Biomedical subjects

S Yokono

Publications and source records attributed to S Yokono.

At least 19 recordsLinked to original sources

PubMed2001

The relationship of brain catecholamine levels to enflurane requirements among three strains of mice with different anesthetic sensitivities.

PURPOSE: . It has been reported that brain catecholamines alter the minimum alveolar concentration (MAC) of anesthetics. The extent of the relation between the levels of brain catecholamine and anesthetic sensitivity should be evaluated by excluding several factors. METHODS: Anesthetic sensitivity was measured by using loss of the righting reflex in three strains of mice with different sensitivities. The mice were decapitated without any anesthesia, adding on ddN and C57BL/6J mice in 2% enflurane, their brains were divided into three parts, and dopamine and norepinephrine levels were analyzed by high-performance liquid chromatography (HPLC). Results. The values of enflurane requirement (%) were 1.30 +/- 0.05 in ddN, 1.10 +/- 0.02 in C57BL/6J, and 1.05 +/- 0.02 in MSM mice. The values of dopamine (microg.g(-1)) in the mesencephalon were 0.23 +/- 0.02 in ddN, 0.15 +/- 0.02 in C57BL/6J, and 0.12 +/- 0.02 in MSM (mean +/- SE). No statistical significance in the values in 2% enflurane could be obtained between ddN and C57BL/6J. The stepwise regression line showed a significant correlation: enflurane requirement (%) = -0.89 + 1.60 x (dopamine levels of mesencephalon) (r(2) = 0.571, P < 0.0001). CONCLUSION: Dopamine in the mesencephalon seems to play an important role in the production of different anesthetic sensitivities, and the anesthetic mechanism might be related to the regulation of dopamine levels that promote arousal.

Journal Article↗

PubMed2001

Effects of ulinastatin (urinary trypsin inhibitor) on ATP, intracellular pH, and intracellular sodium transients during ischemia and reperfusion in the rat kidney in vivo.

PURPOSE: To investigate the effects of ulinastatin on renal ischemia-reperfusion injury, we monitored the dynamic changes in ATP, intracellular pH (pHi), and intracellular sodium (Nai) in rats in vivo. METHODS: Renal ischemia was induced by clamping the abdominal aorta for 30 min followed by reperfusion for 60 min. Ulinastatin, 50,000 U.kg(-1) (UTI group), or normal saline (NS group) was infused for 30 min before ischemia. (31)P- and double quantum (23)Na-NMR were used to monitor ATP, pHi, and Nai. RESULTS: During ischemia, ATP was rapidly depleted and Nai increased to the same extent in both groups. After 60 min reperfusion, Nai in the NS group was almost restored to the preischemic baseline level (117.2 +/- 7.4% of the baseline value), but the recovery of ATP was incomplete (60.9 +/- 7.7%). The recovery of Nai in the UTI group began earlier than in the NS group with better recovery of ATP. The pHi values showed severe acidosis in the NS group compared with the UTI group during ischemia and reperfusion. As for ultrastructural findings, after 60 min reperfusion, the mitochondria were less swollen and less disorganized with respect to the membrane and the cristae in the UTI group. CONCLUSION: The transcellular sodium gradient is restored before the ATP level is normalized during postischemic reperfusion. Ulinastatin might protect mitochondrial conformation during ischemia, and facilitate functional recovery of the ionic pump after reperfusion.

Journal Article↗

PubMed2001

Simultaneous determination of glycyrrhizin, glycyrrhetic acid and glycyrrhetic acid mono-glucuronide in Shakuyaku-kanzo-to incubated with rat feces by semi-micro high-performance liquid chromatography.

A method for semi-micro high-performance liquid chromatography (HPLC) has been established for the simultaneous determination of glycyrrhizin (GL), glycyrrhetic acid (GA) and glycyrrhetic acid mono-glucuronide (GAMG) in incubation mixtures of rat feces with Shakuyaku-kanzo-to decoction (combination of licorice root and peony root). The analysis could be accomplished within 20 min with a TSKgel ODS-80TsQA (150 x 2.0 mm i.d.) column by linear gradient elution using a mobile phase containing aqueous phosphoric acid and acetonitrile at a flow rate of 0.2 ml x min(-1), a thermostatic oven at 25 degrees C, and detection at 254 nm. The detection limits of these compounds were 0.1-0.85 pmol per injection (5 microl). The concentrations of GL and its metabolites in the incubation mixture after continuous consumption of Shakuyaku-kanzo-to were significantly different compared with those of untreated control. GL-hydrolysis of rat feces was enhanced by pre-consumption of Shakuyaku-kanzo-to.

