Ikuto Yoshiya

Spectrophotometric monitoring of arterial oxygen saturation in the fingertip.

A noninvasive oximeter that analyses the oxygen saturation of arterial blood in the fingertip is described. The light, after attenuating the infrared portion to avoid thermal injury, is applied to the fingertip through an optical transmitter made of glass fibres. The transmitted light is transferred to an optical reception system where a spectrophotometric determination of oxygen saturation is performed. The determination is performed by considering only the change in the attenuation of light caused by the inflow of arterial blood into the fingertip. The correlation between the oxygen saturation measured with the present instrument (y) and that with the blood-gas method (x), was y=0·907x+8·592 with a standard deviation and a correlation coefficient of 0·135% and 0·983, respectively. The reproducibility was assessed in a healthy subject by measuring the oxygen saturation repeatedly 60 times. The mean saturation was 95·82±0·675% (mean±standard deviation). The instrument has been useful in monitoring arterial oxygenation in patients with respiratory failure in our intensive-care unit. One of the disadvantages of the instrument is that the measurement is interrupted when the fingertip changes its position against the light beam.

Effects of Crystalloid and Colloid Preload on Blood Volume in the Parturient Undergoing Spinal Anesthesia for Elective Cesarean Section

BACKGROUND The role of crystalloid preloading to prevent hypotension associated with spinal anesthesia in parturients during cesarean section has been challenged. Direct measurement of blood volume should provide insight regarding the volume-expanding effects. The aim of the current study was to clarify the effects of volume preload with either crystalloid or colloid solution on the changes in blood volume of parturients undergoing spinal anesthesia for cesarean section. METHODS Thirty-six healthy parturients scheduled for elective cesarean section during spinal anesthesia were allocated randomly to one of three groups receiving 1.5 l lactated Ringers solution (LR; n = 12), 0.5 l hydroxyethylstarch solution, 6% (0.5 l HES; n = 12), and 1.0 l hydroxyethylstarch solution, 6% (1.0 l HES; n = 12), respectively. Blood volume and cardiac output were measured before and after volume preloading with indocyanine green (ICG), and the indocyanine green blood concentrations were monitored by noninvasive pulse spectrophotometry. RESULTS After volume preload, the blood volume significantly increased in all three groups (P < 0.01). The volume of infused solution remaining in the vascular space in the LR, 0.5-l HES, and 1.0-l HES groups were 0.43+/-0.20 l, 0.54+/-0.14 l, and 1.03+/-0.21 l, respectively, corresponding to 28% of lactated Ringers solution and 100% of hydroxyethylstarch solution infused. Significant increases in cardiac output were observed in the 0.5-l and 1.0-l HES groups (P < 0.01). A significant correlation between the percentage increase in blood volume and that of cardiac output was observed by volume preloading (r2 = 0.838; P < 0.001). The incidence of hypotension was 75% for the LR group, 58% for the 0.5-l HES group, and 17% for the 1.0-l HES group, respectively. CONCLUSIONS The incidence of hypotension developed in the 1.0-l HES group was significantly lower than that in the LR and 0.5-l HES groups, showing that greater volume expansion results in less hypotension. This result indicates that the augmentation of blood volume with preloading, regardless of the fluid used, must be large enough to result in a significant increase in cardiac output for effective prevention of hypotension.

Plasma lipid peroxides and alpha-tocopherol in critically ill patients

Plasma lipid peroxide measured as thiobarbituric acid reactive substances (TBARS) and alpha-tocopherol levels in 24 critically ill patients were compared with those of control subjects. The mean plasma alphatocopherol level was significantly lower and the mean TBARS level was significantly higher in critically ill patients. Eight ICU patients developed disseminated intravascular coagulation (DIC); the mean TBARS level during DIC was significantly above the mean pre-DIC level. These results indicate that lipid peroxidation may contribute to the development of DIC in critically ill patients.

