital (30 mg/kg + 2 mg. kg(-1). h(-1)). Bronchoconstriction and PH were elicited by 5HT (10 microg/kg + 1.0 mg. kg(-1). h(-1)). Pulmonary vascular resistance was used to assess PH. Bronchoconstriction was also assessed by changes in bronchial cross-sectional area obtained from our bronchoscopic method. At 30 min after 5HT infusion started, seven dogs were given milrinone: 0 (saline), 5, 50, 500, and 5000 microg/kg at 10-min intervals. The other 12 dogs were given milrinone 5000 microg/kg 30 min after 5HT infusion, and 5 min later were given propranolol 0.2 mg/kg (n = 6) or saline (n = 6) IV. The 5HT significantly increased percentage of pulmonary vascular resistance to 208% +/- 27% and decreased percentage of bronchial cross-sectional area to 52% +/- 5% of the basal. Milrinone significantly attenuated both PH and bronchoconstriction in a dose-dependent manner. However, -log 50% effective concentration (mean ED(50) in microg/kg) of milrinone for bronchoconstriction: 4.32 +/- 0.13 (47.6) was significantly smaller than that for PH: 3.84 +/- 0.29 (144.9) (P < 0.01). In addition, the spasmolytic effects of milrinone (5000 microg/kg) were not antagonized by propranolol, although this dose significantly increased plasma catecholamines. In conclusion, milrinone attenuates 5HT-induced PH and bronchoconstriction; however, this drug may be more sensitive to phosphodiesterase III in the airway smooth muscle than in pulmonary vascular smooth muscle. In addition, the relaxant effects could not be caused by beta-adrenoceptor activation because beta-blocker did not antagonize. IMPLICATIONS: We studied the effects of milrinone on serotonin-induced pulmonary hypertension and bronchoconstriction in dogs. Milrinone produces pulmonary vasodilation and bronchodilation, whose effects may not be caused by beta-adrenoceptor activation. In addition, this drug may be more sensitive to phosphodiesterase III in the airway smooth muscle than that in pulmonary vascular smooth muscle.

Animals↗
PubMed2000

Cardiopulmonary bypass produces greater pulmonary than systemic proinflammatory cytokines.

Cardiopulmonary bypass (CPB) impairs pulmonary endothelial injury in part by increasing expression of adhesion molecules that results in neutrophil influx. Although numerous proinflammatory cytokines up-regulate these responses, the extent to which systemic and pulmonary proinflammatory cytokines increase remains unknown. We therefore examined systemic and pulmonary gene expression and production of proinflammatory cytokines during CPB. Bronchoalveolar lavage and peripheral blood sampling were performed just after the induction of anesthesia and at the end of surgery in 80 patients undergoing CPB. RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) was measured by semiquantitative polymerase chain reaction using beta-actin as an internal standard. We also measured these cytokines in cultured alveolar macrophages and plasma monocytes in standard medium alone, or in the presence of lipopolysaccharide. We found 2- to 20-fold increases in gene expression for these cytokines in both plasma and alveolar leukocytes at the end of surgery. However, the increases were 4-8 times greater in alveolar than plasma leukocytes. Alveolar macrophages obtained at the end of surgery produced 1.5-3 times more IL-6, IL-8, and TNF-alpha than those obtained at the beginning (P < 0.0001). Although plasma monocytes produced more IL-8 at the end of surgery (P < 0.001), TNF-alpha and IL-6 did not increase. The production of all cytokines was 1.5-3 times greater in alveolar macrophages obtained at the end of surgery than in plasma monocytes obtained simultaneously (P < 0.005). Our data thus suggest that CPB provokes a greater pulmonary than systemic inflammatory response.

Actins↗
PubMed2000

Neutrophil number and interleukin-8 and elastase concentrations in bronchoalveolar lavage fluid correlate with decreased arterial oxygenation after cardiopulmonary bypass.

