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Biomedical subjects

T Matsukawa

Publications and source records attributed to T Matsukawa.

At least 91 records · Page 5Linked to original sources

[Anesthetic managements of a patient with multiple sclerosis using propofol].

We experienced anesthetic management of a 45-yr-old female patient with a 12-yr history of multiple sclerosis who underwent orthopedic surgeries three times under general anesthesia. We chose rapid induction with propofol and maintained the anesthesia with nitrous oxide, oxygen, and sevoflurane. We monitored both core and peripheral temperatures to avoid the rapid increase of core temperature, which might worsen the symptoms of the disease. There is no other report of anesthesia using propofol as induction agent for a patient with multiple sclerosis. We succeeded in the satisfactory perioperative management of the patient.

Anesthesia, General↗

[Transdermal nitroglycerin before induction of anesthesia prevents redistribution hypothermia in patients under general anesthesia].

Initial anesthesic-induced hypothermia results largely from core-to-peripheral redistribution of heat. Administration of transdermal nitroglycerin induces vasodilation. Such vasodilation, induced well before induction of anesthesia, might redistribute heat to peripheral tissues. Minimal redistribution hypothermia might accompany subsequent induction of anesthesia. We studied 32 patients undergoing gastrointestinal surgery. Thirty minutes before induction of anesthesia, they were randomly assigned to: 1. transdermal nitroglycerin 10 mg; 2. transdermal nitroglycerin 5 mg; and, 3. control. Core temperature during the first hour of anesthesia decreased significantly more in the control patients than in those given either dose of nitroglycerin. Vasodilation induced by transdermal nitroglycerin before induction of anesthesia significantly decreased subsequent redistribution hypothermia. Drug-induced modulation of vascular tone thus produces clinically important alterations in intraoperative core temperature.

Administration, Cutaneous↗

Release of opioid peptides, gluten exorphins by the action of pancreatic elastase.

The release of opioid peptides, gluten exorphins A, which have been isolated from the pepsin-thermolysin digest of wheat gluten, with gastrointestinal proteases was examined. High levels of gluten exorphin A5 (Gly-Tyr-Tyr-Pro-Thr) immunoreactive materials were detected in the pepsin-pancreatic elastase digest by a competitive ELISA. From this digest, gluten exorphin A5, B5 and B4 were isolated. This means that these peptides are released in the gastrointestinal tracts after ingestion of wheat gluten. The yield of gluten exorphin A5 in the pepsin-elastase digest was larger than that in the pepsin-thermolysin digest. The gluten exorphin A5 sequence is found 15 times in the primary structure of the high molecular weight glutenin. The region from which gluten exorphin A5 was released by the action of pancreatic elastase was identified using synthetic fragment peptides.

Cross Reactions↗

Analysis of chromatin structure of rat alpha1-acid glycoprotein gene; changes in DNase I hypersensitive sites after thyroid hormone, glucocorticoid hormone and turpentine oil treatment.

Transcription of the ratalpha1-acid glycoprotein (AGP) gene is activated by glucocorticoid, thyroid hormone (T3) and cytokines. Following these treatments, the chromatin structure of this gene was analyzed by means of digestion with DNase I or micrococcal nuclease. Four DNase I hypersensitive sites were observed in the 5'-upstream region of the rat AGP gene of liver cells. They were designated HS1, HS2, HS3 and HS4 (3'-->5'). After T3treatment the sensitivity of HS1 and HS2 increased and after dexamethasone (Dex) treatment that of all four sites did so. Three new sites appeared after turpentine oil treatment, while the sensitivities of HS3 and HS4 increased. We conclude that transcriptional activation of the gene by T3and Dex have very similar mechanisms, but that at the inflammation stage they become slightly different. The increase in sensitivity at HS1 and HS2 after T3treatment in vivo was successfully reproduced in a cell-free system by in vitro treatment with T3. HS1, HS2 and HS3 were also sensitive for micrococcal nuclease.

Animals↗

Parallel polarization electron paramagnetic resonance studies of the S1-state manganese cluster in the photosynthetic oxygen-evolving system.

Magnetic properties of the S1-state manganese cluster in the oxygen-evolving photosystem II were studied by parallel polarization electron paramagnetic resonance spectroscopy. Dark minus light spectra gave rise to a broad S1-state signal with a g value of about 4.9 [Dexheimer, S. L., Klein, M. P. (1992) J. Am. Chem. Soc. 114, 2821-2826]. Temperature variation of the signal intensity between 1.9 and 10 K observed in PS II with a sucrose buffer indicates that the signal originates from an excited state with a spin S of 1 with separation from the ground state (S = 0) of about 2.5 K. The S1-state signal was also observed in the sucrose buffer supplemented by 50% glycerol. However, no S1-state signal was detected by addition of 3% methanol or 30% ethylene glycol in the sucrose buffer, although illumination at 200 K in the presence of these alcohols induced the normal multiline S2 signal. Furthermore, modification of the Mn cluster by Cl- or Ca2+ depletion from PS II membranes failed to produce a detectable S1-state signal. A possible magnetic structure of the Mn cluster responsible for the generation of the S1-state signal is discussed on the basis of these observations.