Anaerobiosis↗

PubMed2000

Dose-dependent effects of propofol on renal sympathetic nerve activity, blood pressure and heart rate in urethane-anesthetized rabbits.

To evaluate the role of the autonomic nervous system in hemodynamic changes after propofol bolus injection, we used direct recordings of renal sympathetic nerve activity to examine the dose-dependent effects of propofol (2.5, 5, 10, and 20 mg/kg) on heart rate, mean blood pressure and renal sympathetic nerve activity in urethane-anesthetized rabbits. The animals were divided into four groups: animals with an intact neuraxis (intact group), cervical vagal nerve-sectioned animals (vagotomy group), carotid sinus and aortic-nerve sectioned animals (SAD group), and animals with SAD plus vagotomy (SADV group). Heart rate did not change significantly even after administration of 2.5 and 5 mg/kg but decreased markedly on 20 mg/kg injection in all groups. The intact and vagotomy groups had augmented renal sympathetic nerve activity with insignificant changes in mean blood pressure after 5 mg/kg injection of the agent. Insignificant changes of renal sympathetic nerve activity but a remarkable decrease of mean blood pressure appeared after 10 mg/kg propofol. Sustained hypotension in parallel with a profound depression of renal sympathetic nerve activity developed at the dose of 20 mg/kg. In SAD and SADV groups, however, dose-dependent depressions of renal sympathetic nerve activity were accompanied by decreases of mean blood pressure. These results suggest the following: (1) propofol-induced hypotensive effects are probably produced by the central-mediated sympathetic depression. (2) The baroreceptor reflex may be preserved at the lower dose of the agent. (3) Heart rate does not change significantly unless a large dose of propofol is used. The difference in effects on heart rate and on mean blood pressure may denote a greater inhibition of sympathetic vascular outflow than of the cardiac sympathetic outflow regulating cardiac rate and contractility. This hypothesis needs further clarification.

Anesthesia↗

PubMed2000

Serum glutathione S-transferase alpha as a measure of hepatocellular function following prolonged anaesthesia with sevoflurane and halothane in paediatric patients.

We studied the effects of prolonged anaesthesia (4.3-7.7 h) with sevoflurane and halothane on hepatic function in 14 paediatric patients. Hepatic function was assessed using serum concentrations of liver-specific glutathione S-transferase alpha (GSTA) before and 0, 3 and 15 h after the end of anaesthesia. A transient significant increase in GSTA over baseline was observed in the sevoflurane group, but not in the halothane group, and the difference between the groups was not significant. These data suggest that, although statistically insignificant, the use of sevoflurane for prolonged anaesthesia in paediatric patients is more likely than halothane to be involved in damage to hepatic function.

Analysis of Variance↗

PubMed2000

Effects of induced hypothermia on renal sympathetic nerve activity and baroreceptor reflex in urethane-anesthetized rabbits.

OBJECTIVE: To evaluate the role of the autonomic nervous system in hemodynamic changes during induced hypothermia. DESIGN: Prospective, randomized animal study. SETTING: An animal research laboratory in a medical university. SUBJECTS: A total of 29 anesthetized rabbits. INTERVENTIONS: Animals were anesthetized by intraperitoneal urethane. After tracheostomy and administration of gallamine, respiration was maintained by mechanical ventilatory support. The animals were divided into five groups (one control and the four experimental groups); animals were treated with an intact neuraxis and normothermia (control group), animals with an intact neuraxis (intact group), cervical vagotomized animals (vagotomy group), the carotid sinus and aortic nerves denervated animals (SAD group), and animals with SAD plus vagotomy (SADV group). The left renal sympathetic nerves were exposed by a retroperitoneal approach. MEASUREMENTS AND MAIN RESULTS: We examined the effects of surface cooling on HR, mean arterial pressure, central venous pressure, and renal sympathetic nerve activity (RSNA) in the animals. Changes of baroreflex sensitivity and plasma catecholamines were also measured simultaneously. Surface cooling caused progressive and profound decreases in HR in all experimental groups. In all groups, RSNAs increased at the early phase, which were followed by return to the precooling level. CONCLUSIONS: Hemodynamics and RSNA during induced hypothermia are regulated by mechanisms other than the baroreceptor reflex system, possibly the dermal cold receptors. Suppression of the baroreflex occurred on HR but not on RSNA during hypothermia, which may indicate direct effects of hypothermia on the heart. RSNA responses may be activated earlier than systemic catecholamine responses during induced hypothermia.