Atelectasis is a major cause of decreased arterial oxygenation after cardiopulmonary bypass (CPB). There is a close relationship between atelectasis and inflammatory responses. We therefore tested the hypothesis that neutrophil number and the concentrations of proinflammatory cytokines and elastase in plasma and bronchoalveolar lavage fluid correlate with changes in arterial oxygenation. Bronchoalveolar lavage was performed just after the induction of anesthesia and at the end of surgery in 80 patients undergoing CPB. Peripheral blood was sampled simultaneously. Arterial oxygenation was quantified by PaO(2)/fraction of inspired oxygen (FIO(2)) and intrapulmonary shunt (Q(s)/Q(t)). PaO(2)/FIO(2) and Q(s)/Q(t) decreased significantly at the end of surgery, whereas neutrophil number, interleukin (IL)-6, IL-8, tumor necrosis factor-alpha, and elastase concentrations in the lavage fluid increased significantly. The increase in neutrophil count from the lavage fluid correlated significantly with the increases in IL-8 and elastase concentrations. The increase in neutrophil number and IL-8 and elastase concentrations in the lavage fluid correlated significantly with PaO(2)/FIO(2) and Q(s)/Q(t) at the end of surgery. In contrast, none of the plasma values correlated with these variables. Significant correlation between immune mediators and decreased arterial oxygenation suggests that inflammatory responses in the distal airway are strongly related to a decrease in arterial oxygenation after CPB.

Bronchoalveolar Lavage Fluid↗
PubMed2000

Sevoflurane stimulates inositol 1,4,5-trisphosphate in skeletal muscle.

UNLABELLED: Inositol 1,4,5-triphosphate (IP(3)) plays an important role in excitation-contraction coupling and malignant hyperthermia in skeletal muscle. We investigated whether sevoflurane affects IP(3) formation in L(6) skeletal muscle cells and studied the mechanisms that modulate IP(3). Sevoflurane stimulated IP(3) production from a basal level of 78.4 +/- 6.1 to 730.0 +/- 53.1 pmol. mg. protein(-1) in 2 mM of sevoflurane in a dose-dependent manner. A dose of 10 microM of U73122 (a phospholipase C antagonist) significantly decreased 0.8 mM of sevoflurane-stimulated IP(3) production from 387. 8 +/- 24.7 to 247.8 +/- 19.8 pmol. mg. protein(-1). A dose of 100 microM of (p-amylcinnamoyl) anthranilic acid (a PLA(2) antagonist) also significantly decreased sevoflurane-stimulated IP(3) production to 282.0 +/- 24.0 pmol. mg. protein(-1). Exposure to 1 microM of genistein and tyrphostin A23 (tyrosine kinase inhibitors) significantly decreased sevoflurane-stimulated IP(3) production to 241.0 +/- 35.3 and 267.4 +/- 32.9 pmol. mg. protein(-1). Sevoflurane-stimulated IP(3) production was significantly decreased by 10 microM of 8-(N,N-diethylamino) octyl-3,4-5-trimathoxybenzoate (an intracellular calcium antagonist) and 100 microM and 1 mM of guanosine 5'-O-(2-thiodiphosphate) (GDPbetaS), a guanosine 5'triphosphate-binding protein inhibitor. Elevation of IP(3) production was significantly higher in halothane than in sevoflurane and isoflurane at the same concentration of 0.8 mM. We conclude that sevoflurane-stimulated IP(3) production involves phospholipase C, phospholipase A(2), tyrosine kinase, and guanosine 5'triphosphate-binding protein and the stimulation is associated with concentration of intracellular ionized calcium. IMPLICATIONS: Inhaled anesthetics increase intracellular ionized calcium in the skeletal muscle cell and the ionized calcium increase is partly released from the intracellular store by inositol 1,4,5-triphosphate (IP(3)) formation. IP(3) plays an important role in excitation-contraction coupling and malignant hyperthermia. We studied whether sevoflurane affects IP(3) formation and the mechanisms that modulate IP(3).

Anesthetics, Inhalation↗
PubMed2000

Halothane and sevoflurane decrease norepinephrine-stimulated glucose transport in neonatal cardiomyocyte.