Buffers↗

Effect of heat stress on muscle sympathetic nerve activity in humans.

To elucidate the effect of heat stress on the sympathetic nervous system, we evaluated changes in muscle sympathetic nerve activity (MSNA), plasma arginine vasopressin (AVP), tympanic temperature, skin blood flow, cardiac output, mean blood pressure, and heart rate in 9 subjects in response to acute heat stress induced by raising the ambient temperature from 29 to 34 degrees C and then to 40 degrees C. With the heat exposure, MSNA was significantly increased with a significant increase in tympanic temperature. Skin blood flow and heart rate were also significantly increased, while mean blood pressure tended to decline and cardiac output tended to increase. The combination of the increased MSNA and skin blood flow may have caused the redistribution of the circulatory blood volume from the muscles to the skin, facilitating convection heat loss. The increases in MSNA counteracted the lowered blood pressure during heat exposure. Thus, the increased MSNA may play an important role both in thermoregulation and in the maintenance of blood pressure against heat stress.

Adult↗

Comparison of distal oesophageal temperature with "deep" and tracheal temperatures.

PURPOSE: To compare distal oesophageal (reference) temperature with "deep-sternal," "deep-forehead," and tracheal temperatures, establishing the accuracy and precision of each. METHODS: We studied 20 patients undergoing general anaesthesia for gynaecological surgery. Their lungs were mechanically ventilated with a circle system, at a fresh-gas flow rate of 6 L.min-1 Respiratory gases were not warmed or humidified. Tracheal temperatures were recorded from a Trachelon tube inserted approximately 21 cm. Deep-body temperatures were measured at the sternum and forehead using a Coretemp thermometer. The principle of the method is to null thermal flux through a cutaneous disk, thus obliterating thermal gradients between the sides of the disk, skin surface, and subcutaneous tissues. Distal oesophageal temperatures were measured from thermocouples incorporated into oesophageal stethoscopes. Tracheal and deep-tissue temperatures were compared with oesophageal temperature using regression and Bland and Altman analyses. RESULTS: Tracheal, sternal, and forehead temperatures correlated similarly with distal oesophageal temperature, correlation coefficients (r2) being 0.7 in each case. The offset (oesophageal temperature minus study site) was considerably larger for tracheal temperature (0.7 degree C) than for the other sites (0.2 degree C). However, the precision was only 0.3 degree C at each site. CONCLUSION: Our data suggest that tracheal temperatures may not be an adequate substitute for conventional core-temperature monitoring sites. In contrast, the accuracy and precision of deep-tissue temperature monitoring at the sternum and forehead was sufficient for clinical use.

Anesthesia, General↗

Interactions between nicardipine and enflurane, isoflurane, and sevoflurane.

PURPOSE: During nicardipine induced hypotension, different inhalational anaesthetics may have different effects on haemodynamic variables, sympathetic function and drug metabolism. Therefore, the haemodynamic effects and pharmacokinetics of nicardipine were studied in the presence of the three inhalation anaesthetics enflurane, isoflurane and sevoflurane. METHODS: Thirty patients scheduled for neurosurgery were randomly assigned to one of three anaesthetic techniques: enflurane, isoflurane or sevoflurane. Nicardipine (0.017 mg.kg-1) was administered during stable anaesthesia and the following measurements made for 30 min: blood pressure, heart rate, and plasma concentration of norepinephrine, epinephrine and nicardipine. RESULTS: With sevoflurane, plasma concentrations of nicardipine, five minutes after administration, (39.8 +/- 3.5 ng.ml-1, mean +/- SEM) were higher (P < 0.05) than in the other two groups (28.3 +/- 2.9 ng.ml-1, 32.6 +/- 4.3 ng.ml-1, enflurane and isoflurane, respectively). With isoflurane, the approximated half-life of nicardipine (14 +/- 4 min) was shorter and clearance (2.1 +/- 0.3 l.min-1) more rapid. Peak heart rates were similar in all groups but elevated rates continued longer with isoflurane (> 30 min). Nicardipine-induced reduction in blood pressure was greater with sevoflurane but low pressures persisted for longer with isoflurane. Plasma catecholamine concentrations increased with isoflurane and enflurane, but not with sevoflurane: considerably higher epinephrine concentrations were seen with isoflurane. CONCLUSION: This study showed that the action of nicardipine is modified by different inhalational anaesthetic agents. Nicardipine has a prolonged duration of action in the presence of isoflurane and produces greater initial hypotension with sevoflurane.