Adrenergic Fibers↗

PubMed2000

Moderate hypothermia improves imbalances of thromboxane A2 and prostaglandin I2 production after traumatic brain injury in humans.

OBJECTIVE: To examine the levels of thromboxane B2 (TXB2) and 6-keto prostaglandin F1alpha (6-keto PGF1alpha) production in arterial and internal jugular bulb sera in patients with traumatic brain injury (TBI). TBI is associated with arachidonate release and may be associated with an imbalance of vasoconstricting and vasodilating cyclooxygenase metabolites. DESIGN: A prospective, randomized study. SETTING: The intensive care unit of a medical university hospital. INTERVENTIONS: Twenty-six ventilated TBI patents (Glasgow Coma Scale score on admission, < or = 8 points) were divided randomly into two groups: a hypothermic group (n = 15), in which the patients were cooled to 32 to 33 degrees C after being giving vecuronium, midazolam, and buprenorphine; and a normothermic group (n = 11), in which the patients' body temperature was controlled at 36 to 37 degrees C by surface cooling using the same treatment as the hypothermic group. Body temperature control including normothermia was started 3 to 4 hrs after injury. The duration of hypothermia usually lasted for 3 to 4 days, after which the patients were rewarmed at a rate of approximately 1 C per day. MEASUREMENTS AND MAIN RESULTS: Blood sampling for TXB2 and 6-keto PGF1alpha was started shortly after admission in both groups. Arterial TXB2 levels on admission in both groups were elevated remarkably, but not 6-keto PGF1alpha, thereby causing an imbalance of the prostanoids after injury. In the normothermic group, TXB2 decreased transiently, but this prostanoid increased again 3 days after the injury. In the hypothermic group, such prostanoid differences disappeared shortly after therapy, and the condition was sustained for 10 days. Hypothermia attenuated differences in TXB2 levels between arterial and internal jugular bulb sera, which may reflect reduced cerebral prostanoid production. The Glasgow Outcome Scale score 6 months after the insult in the hypothermic group was significantly higher than that in the normothermic group (p = .04). CONCLUSION: The current results from a limited number of patients suggest that moderate hypothermia may reduce prostanoid production after TBI, thereby attenuating an imbalance of thromboxane A2 and prostaglandin I2. However, it must be clarified whether the changes in the prostanoid after moderate hypothermia are a secondary effect of other mediator changes or whether they simply represent an epiphenomenon that is mechanistically unrelated to damage in TBI.

6-Ketoprostaglandin F1 alpha↗

PubMed2000

[Supplement of ulinastatin on renal function after cardiopulmonary bypass].

The effects of Miraclid (ulinastatin) on renal tubular function after open thorax surgery under cardiopulmonary bypass were investigated. On the 3rd day after open thorax surgery, which had lasted more than 127 min under cardiopulmonary bypass, the levels of urinary ulinastatin in the Miraclid group and control (without Miraclid) were 170 IU.mg Cr-1 and 95 IU.mg Cr-1, respectively. In the Miraclid group, 300,000 units.day-1 of Miraclid was administrated for three postoperative days. N-acetyl-beta-d-glucosaminidase in urine as a marker of tubular function rose significantly on the seventh postoperative day in the control group but not in patients with Miraclid group. These data suggested that Miraclid 300,000 units.day-1 was needed to protect renal tubular function and more than that dose was needed to prevent the deterioration of renal function after open thorax surgery after cardiopulmonary bypass lasting more than 127 min.