UNLABELLED: Catecholamine regulates myocardial glucose use. However, the effect of inhaled anesthetics on myocardial glucose transport stimulated by catecholamine is unclear. We studied the effect of halothane and sevoflurane on uptake of 2-deoxyglucose stimulated by norepinephrine in neonatal cardiomyocytes and the mechanism that modulates glucose transport. We studied the effects of halothane and sevoflurane on norepinephrine (NE)-stimulated glucose uptake and the effects of halothane and sevoflurane on glucose uptake stimulated by W7 (a calcium releasing agent), phorbol 12 myristate-13-acetate (a protein kinase C agonist), and LiCl. Sevoflurane decreased NE-stimulated glucose uptake from 63.7 +/- 7.0 to 41.2 +/- 3.7 pmol h(-1) mg protein(-1), and halothane also attenuated NE-stimulated glucose uptake to 37.8 +/- 5.7 pmol h(-1) mg protein(-1). W7 at 10 micromol/L increased glucose uptake from 16.4 +/- 1.4 to 41.2 +/- 3. 4 pmol h(-1) mg protein(-1). The stimulation was inhibited in the presence of 0.8 mmol/L sevoflurane and 0.58 mmol/L halothane to 23.9 +/- 3.7 and 25.6 +/- 3.6 pmol h(-1) mg protein(-1), respectively. Halothane and sevoflurane did not significantly affect the glucose uptake stimulated by 1 nmol/L insulin, 10 micromol/L PMA, or 10 mmol/L LiCl. We conclude that halothane and sevoflurane decrease NE-stimulated glucose uptake through decrease in intracellular calcium in cardiomyocytes. IMPLICATIONS: The effect of inhaled anesthetics on myocardial glucose uptake during administration of catecholamine is unclear. The myocardial glucose uptake is stimulated not only by catecholamine, but also by insulin, protein kinase C, and increase of intracellular calcium. We examined the effects of halothane and sevoflurane on glucose uptake.

Adrenergic alpha-Agonists↗
PubMed2000

A comparison of the spasmolytic effects of olprinone and aminophylline on serotonin-induced pulmonary hypertension and bronchoconstriction with or without beta-blockade in dogs.

In the present study in dogs, we compared with aminophylline the spasmolytic effects of olprinone, a novel phosphodiesterase 3 inhibitor, on serotonin-induced pulmonary hypertension (PH) and bronchoconstriction. Mongrel dogs were anesthetized with pentobarbital. PH and bronchoconstriction were induced with serotonin: 10 microg/kg + 1 mg x kg(-1) x h(-1), and assessed as % changes in pulmonary vascular resistance and bronchial cross-sectional area (basal = 100%). Initially, the relaxant effects of olprinone (n = 8: 0-1000 microg/kg) and aminophylline (n = 8: 0-100 mg/kg) were compared. Pulmonary vascular resistance and bronchial cross-sectional area were assessed before and 30 min after serotonin infusion began and 5 min after each dose of olprinone or aminophylline. We then determined whether propranolol (0.4 mg/kg) reversed the relaxation induced by olprinone (1000 microg/kg, n = 6) or aminophylline (100 mg/kg, n = 6) compared with saline (n = 6 each). Olprinone and aminophylline dose-dependently attenuated both PH and bronchoconstriction (olprinone > aminophylline: -logED(50)[mean] for PH and bronchoconstriction 5.37+/- 0.35[4.24 microg/kg] vs. 1.60+/-0.23[25.4 mg/kg] and 4.06+/-0.12[87.8 microg/kg] vs. 1.51+/-0.21[30.6 mg/kg], respectively). In addition, olprinone produced more potent pulmonary vasodilation than bronchodilation while aminophylline was equipotent. In addition, there was a significant increase in plasma catecholamines after olprinone (> or =100 microg/kg) and aminophylline (> or =10 mg/kg). With the exception of aminophylline-induced bronchodilation, propranolol did not reverse any of the other effects measured. Therefore, the spasmolytic effects of olprinone are independent of plasma catecholamines, while the bronchodilating effect of aminophylline may partially involve increased levels of circulating catecholamines.