Adult↗

Percutaneous microwave coagulation therapy in liver tumors. A 3-year experience.

PURPOSE: Percutaneous microwave coagulation therapy (PMCT) is an interventional alternative for inoperable malignant liver tumors. In this paper, we report the results of our 3-year experience of PMCT in order to establish suitable indications for this treatment. MATERIAL AND METHODS: We studied a total of 27 inoperable liver tumors in 24 patients. Histology of the tumors showed 20 hepatocellular carcinomas (HCCs) (13 well differentiated, 4 moderately differentiated, and 3 poorly differentiated) and 7 metastases. These tumors were treated by PMCT and were followed for 4-40 months (average 18 months). Under US guidance, the tumors were coagulated by microwaves emitted from an electrode. The changes of tumor size after PMCT were evaluated by CT. When the tumors disappeared or were reduced in size after treatment, PMCT was regarded as effective. Complications from PMCT were also evaluated. The patient survival rate was obtained by means of the Kaplan-Meier method. RESULTS: In tumors of 30 mm or less, treatment response was obtained in 70% of cases, while 55% of tumors larger than 30 mm responded. The tumor became smaller or disappeared in 85% of the well differentiated HCCs, and in 25% of the moderately differentiated HCCs, but none of the poorly differentiated HCCs responded. In metastatic tumors, PMCT was effective in 57% of cases. Slight pain (24%), fever (20%) and subcutaneous hematoma (8%) were experienced immediately after PMCT. In 2 poorly differentiated HCCs, needle tract seeding was observed. No case of liver dysfunction was seen after PMCT. The overall survival rate was 83.1% at 1 year and 68.7% at 2 years. CONCLUSION: Good therapeutic results were achieved with PMCT in lesions of 30 mm or less, and in well differentiated HCCs.

Aged↗

I.m. midazolam as premedication produces a concentration-dependent decrease in core temperature in male volunteers.

We tested the hypothesis that premedication with i.m. midazolam decreases core temperature dose-dependently. We studied six male volunteers, in random order, on 3 days: (1) no midazolam administration (control day), (2) midazolam 0.025 mg kg-1 i.m., (3) midazolam 0.075 mg kg-1 i.m. On the first day, subjects were maintained alert during a 30-min control period. On the second and third days, midazolam 0.025 or 0.075 mg kg-1 was administered i.m. Core temperatures were measured at the right tympanic membrane. Four adhesive skin surface probes were fixed on the chest, upper right arm, lateral calf and thigh. Finger tip perfusion was evaluated using forearm minus fingertip and calf minus toe, skin surface temperature gradients. Thirty minutes after midazolam i.m., the level of sedation in the volunteers was assessed. Peripheral venous blood was obtained immediately after the assessment of the level of sedation. Tympanic membrane temperatures after administration of midazolam 0.075 mg kg-1 i.m. were significantly lower than those on the control and midazolam 0.025 mg kg-1 i.m. days at 20 and 30 min. The decreases in tympanic membrane temperatures at 30 min after midazolam i.m. became larger as the volunteers were more deeply sedated. i.m. midazolam produced a concentration-dependent decrease in tympanic membrane temperature at 30 min after midazolam 0.025 and 0.075 mg kg-1 i.m. We conclude that midazolam impaired tonic thermoregulatory vasoconstriction, allowing core-to-peripheral heat redistribution in a dose-dependent manner after i.m. administration.

Adult↗

The threshold for thermoregulatory vasoconstriction during nitrous oxide/sevoflurane anesthesia is reduced in the elderly.

Elderly patients become more hypothermic during surgery, shiver less postoperatively, and take longer to rewarm than younger patients. Similarly, the vasoconstriction threshold (triggering core temperature) is reduced approximately 1 degree C in elderly patients during nitrous oxide/isoflurane anesthesia. Accordingly, we tested the hypothesis that the vasoconstriction threshold in the elderly is also reduced approximately 1 degree C during nitrous oxide and sevoflurane anesthesia. Eleven young patients aged 30-50 yr and 14 elderly patients aged 60-80 yr were anesthetized with nitrous oxide (50%) and sevoflurane (1%). Mean skin temperature was calculated from four sites. Fingertip blood flow was estimated using forearm minus fingertip skin-temperature gradients, with a gradient of 0 degree C identifying onset of vasoconstriction. The distal esophageal temperature triggering onset of vasoconstriction identified the threshold for this thermoregulatory defense. The data from five patients who did not vasoconstrict at minimum core temperatures of 33-34 degrees C were eliminated, leaving 10 patients in each group. The vasoconstriction threshold was significantly less in the elderly (35.0 +/- 0.8 degrees C) than in younger patients (35.8 +/- 0.3 degrees C), despite similar mean skin temperatures (mean +/- SD, P < 0.01, Student's t-test). Age dependence of thermoregulatory vasoconstriction during nitrous oxide/sevoflurane anesthesia is similar to that previously observed during nitrous oxide/isoflurane anesthesia.