Acute Kidney Injury↗

PubMed1999

Intra-axonal continuous measurement of lidocaine concentration and pH in squid giant axon.

PURPOSE: To measure the dynamic penetration process of lidocaine, lidocaine concentration (Ci) and pH (pHi) in squid giant axon, and to determine the times and Ci of disappearance and reappearance of action potentials (AP). METHODS: Lidocaine solutions adjusted to four different pHs (pH = 5.5, 6.8, 7.8 and 9.0) were externally administered to the axon and Ci and pHi were measured using lidocaine and pH microsensors. The times and Ci when the AP just disappeared and reappeared were recorded. In addition, for comparison with Ci, the lidocaine content in the whole axon (Cw) was measured with high-performance liquid chromatography (HPLC). RESULTS: The Ci (charged plus uncharged) was 1.5 times greater than the uncharged form of administered lidocaine. The changes in pHi depended on the increase in Ci. The AP disappeared only after administration of high pH lidocaine solutions (pH = 7.8, 9.0) and reappeared by washing out the solution in the chamber. Nerve block occurred more rapidly at pH 9.0 than at pH 7.8, and the time after washing out the lidocaine was longer at pH 9.0 than at pH 7.8. The mean Ci and charged lidocaine concentration in the axoplasm, when the AP disappeared or reappeared, were lower at pH 9.0 than at pH 7.8 (P < 0.05). CONCLUSION: Uncharged lidocaine penetrates the axon membrane to the axoplasm where it changes to the charged form and is concentrated in the axon membrane and axoplasm. External application of uncharged lidocaine plays a role in modulating nerve conduction.

Action Potentials↗

PubMed1999

Activated cytokine production in patients with accidental hypothermia.

We have demonstrated recently that therapeutic moderate hypothermia of 32-33 degrees C, induced by surface cooling under the administration of narcotics, sedatives and muscle relaxant, suppresses cytokine production after traumatic brain injury. We present here the first documented case report of augmented cytokine production in two accidental hypothermia patients, unconscious 84- (acute immersion) and 87- (non-immersion) year-old women, whose rectal temperatures were below 28 degrees C. The victims were artificially ventilated after sedation with midazolam and buprenorphine in accordance with our protocol. Rewarming at the rate of approximately 1 degrees C/h was done by blowing forced-air with appropriate fluid resuscitation. Plasma interleukin(IL)-6 and/or IL-8 levels were measured using ELISA in the patients. In both patients, plasma IL-6 levels on admission were already elevated and the cytokine levels further increased during and after the rewarming period. In the patient with the poorer prognosis, the plasma IL-8 level on admission was not elevated remarkably but after rewarming the level rose significantly. Augmented IL-6 production in accidental hypothermia was sustained for 6 days in the patient with the poorer prognosis but not in the subject with good recovery, who was treated with anti-thrombin III in the early phase. Since the mechanisms for developing accidental hypothermia were different, simple comparisons between the two cases should be limited. But, these findings may suggest a need for testing a hypothesis whether cytokine modulation could be a therapeutic approach worthy of consideration. The results presented here also suggest that in hypothermia, changes in cytokine release may vary depending on procedures such as the anesthetic drugs used, the duration of the therapy, or the rate of rewarming from hypothermia.

Aged↗

PubMed1999

Effect of moderate hypothermia on systemic and internal jugular plasma IL-6 levels after traumatic brain injury in humans.