Adrenergic beta-Antagonists↗
PubMed2000

Smoking decreases alveolar macrophage function during anesthesia and surgery.

BACKGROUND: Smoking changes numerous alveolar macrophage functions and is one of the most important risk factors for postoperative pulmonary complications. The current study tested the hypothesis that smoking impairs antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery. METHOD: The authors studied 30 smoking and 30 nonsmoking patients during propofol-fentanyl general anesthesia. Alveolar immune cells were harvested by bronchoalveolar lavage immediately and 2, 4, and 6 h after induction of anesthesia and at the end of surgery. The types of alveolar immune cell and macrophage aggregation were determined. The authors measured opsonized and unopsonized phagocytosis. Microbicidal activity was determined as the ability of the macrophages to kill Listeriamonocytogenes directly. Finally, RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin 1beta, 6, and 8, interferon gamma, and tumor necrosis factor alpha were measured by semiquantitative polymerase chain reaction using beta-actin as an internal standard. RESULTS: The fraction of aggregated macrophages increased significantly over time in both groups, whereas phagocytosis of opsonized and nonopsonized particles and microbicidal activity of alveolar macrophages decreased significantly. The changes, though, were nearly twice as great as in patients who smoked. Gene expression of all proinflammatory cytokines in alveolar immune cells except interleukin 6 increased 2- to 20-fold over time in both groups. The expression of interleukin 1beta, interferon gamma, and tumor necrosis factor alpha, however, increased only half as much in smokers as in nonsmokers. CONCLUSION: Smoking was associated with macrophage aggregation but markedly reduced phagocytic and microbicidal activity-possibly because expression of proinflammatory cytokines was reduced in these patients. Our data thus suggest that smokers may have a limited ability to mount an effective pulmonary immune defense after anesthesia and surgery.

Anesthesia, General↗
PubMed2000

Supplemental intraoperative oxygen augments antimicrobial and proinflammatory responses of alveolar macrophages.

BACKGROUND: The first goal was to test the hypothesis that 100% inspired oxygen maintained for approximately 8 h intraoperatively is not associated with impaired pulmonary oxygenation. The authors also tested the hypothesis that intraoperative inhalation of 100% oxygen augments proinflammatory and antimicrobial responses of alveolar macrophages during anesthesia and surgery. METHODS: The authors studied patients administered 100% oxygen (n = 30) and 30% oxygen (n = 30) during propofol-fentanyl general anesthesia. Alveolar macrophages were harvested by bronchoalveolar lavage immediately, 2, 4, and 6 h after induction of anesthesia, and at the end of surgery. The authors measured "opsonized" and "unopsonized" phagocytosis and microbicidal activity. RNA was extracted from harvested cells and cDNA was synthesized. The expression of interleukin(IL)-1beta, IL-6, IL-8, interferon-gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) was measured by semiquantitative polymerase chain reaction. RESULTS: Gene expression of all proinflammatory cytokines except IL-6 increased fourfold to 20-fold over time in both groups. However, expression of TNF-alpha and IL-8, IFN-gamma, and IL-6 and IL-1beta was 2-20 times greater in patients administered 100% than in those administered 30% oxygen. Unopsonized and opsonized phagocytosis and microbicidal activity decreased progressively, with the decreases being nearly twice as great during inhalation of 30% oxygen versus 100% oxygen. CONCLUSION: Inhalation of 100% oxygen improved intraoperative decreases in phagocytic and microbicidal activity possibly because expression of proinflammatory cytokines was augmented. These data therefore suggest that intraoperative inhalation of 100% oxygen augments antimicrobial and proinflammatory responses in alveolar macrophages during anesthesia and surgery.

Anesthesia, Intravenous↗
PubMed2000

Detection of capillary protein leakage by indocyanine green and glucose dilutions in septic patients.