The effects of propofol, isoflurane, and sevoflurane on oxygenation and shunt fraction during one lung ventilation

Propofols effect on hypoxic pulmonary vasoconstriction during one-lung ventilation (OLV) has not been determined. Twenty patients who had long-term OLV for esophageal surgery were allocated randomly to one of two study groups; one in which isoflurane administration preceded propofol, and another in which sevoflurane administration preceded propofol. Arterial and mixed venous blood samples and hemodynamics were measured as follows: before OLV, during OLV, OLV at 4 cm of positive end-expiratory pressure (PEEP), OLV after conversion from volatile anesthetics to propofol, OLV at 4 cm of PEEP, and after OLV. After the application of 4 cm of PEEP during propofol anesthesia, PaO2 increased significantly in both groups. The shunt fraction (Qs/Qt) increased significantly after the initiation of OLV in both groups and decreased significantly after the conversion from volatile anesthetics to propofol in both groups. Propofol can be used safely during OLV because PaO2 increased after the application of 4 cm of PEEP during propofol anesthesia, and Qs/Qt decreased significantly after the conversion from inhaled anesthetics to propofol anesthesia. Implications: During one-lung ventilation, the arterial partial pressure of oxygen values with propofol were greater than those with isoflurane and sevoflurane, and shunt fraction values with propofol were lower than those with both volatile anesthetics. Propofol improved oxygenation and shunt fraction during one-lung ventilation compared with volatile anesthetics. (Anesth Analg 1998;87:1164-9)

Practical issues in bispectral analysis of electroencephalographic signals.

IMPLICATIONS The aim of this report was to confirm the methodology of bispectral analysis of electroencephalogram. In developing a software for real-time bispectral analysis, we encountered several practical problems in bispectrum calculation. We settled those and concluded that 3 min of monitoring are required to obtain reliable and reproducible bicoherence values.

Prolongation of canine epidural anesthesia by liposome encapsulation of lidocaine.

The purpose of our study was to produce a long-acting lidocaine by using a liposome that would entrap the drug. Egg yolk phosphatidylcholine and cholesterol were used as liposome materials. After epidural administration, the pharmacodynamics and pharmacokinetics of liposomal and free lidocaine were studied in 20 dogs. Two percent liposomal or free lidocaine (3.0 mL) was injected into the lumbar epidural space. Nerve blocking effects were estimated by measuring somatosensory evoked potentials. Recovery time from the epidural block in the liposomal lidocaine group (170 +/- 49.5 min) was approximately three times longer than that in the free lidocaine group (61 +/- 18.1 min). The areas under the drug concentration-time curves (AUC0-infinity) and time to maximal concentration (Tmax) in the liposomal lidocaine group were significantly larger than those in the free lidocaine group. These results suggest that the prolongation of epidural blockade by liposomal lidocaine is caused by a slow release of the drug from liposomes. The present study suggests that liposomal lidocaine can be used as a long-acting local anesthetic.

A comparative study of the antinociceptive action of xenon and nitrous oxide in rats

We attempted to clarify the mechanism of antinociceptive action induced by xenon and nitrous oxide.Eighty percent of nitrous oxide or 80% xenon was applied to rats inside enclosed clear plastic glass cylinders with their tails protruding for assessment of the tail-flick response to radiant heat. With repeated testing, there was a rapid reduction to nitrous oxide antinociception within 90 min, which was interpreted as development of tolerance, but not to xenon antinociception. Nitrous oxide antinociception was blocked by the intraperitoneal administration of 0.1 or 1.0 mg/kg yohimbine, but not by 1.0 or 5.0 mg/kg L659-066 or by 5.0 or 10 mg/kg naloxone. Xenon antinociception was not affected by any of these drugs. Yohimbine and L659-066 are characterized as alpha2-adrenoceptor antagonists. Although yohimbine penetrates the blood-brain barrier after systemic administration, L659-066 does not penetrate it and act peripherally. Therefore, the results indicate that alpha2-adrenoceptors, but not opioid receptors, may play a key role in antinociception induced by nitrous oxide in the central nervous system. Furthermore, the mechanism of xenon antinociception differs from that of nitrous oxide because it does not involve either alpha2 or opioid receptors. Implications: The precise mechanism of antinociceptive action of nitrous oxide and xenon remains unknown. It is still controversial whether an opioid system plays a role in antinociception induced by nitrous oxide. The results of the study showed that antagonism of central alpha2-adrenoceptors, but not opioid receptors, reverses the antinociception induced by nitrous oxide but not by xenon, which indicates that alpha2-adrenoceptors may play a key role in nitrous oxide antinociception. (Anesth Analg 1997;85:931-6)

Ketamine inhibits monoamine transporters expressed in human embryonic kidney 293 cells.