Moderate hypothermia may reduce subsequent neuronal damage after traumatic brain injury. Interleukin (IL)-6 may have a role in the pathogenesis of traumatic neuronal damage or repair. Using the enzyme-linked immunological sorbent assay (ELISA), we serially measured IL-6 levels in plasma obtained from the radial artery (systemic) and internal jugular vein (regional) in 13 cerebral trauma patients who underwent hypothermia of 32-33 degrees C ranged from 4-9 days postinjury and 10 head-injured patients who were maintained at normothermic levels (36-37 degrees C). In both patient populations, surface cooling was used since even in the normothermic group, cooling was needed to maintain patient temperature in the normothermic range. All patients were mechanically ventilated after injection of midazolam and vecuronium. The administration of these agents were continued until the end of the study. Hypothermia was typically maintained for four days, however, in some cases based upon CT findings and/or intra-cranial pressure change, the duration was prolonged. No significant differences were found between the two groups in age, gender and Glasgow Coma Scale upon admission. Further, no differences were found in terms of the classification of computed tomography findings or the occurrence of pupillary abnormalities on admission. The patients in this study had not sustained either abdominal or thoracic trauma. Before inducing hypothermia, IL-6 levels in the arterial and internal jugular venous blood exceeded the normal range. Specifically, the internal jugular plasma levels were significantly higher than those in the arterial plasma. While IL-6 levels in the normothermic group did not decrease even at 4 days postinjury, the plasma cytokine levels fell at both sites sharply after moderate hypothermia. The cytokine suppression found in the hypothermic group continued even after rewarming in these patients showing an improved clinical course, but not in those whose condition worsened. In addition to these changes in cytokine levels, the Glasgow Outcome Scale at 6 months postinjury was significantly higher in the hypothermic group than in the normothermia group. Based on the above, this clinical study with its small patient sample size suggests the need for further prospective randomized studies to examine the role of cytokine suppression in the beneficial effects of moderate hypothermia in patients with traumatic brain injury.

Adolescent↗

PubMed1998

The effect of volatile anesthetics on light-induced phosphorylation in spinach chloroplasts.

(1) The light-induced phosphorylation in spinach chloroplast is coupled with proton transfer. (2) We investigated the effect of volatile anesthetics (halothane, enflurane, isoflurane) on the cyclic and/or non-cyclic light-induced phosphorylation. (3) We used potassium ferricyanide as a Hill oxidant for non-cyclic phosphorylation and phenazin-methosulfate as an oxidation-reduction indicator for cyclic phosphorylation. (4) These three anesthetics inhibit the Hill reaction in light induced phosphorylation. The inhibition rate of this reaction generates concave curves with minimum values at 303 K in each of the anesthetics.

Anesthetics, Inhalation↗

PubMed1998

Effects of halothane and supporting membrane lipids on the activity of acetylcholinesterase.

1. The activity of acetylcholinesterase in the human erythrocyte membrane was measured with and without halothane. 2. To evaluate the roles of the supporting membrane lipids, the enzyme protein was solubilized from the membrane with a surfactant, Triton X-100. 3. It is confirmed that membrane lipids alter the activation energy of the enzyme bound to the membrane, and strengthen the effects of halothane and Triton X-100 on the enzyme activity by providing a high concentration field of them around the enzyme.

Acetylcholinesterase↗

PubMed1998

Repetitive post-training exposure to enflurane modifies spatial memory in mice.

BACKGROUND: Previously the authors found that a single post-training exposure to enflurane or isoflurane, but not halothane, enhanced memory storage in an active avoidance task, which is a behavior with underlying mechanisms that are poorly understood and still debated. In contrast, spatial tasks are known to depend on hippocampal functions. This study investigated the effects of repetitive post-training exposure to enflurane on spatial memory in mice. METHODS: Using an eight-arm radial maze, 80 mice were trained to eat a pellet placed on the end of each of the eight arms. Training occurred on four consecutive days with one trial per day. The number of errors in the first eight choices was recorded to determine performances for each day of training. Immediately after each training session, mice in the enflurane group received 1 h exposure to 0.5%, 1%, or 2% enflurane in air through a calibrated vaporizer. The performance ratios (the ratio of errors on each day compared with the first day of the 4 days) in the control and the enflurane groups were compared. RESULTS: The performance ratios (which equals the mean of the error in the fourth day/the error in the first day) in the control, and 0.5%, 1%, and 2% enflurane groups were 0.66, 0.65, and 0.32 (P < 0.01, vs. control), and 0.46 (P < 0.05, vs. control), respectively. CONCLUSIONS: Repetitive post-training exposure to 1% and 2% enflurane significantly enhanced spatial memory in the eight-arm radial maze task. Enflurane enhances consolidation of spatial memory, possibly by affecting hippocampal activity.

Anesthetics, Inhalation↗

PubMed1997

Spontaneous breathing with the use of a laryngeal mask airway in children: comparison of sevoflurane and isoflurane.

