Katsuyasu Kitaguchi

A comparison of the INVOS 4100 and the NIRO 300 near-infrared spectrophotometers

We determined whether two different devices for measuring near-infrared spectroscopy (NIRS)—the INVOS 4100 and the NIRO 300—produce similar cerebral oxygenation data during the CO2 challenge test. Nineteen patients anesthetized with sevoflurane, 67% nitrous oxide in oxygen, and fentanyl were studied. A series of measurements of regional cerebral oxygen saturation (rSo2), measured by the INVOS 4100, and tissue oxygen index (TOI), measured by the NIRO 300, were performed in the following conditions: 1) normocapnia (Paco2, 35–45 mm Hg); 2) hypocapnia (Paco2, 25–35 mm Hg); 3) normocapnia; and 4) hypercapnia (Paco2, 45–55 mm Hg). Hemodynamic variables, including arterial blood gases and cerebral blood flow velocity, were measured at the same time with transcranial Doppler. The values and percentage changes of rSo2 and TOI were compared by using regression analysis and Bland and Altman analysis. The rSo2 showed a significant positive correlation with TOI (r = 0.58, P < 0.01). The percentage change of rSo2 also showed a significant positive correlation with the percentage change of TOI during the CO2 challenge (r = 0.85, P < 0.01). Bland and Altman analysis revealed a bias of −0.5% with 2 sd of 15.6% when comparing the rSo2 value with the TOI value, and it showed a bias of −3.4% with 2 sd of 15.2% when comparing the percentage change of rSo2 with the percentage change of TOI, indicating unacceptable disagreement of these data. These results indicate that cerebral oxygen saturation and its relative change during the CO2 challenge may vary depending on the type of NIRS used. Because the measurement technique and algorithm were different in each device, we should carefully consider the clinical application of the values produced by NIRS.

The effect of sevoflurane on myogenic motor-evoked potentials induced by single and paired transcranial electrical stimulation of the motor cortex during nitrous oxide/ketamine/fentanyl anesthesia.

To overcome anesthetic-induced depression of myogenic motor-evoked potentials (MEPs), several techniques of stimulation using paired pulses or trains of pulses are used. This study investigated the effect of sevoflurane on myogenic MEPs induced by single and paired transcranial electrical stimulation of the motor cortex. Nine patients undergoing elective spinal surgery were anesthetized with fentanyl-N2O-ketamine. Partial neuromuscular blockade (single-twitch height 15% of baseline) was maintained with vecuronium. Single and paired (interstimulus interval 2 milliseconds) electrical stimuli were delivered to the scalp, and compound muscle action potentials were recorded from the left and right tibialis anterior muscles. In all patients, baseline MEPs were recorded from both the left and right anterior tibialis muscles (in a total of 18 legs). During the administration of 0.25 MAC and 0.5 MAC sevoflurane, MEPs induced by stimulation with a single pulse could be recorded in 12 of 18 and 4 of 18 legs, respectively, and MEP amplitude was significantly reduced to 48% and 4% of the control value, respectively. During the administration of 0.75 MAC sevoflurane, MEPs following single-pulse stimulation could not be recorded in any legs. The success rate of MEP recording during the administration of sevoflurane was greater after paired stimulation than after single stimulation, and percentage MEP amplitude (percentage of the control value after single stimulation but before sevoflurane) after paired stimulation was significantly higher than after single stimulation before and during the administration of 0.25 MAC and 0.5 MAC sevoflurane. The success rate of MEP recording and MEP amplitude after paired stimulation decreased in a dose-dependent manner during the administration of sevoflurane. These results suggest that although facilitation by the second stimulus was considerable, paired stimuli are still not sufficient to overcome the depressant effects of sevoflurane in clinically used concentrations.

The influence of induced hypothermia for hemostatic function on temperature-adjusted measurements in rabbits.

In hypothermic patients, a tendency to bleed may be observed even when hemostatic tests seem to be normal. Coagulation and platelet function tests are usually performed at 37°C. We investigated the influence of induced hypothermia on temperature-adjusted hemostasis function testing using Sonoclot Analyzer® (Sonoclot®) and Thromboelastography® (TEG®). Anesthesia was induced and maintained with IV ketamine and fentanyl on 15 male New-Zealand White rabbits. A water blanket was used to induce hypothermia to 30°C and to rewarm to 37°C. Blood samples were obtained at four points: before hypothermia, at 34°C, at 30°C, and after rewarming. Standard coagulation tests were performed at 37°C (C method), and simultaneously, real temperature hemostasis function tests (R method) were run. In Sonoclot®, activated clotting time and time to peak increased and clot rate decreased significantly at 30°C in the R method compared with those in the C method. In TEG®, reaction time and clot formation time were prolonged and clot formation rate was diminished at 30°C in the R method compared with those in the C method. Induced hypothermia delayed the coagulation cascade and reduced platelet function. During hypothermia, hemostatic measurements should be performed at real temperature to avoid overestimating patient hemostatic function based on results measured at the standard 37°C.