OBJECTIVE: To determine whether indocyanine green (ICG) and glucose dilutions can detect generalized capillary protein leakage in septic patients without requiring repeated measurements. DESIGN: Prospective, clinical study. SETTING: General intensive care unit. PATIENTS: Twelve consecutive patients who met the criteria of sepsis and 16 consecutive acute myocardial infarction (AMI) patients without any underlying pathology inducing generalized protein capillary leakage. INTERVENTIONS: Both ICG 25 mg and glucose 5 g were administered simultaneously, to calculate the plasma volume determined by the ICG dilution method (PV-ICG) and the initial distribution volume of glucose (IDVG), on day 1 of sepsis or on day 1 of hospitalization for the AMI patients. The relationship between these two volumes and the PV-ICG/IDVG ratio was evaluated in two patient groups. MEASUREMENTS AND MAIN RESULTS: Although the IDVG of the two patient groups was not statistically different, the PV-ICG in the septic patients was higher than that in the AMI patients (p < .01). Consequently, the PV-ICG/IDVG ratio in the septic patients was higher than that in the AMI patients (p < .01). Eight of the 12 septic patients had a PV-ICG/IDVG ratio of >0.45, which was not observed in any of the AMI patients. The PV-ICG/IDVG ratio in the septic patients correlated inversely with the total plasma protein concentration (r2 = .46, p < .025) and mean arterial pressure (r2 = .42, p < .05). CONCLUSIONS: Our results indicate that overestimation of the PV-ICG can occur in septic patients and, further, suggest that simultaneous measurement of the two distribution volumes would help predict generalized capillary protein leakage in septic patients without repeated measurement.

Adult↗
PubMed2000

Bradykinin-induced inositol 1,4,5-triphosphate in neonatal rat cardiomyocytes is activated by endotoxin.

We studied the effect of endotoxin on bradykinin-induced inositol 1,4,5-triphosphate (IP3) production and the relationship between IP3 and phospholipase A2 or thromboxane A2. When exposed with 0.1, 1.0, and 10 microg ml(-1) lipopolysaccharide (LPS) for short-term (60 min), 100 nmol L(-1) bradykinin-induced IP3 production was stimulated in a dose-dependent manner from 569.2+/-42.4 in absence of LPS to 714.3+/-52.8, 804.5+/-42.6, and 894.1+/-62.6 pmol mg protein(-1). Treatment of 100 micromol L(-1) ACA (a phospholipase A2 inhibitor) and 10 micromol L(-1) BM13.177 (a thromboxane A2 inhibitor) significantly decreased bradykinin-induced IP3 production and LPS (1.0 microg mL(-1)) modulation of bradykinin-induced IP3 formation from 804.5+/-42.6 to 217.4+/-12.7 and 208.6+/-17.1 pmol mg protein(-1), respectively. LPS modulation of bradykinin-induced IP3 production was significantly blocked by 1 micromol L(-1) TMB-8 (an intracellular Ca2+ antagonist) from 804.5+/-42.6 to 507.8+/-33.4 pmol mg protein(-1). LPS modulation of bradykinin-induced IP3 production was significantly inhibited from 804.5+/-42.6 to 397.4+/-30.3 pmol mg protein(-1) by treatment of 10 micromol L(-1) indomethacin. In conclusion, short-term administration of LPS stimulates bradykinin-induced IP3 formation through activation of phospholipase A2 and thromboxane A2 and the stimulation is associated with an elevation of intracellular Ca2+.

Animals↗
PubMed2000

Effects of angiotensin-converting enzyme inhibitors on glucose uptake.