We compared respiratory parameters during anaesthesia with sevoflurane and isoflurane through a laryngeal mask airway (LMA). Children were anaesthetized with O2 and air with 2.3% (1MAC) sevoflurane (n = 20) or 1.5% (1MAC) isoflurane (n = 20). After insertion of LMA, patients were allowed to breathe spontaneously and respiratory rate (RR) and PECO2 were measured (presurgery state). After the measurement, anaesthetic concentration was increased to 1.3 MAC (3.0% sevoflurane or 2.0% isoflurane) and surgical stimulation was added. Fifteen min after incision, the measurements were again performed (during surgery). In the sevoflurane group, mean RR and PECO2 were 32 breaths.min-1, and 6.0 kPa (45 mmHg) respectively, before surgery, and 35 breaths.min-1 and 7.0 kPa (52 mmHg) during surgery. In the isoflurane group, mean RR and PECO2 were 32 breaths.min-1 and 6.1 kPa (46 mmHg) respectively, before surgery, and 37 breaths.min-1 and 6.7 kPa (52 mmHg) during surgery. There were no statistical differences between the two anaesthetic groups. Clinical respiratory and cardiovascular parameters during spontaneous breathing with LMA in children are similar during sevoflurane and isoflurane anaesthesia.

Anesthetics, Inhalation↗

PubMed1997

[Significance of postoperative elevation of urinary ulinastatin after open heart surgery under cardiopulmonary bypass].

To investigate the role of ulinastatin in perioperative stress, we measured the urinary levels of ulinastatin (UTI) in patients subjected to open heart surgery under cardiopulmonary bypass. The UTI levels began to increase on the first postoperative day and reached its maximum level on the third postoperative day. There is a good correlation between the maximum level of urinary UTI and cardiopulmonary bypass time. These results indicate that urinary UTI level can be an indicator of surgical stress.

Aged↗

PubMed1997

[Effects of ulinastatin on postoperative renal function in hepatectomized patients with liver cirrhosis].

Posthepatectomy patients with liver cirrhosis have a high incidence of multiple organ failure including renal failure. The depression of urinary ulinastatin (UTI) might be involved in renal derangements in the posthepatectomy patients with liver cirrhosis. We evaluated the relationship between the renal functions and the level of urinary UTI in perioperative period in the posthepatectomy patients with liver cirrhosis, and evaluated whether or not the renal function in the posthepatectomy patients with liver cirrhosis was protected by receiving synthetic UTI, Miraclid. In posthepatectomy patients with liver cirrhosis, the urinary UTI level was 26.3 +/- 13.0 IU. mg x Cr-1 on the first day and renal tubular dysfunction was noticed. On the other hand, in posthepatectomy patients with liver cirrhosis receiving Miràclid administered intravenously during the operation and postoperative three days, the urinary UTI level was 121.2 +/- 85.0 IU. mg x Cr-1 on the first day and renal function was maintained. These results indicate that in posthepatectomy patients with liver cirrhosis, an increase in urinary UTI level observed in response to surgical stress may not occur and this low level of urinary UTI may cause renal dysfunction in the postoperative period. The synthetic UTI, Miraclid, may have beneficial effects reversing the renal derangements resulting from the stress in posthepatectomy patients with liver cirrhosis.

Aged↗

PubMed1997

[Urinary excretion of ulinastatin and NAG after cardiopulmonary bypass].

Although urinary trypsin inhibitor (ulinastatin, UTI) is excreted into urine, its physiological function has not been clarified well. Administration of UTI during surgical procedure was reported to protect renal function from surgical stress. This result suggests participation of UTI excretion in renal tubular function. In this study, the amount of urinary excretion of UTI and that of N-acetyl-beta-D-glucosaminidase (NAG) after cardiopulmonary bypass (CPB) were measured. The urinary UTI excretion increased after surgery and reached the maximum on the third postoperative day. NAG also increased gradually and was three times greater than control on the seventh postoperative day. There was a good correlation between NAG and UTI on the first postoperative day. It is suggested that UTI might correlate with the renal tubular function after CPB.

Acetylglucosaminidase↗