The association of high jugular bulb venous oxygen saturation with cognitive Decline after hypothermic cardiopulmonary bypass

This study was conducted to investigate whether jugular bulb venous oxygen saturation (Sjvo2) predicted cognitive decline after cardiac surgery with hypothermic cardiopulmonary bypass (CPB). We studied 35 patients undergoing cardiac surgery. After the induction of anesthesia, a 5.5F fiberoptic oximetry catheter was retrogradely inserted into the jugular bulb, and Sjvo2 and other cerebral oxygenation variables were analyzed before, during, and after CPB. At each point, an oxyhemoglobin dissociation curve was drawn, and the P50 value of jugular bulb venous blood was calculated by computer analysis. Cognitive function was assessed with the revised version of Hasegawa’s Dementia Scale and the Benton Revised Visual Retention Test before and early after the operation. In 15 patients (the Decline group), cognitive function was declined after surgery, whereas it remained unchanged in 20 patients (the Normal group). Sjvo2 was significantly higher and cerebral oxygen extraction was significantly lower before and during CPB in the Decline group than in the Normal group (P < 0.05). The oxygen pressure at an oxygen saturation of 50% was significantly lower before and after CPB in the Decline group than in the Normal group (P < 0.05). Logistic regression analysis showed that high Sjvo2 was a predictor of cognitive decline after cardiac surgery. We conclude that high Sjvo2 was associated with cognitive decline after cardiac surgery with hypothermic CPB.

Postoperative neurological deterioration following the revascularization surgery in children with moyamoya disease.

We describe four children with moyamoya disease who developed neurologic deterioration following revascularization surgery. In all cases, anesthesia was smoothly induced and the intraoperative course was uneventful. Emergence from anesthesia was prompt and no new neurological deficit was observed. However, the children suffered strokes on 2, 4, 5, and 10 days, postoperatively, respectively. Dehydration and crying were thought to be closely associated with the stroke in each case. This report suggests that attention should be paid during entire the perioperative period to avoid stroke in patients with moyamoya disease.

Amplitudes and intrapatient variability of myogenic motor evoked potentials to transcranial electrical stimulation during ketamine/N2O- and propofol/N2O-based anesthesia.

The aim of the current study was to investigate whether there are differences in amplitudes and intrapatient variability of motor evoked potentials to five pulses of transcranial electrical stimulation between ketamine/N2O- and propofol/N2O-based anesthesia. Patients in the propofol group (n = 13) and the ketamine group (n = 13) were anesthetized with 50% N2O in oxygen, fentanyl, and 4 mg/kg/hr of propofol or 1 mg/kg/hr of ketamine, respectively. The level of neuromuscular blockade was maintained at an M-response amplitude of approximately 50% of control. Motor evoked potentials in response to multipulse transcranial electrical stimulation were recorded from the right adductor pollicis brevis muscle, and peak-to-peak amplitude and onset latency of motor evoked potentials were evaluated. To estimate intrapatient variability, the coefficient of variation (standard deviation/mean × 100%) of 24 consecutive responses was determined. Motor evoked potential amplitudes in the ketamine group were significantly larger than in the propofol group (mean, 10th–90th percentile: 380 &mgr;V, 129–953 &mgr;V; 135 &mgr;V, 38–658 &mgr;V, respectively;P < .05). There were no significant differences in motor evoked potential latency (mean ± standard deviation: 20.9 ± 2.2 msec and 21.4 ± 2.2 msec, respectively) and coefficient of variation of amplitudes (median [range]: 32% [22–42%] and 26% [18–41%], respectively) and latencies (mean ± standard deviation: 2.1 ± 0.7% and 2.1 ± 0.7%, respectively) between the ketamine and propofol groups. In conclusion, intrapatient variability of motor evoked potentials to multipulse transcranial stimulation is similar between ketamine/N2O- and propofol/N2O-based anesthesia, although motor evoked potential amplitudes are lower during propofol/N2O-based anesthesia than ketamine/N2O-based anesthesia.

Nitric oxide involvement in hypoxic dilation of pial arteries in the cat.

Background The reactivity of cerebral arteries to different stimuli varies according to vessel size. Whether nitric oxide mediates hypoxic vasodilation is controversial The authors considered this question by measuring the diameter of pial arteries and arterioles with or without exposure to the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME). Methods The cranial window technique, combined with microscopic video recording, was used in an experiment involving 20 cats anesthetized with fentanyl and midazolam. The diameters of pial arteries and arterioles were measured under the following conditions: (1) normoxia (PaO2 > 100 mmHg); (2) hypoxia (PaO2 < 45 mmHg); (3) normoxia with L-NAME infusion; and (4) hypoxia with L-NAME infusion. Changes in vessel diameter were analyzed with respect to artery size. Results Under hypoxic conditions, arteries and arterioles smaller than 200 micro meter were dilated significantly (P < 0.05). In arterioles smaller than 200 micro meter, L-NAME attenuated this hypoxic vasodilation (P < 0.05). In contrast, under normoxic conditions, L-NAME caused significant vasoconstriction in arteries larger than 100 micro meter but not in arteries smaller than 100 micro meter. Conclusions Arteries and arterioles smaller than 200 micro meter are dilated by hypoxia, and nitric oxide contributes to this process. Nitric oxide synthesis may also be related to the regulation of resting vascular tone in arteries larger than 100 micro meter.