We investigated the effect of angiotensin-converting enzyme inhibitors on glucose uptake regulation as well as the effect of bradykinin (BK) on glucose uptake and its regulation by using inhibitors of phospholipase C, BK B2 receptor, protein kinase C, phosphatidylinositol 3-kinase, tyrosine kinase, and intracellular Ca(2+). We measured 2-deoxyglucose uptake by using L(6) skeletal muscle cells. In the presence of 1 nmol/L of insulin, 1 micromol/L of enalaprilat enhanced insulin-induced glucose uptake from 89.2+/-8. 1 to 138.0+/-13.6 pmol/h per mg protein. The stimulation of glucose uptake with enalaprilat was blocked to 92.7+/-7.8 pmol/h per mg protein by 10 micromol/L HOE 140 (a BK B2 receptor antagonist). In the presence of 1 nmol/L of insulin, exposure to 10 micromol/L BK stimulated glucose uptake from 89.2+/-8.1 to 171.6+/-10.1 pmol/h per mg protein. However, in the absence of insulin, BK could not enhance glucose uptake. One hundred nanomoles per liter of tyrphostin A-23 and genistein, which are tyrosine kinase inhibitors, significantly decreased the BK-induced glucose uptake from 142.0+/-8.4 to 87.6+/-6. 4 and 85.2+/-7.3 pmol/h per mg protein, respectively. BK-induced glucose uptake was inhibited significantly by 10 micromol/L U73122 (a phospholipase C antagonist) from 142.0+/-8.4 to 95.7+/-9.5 pmol/h per mg protein. One and 20 micromol/L of TMB-8 (an intracellular calcium antagonist) significantly decreased BK-induced glucose uptake from 142.0+/-8.4 to 108.0+/-9.6 and 100.8+/-11.4 pmol/h per mg protein. Angiotensin-converting enzyme inhibitors enhanced insulin-induced glucose uptake via the BK B2 receptor. BK-stimulated glucose uptake is related to phospholipase C, tyrosine kinase, and an increase in intracellular calcium.

Androstadienes↗
PubMed2000

[Tracheal mucosal bulla found on tracheal extubation in a patient with pemphigus vulgaris--a case report].

A 49-year-old female with pemphigus vulgaris underwent the removal of a meningioma under general anesthesia. Neither bulla nor erosion was observed on her skin and oral cavity mucosa. She had been on prednisolone 15 mg for six years daily to avoid the recurrence of skin lesion. Anesthesia was induced and maintained with total intravenous anesthesia with propofol and fentanyl. No adverse episodes were encountered during the operative procedure. We checked the tracheal mucosa using bronchofiberscope before extubation. A small bulla was found on the tracheal mucosa, where the cuff of the tracheal tube was located. The trachea was extubated slowly under bronchofiberscopic observation, and no other bullae were found. It would have been formed by mechanical stimulation of the tracheal tube. This case suggests that we have to pay careful attention to the formation of bullae at any part of the body by mechanical stimuli during anesthetic management of patients with pemphigus vulgaris.

Anesthesia, General↗
PubMed2000

[Anesthesia, department of anesthesiology and anesthesiology--why has anesthesiology not been accepted socially in Japan?].

An incorrect Japanese terminology of "Masuigaku [symbol: see text]" has been used widely to express "anesthesiology" or "anaesthetics" [symbol: see text] since the first Department of Anesthesiology was established in Tokyo University in 1952. The reason why the nomenclature "Masui-gaku" is wrong is as follows: Japanese nomenclatures for clinical medical sciences should include a Chinese character "Ka [symbol: see text]" such as "nai-ka-gaku" for internal medicine, "ge-ka-gaku" for surgery and "gan-ka-gaku" for ophthalmology. Accordingly the name "Masui-gaku" is erroneous to mean "Anesthesiology" and it should be "Masui-ka-gaku" [symbol: see text]. Thus a big confusion has occurred among lay people as well as many physicians in medical field. "Ma-sui" is etymologically a Japanese word which Dr Seikei Sugita coined when he translated a Dutch edition of J. Schlesinger's monograph on ether anesthesia in 1850. "Ma [symbol: see text]" means analgesia or loss of regional sensation and "Sui [symbol: see text]" means loss of consciousness. Most people consider that "Ma [symbol: see text]" is originated from "[symbol: see text] (Hemp, Asa)" or "[symbol: see text] (Marihuana, Taima)", however, this is definitely incorrect and "Ma [symbol: see text]" of "Ma-sui" has no direct relation with the pharmacological effect of hemp. Thus the misuse of "Masui-ga-ku" might have caused serious academic and social confusions, such as misunderstanding of anesthesiologists as comedical technicians, leading to a poor social acceptance of anesthesiology and anesthesiologists for these fifty years in Japan. To correct this confused situation I would like to ask our colleagues to use correctly these nomenclatures.

Anesthesia Department, Hospital↗