Background Ketamine has been characterized as having psychotomimetic and sympathomimetic effects. These symptoms have raised the possibility that ketamine affects monoaminergic neurotransmission. To elucidate the relation between ketamine and monoamine transporters, the authors constructed three cell lines that stably express the norepinephrine, dopamine, and serotonin transporters and investigated the effects of ketamine on these transporters. Methods Human embryonic kidney cells were transfected using the Chen‐Okayama method with the human norepinephrine rat dopamine, and rat serotonin transporter cDNA subcloned into the eukaryotic expression vector. Using cells stably expressing these transporters, the authors investigated the effects of ketamine on the uptake of these compounds and compared them with those of pentobarbital. Results Inhibition analysis showed that ketamine significantly inhibited the uptake of all three monoamine transporters in a dose‐dependent manner. The Ki (inhibition constant) values of ketamine on the norepinephrine, dopamine, and serotonin transporters were 66.8 micro Meter, 62.9 micro Meter, and 162 micro Meter, respectively. Pentobarbital, a typical general anesthetic agent with no psychotic symptoms, did not affect the uptake of monoamines, however. Further, neither the glycine transporter 1 nor the glutamate/aspartate transporter was affected by ketamine, indicating that ketamine preferentially inhibits monoamine transporters. Conclusions Ketamine inhibited monoamine transporters expressed in human embryonic kidney cells in a dose‐dependent manner. This result suggests that the ketamine‐induced inhibition of monoamine transporters might contribute to its psychotomimetic and sympathomimetic effects through potentiating monoaminergic neurotransmission.

Dexmedetomidine Prevents Epinephrine-induced Arrhythmias Through Stimulation of Central α2 Adrenoceptors in Halothane-anesthetized Dogs

Since alpha 2-adrenergic agonists have important effects on the adrenergic system that have recently been applied to the anesthetic setting, we investigated the effect of stimulation of alpha 2 adrenoceptors on epinephrine-induced arrhythmias in halothane-anesthetized dogs. The arrhythmogenic threshold for epinephrine was determined during halothane anesthesia in the presence of dexmedetomidine, a selective alpha 2 agonist, and L-medetomidine, a stereoisomer of medetomidine that lacks alpha 2-agonist activity. Dexmedetomidine increased the arrhythmogenic threshold for epinephrine in a dose-dependent manner during halothane anesthesia. At the highest dose of dexmedetomidine, 0.5 microgram.kg-1.min-1, there was a three-fold increase in both the arrhythmogenic dose of epinephrine and the plasma epinephrine concentration that was reached at this dose. On the other hand, L-medetomidine over the same dose range did not effect the arrhythmogenic dose of epinephrine. Atipamezole, a central alpha 2 antagonist that crossed the blood-brain barrier, blocked the antiarrhythmic action of dexmedetomidine. L-659,066 a peripheral alpha 2 antagonist that does not penetrate the blood-brain barrier, did not affect the antiarrhythmic action of dexmedetomidine. Thus, dexmedetomidines antiarrhythmic effect on epinephrine-induced arrhythmias during halothane anesthesia appears to be mediated at least in part by stimulation of central alpha 2 adrenoceptors.

Effects of multiple scattering and peripheral circulation on arterial oxygen saturation measured with a pulse-type oximeter

NONINVASIVE monitoring of arterial oxygenation is essential for the management of patients with respiratory insufficiency. We previously developed a pulse-type oximeter which estimates the absolute value of oxygen saturation (YOSHIYA et al., 1980). The determination is performed by considering just the change in the attenuation of light caused by the inflow of arterial blood into the fingertip. However, SARNQU[ST et al. (1980) recently reported that the device overestimates arterial oxygen saturations below 90 per cent. If this is the case, there would be serious limitations in its use as a monitoring device for hypoxaemic patients. We re-evaluated the device and found similar overestimation. We then performed an in vitro study to clarify the possible contribution of multiple scattering on the saturation measurement. We also evaluated the effects of an impaired peripheral circulation on the arterial oxygen saturation values of the pulse-type oximeter.