Treatment of pulmonary embolism during cesarean section with recombinant tissue plasminogen activator.

ALTHOUGH pulmonary embolism is a rare complication of pregnancy, it is one of the leading causes of maternal mortality It was estimated that two thirds of deaths caused by pulmonary embolism occur during the first hour after the event, and the remainder occurred within 4 to 6 h. 3 Therefore, we believe that early detection and subsequent treatment of pulmonary embolism are important clinical challenges. In this report, we describe a patient with abruptio placenta and preeclampsia who underwent general anesthesia for cesarean section, in which life-threatening pulmonary embolism developed intraoperatively and was treated with recombinant tissue plasminogen activator (rt-PA).

Mild hypothermia can attenuate nitroglycerin-induced vasodilation of pial arterioles in the cat.

The purpose of the present study was to investigate the effect of mild hypothermia on nitroglycerin-induced vasodilation of cerebral vessels. The cranial window technique, combined with microscopic video recording, was used in an experiment involving 26 cats anesthetized with isoflurane. Animals were randomly assigned to either a normothermic or a mildly hypothermic group (33[degree sign]C). We administered three different concentrations of nitroglycerin (10-6, 10-5, 10-4 M) under the window and measured the diameter of small (<100 [micro sign]m) and large (100-200 [micro sign]m) pial arterioles. In the normothermic group (n = 13), nitroglycerin produced a significant dilation of both small and large arterioles in a dose-dependent manner. In the hypothermic group (n = 13), a significant dilation of arterioles was observed only after topical application of nitroglycerin at a concentration of 10-4 M. The percent increase in diameter of small and large arterioles was less in the hypothermic group than the normothermic group. Our in vivo study demonstrates that topically applied nitroglycerin produces a dose-dependent dilation of pial arterioles in normothermic cats anesthetized with isoflurane, but the reduction of temperature to 33[degree sign]C significantly attenuates nitroglycerin-induced vasodilation of pial arterioles. Implications: Although nitroglycerin may be used in hypothermic patients, the effect of mild hypothermia on nitroglycerin-induced vasodilation of cerebral vessels is unknown. In this study, we investigated the effects of nitroglycerin on pial arteriolar diameter in normothermic and hyperthermic cats. Hypothermia was found to attenuate nitroglycerin-induced vasodilation. (Anesth Analg 1998;86:546-51)

Mild hypothermia can enhance pial arteriolar vasodilation induced by isoflurane and sevoflurane in cats.

ObjectiveVolatile anesthetics have been shown to dilate cerebral vessels. Recent evidence suggests that mild hypothermia can alter vascular reactivity of the cerebral vessels. However, the effect of mild hypothermia on volatile anesthetic-induced vasodilation of cerebral vessels is unknown. In the present study, we investigated the effect of mild hypothermia on pial arteriolar vasodilation induced by isoflurane and sevoflurane in cats. DesignProspective, randomized, experimental study with repeated measures. SettingInvestigational animal laboratory. SubjectsForty cats were used for the study of systemic administration of volatile anesthetics, and 22 cats were used for the study of topical administration of volatile anesthetics. InterventionsThis study was approved by the Animal Experiment Committee of Nara Medical University. Animals were anesthetized with pentobarbital to maintain suppressive electroencephalographic patterns, which were introduced to measure direct effects of anesthetic agents after removing metabolic effects. The cranial window technique, combined with microscopic video recording, was used for the measurement of small (50–100 &mgr;m) and large (100–200 &mgr;m) pial arteriolar diameter in an experiment. Animals were randomly assigned to either a normothermic (37°C) or a hypothermic group (33°C). Desired temperatures were maintained by using a water blanket. In the first phase of the study, the effect of hypothermia on pial arteriolar vasodilation induced by systemic administration of isoflurane or sevoflurane was assessed. Each cat received isoflurane or sevoflurane at 0.5, 1.0, 1.5, and 2.0 minimum alveolar anesthetic concentrations, and the diameter of pial arterioles was measured. In the second group of animals, the direct effect of isoflurane and sevoflurane on pial vessels was evaluated. The artificial cerebrospinal fluid bubbled with isoflurane or sevoflurane (minimum alveolar anesthetic concentrations of 1 or 3) was topically administered in the cranial window. Measurements and Main ResultsSystemic and topical administration of isoflurane and sevoflurane produced significant dilation of both small and large pial arterioles in a dose-dependent manner during normothermia. In the hypothermic group, vasodilation of small pial arterioles by systemic administration of isoflurane and sevoflurane at a high concentration was significantly larger than in the normothermic group (p < .05). Vasodilation of both small and large pial arterioles by topical administration of isoflurane and sevoflurane was significantly greater in the hypothermic group than in the normothermic group (p < .05). ConclusionsThese results suggest that pial arteriolar vasodilation induced by isoflurane and sevoflurane can be enhanced by mild hypothermia in cats anesthetized with pentobarbital.