Adult↗

A rapid increase in foot tissue temperature predicts cardiovascular collapse during anaphylactic and anaphylactoid reactions.

BACKGROUND: Cardiovascular collapse during anaphylactic and anaphylactoid reactions results from release of histamine and other vasoactive substances. Intense arteriolar vasodilation associated with severe allergic reactions is likely to increase convective transfer of heat and peripheral tissue temperature, and finally to provoke cardiovascular collapse. Therefore the authors tested the hypothesis that during anaphylactic and anaphylactoid reactions, an acute increase in peripheral tissue temperature precedes cardiovascular collapse and that the magnitude of the increase correlates with the severity of the reaction. METHODS: During a 13-yr period, approximately 120,000 patients were screened for clinical evidence of intraoperative anaphylactic and anaphylactoid reactions. Core temperature was measured in the distal esophagus, and "deep" foot tissue temperature was measured on the sole of one foot in all these patients. Otherwise unexplained cardiovascular collapse accompanied by bronchospasm and/or cutaneous signs such as urticaria, flushing, or angioedema occurred in 32 patients who were entered into a prospective diagnostic protocol. Among these, 15 met laboratory criteria for anaphylactic or anaphylactoid reactions. Anaphylaxis was confirmed in nine of them by a positive skin test to the suspected agent, the in vitro leukocyte histamine-release test, or the Praunitz-Küstner test. Reactions were considered anaphylactoid in six others when laboratory evidence did not support anaphylaxis, but plasma histamine or tryptase concentrations were much greater during episodes than 6 weeks later. RESULTS: Development of anaphylactic and anaphylactoid reactions followed a characteristic pattern: (1) Foot temperature, which was initially 3.3 +/- 1.7 degrees C less than core temperature, increased to within 0.3 degrees C of core temperature 3.2 +/- 1.4 min after drug administration; (2) onset of cardiovascular collapse ensued 1.8 +/- 0.8 min later; and (3) core temperature increased from 34.7 +/- 1.0 degrees C to peak values 37.1 +/- 0.6 degrees C 13 +/- 5 min after drug administration. The most severe reactions were associated with shorter times to comparable core and foot temperatures, faster onset of cardiovascular collapse, and higher maximum core temperatures. CONCLUSIONS: The normal core-to-peripheral tissue temperature gradient was obliterated several minutes before hemodynamic consequences associated with anaphylactic and anaphylactoid reactions. Further, a rapid increase in deep foot temperature and maximum core temperature correlated with clinical severity.

Adolescent↗

Sympatho-vagal responses in humans to thermoneutral head-out water immersion.

To clarify the role of autonomic nervous functions in cardiovascular adaptation to microgravity, heart rate variability (HRV) and blood pressure variability (BPV) were evaluated during thermoneutral head-out water immersion (HOI) of eight healthy young subjects 23 to 31 yr of age. The very low-frequency (VLF; 0.00-0.04 Hz) component of BPV tended to increase during HOI, whereas the low-frequency (LF; 0.04-0.15 Hz) component of BPV and the ratio of LF power to high-frequency (HF; 0.15-0.40 Hz) component (LF/HF ratio) of HRV decreased. The HF component of HRV increased in all the subjects during immersion up to the shoulder. Concomitantly, we found a decrease in heart rate and increases in stroke volume and cardiac output with no significant changes in BP and respiration rate during HOI. These results suggest that both vasomotor and cardiac sympathetic activities are suppressed and that the parasympathetic (vagal) activity is enhanced during HOI.

Adult↗

Skin sympathetic nerve activity and event-related potentials during auditory oddball paradigms.

Skin sympathetic nerve activity (SSNA) from the tibial nerve and event-related brain potentials (ERPs) were recorded simultaneously during auditory oddball paradigms with a counting task in 10 healthy subjects to elucidate the relationships between the autonomic nervous system and the cognitive process. After the target tones. SSNA bursts were observed more frequently than after the non-target tones. Moreover, the amplitudes of SSNA bursts elicited after the target tones were higher than those elicited after the non-target tones. However, when subjects ignored the series of tones, there was no significant difference between the incidence of SSNA bursts after rare tones and frequent tones. The P300 latencies for the target trials with SSNA bursts were shorter than those for the target trials without SSNA bursts. The average ERP wave forms for the target trials with SSNA bursts showed larger positive deflection in the early part of the P300 component than those for the target trials without SSNA bursts. We conclude that SSNA is generated in relation to the conscious cognitive process, as well as to the reactive automatic process to changes in repeating stimuli. The early part of the P300 component, possibly P3a, may be related to the mechanisms that generate SSNA.

Adult↗

Age-related changes in baroreflex control of heart rate and sympathetic nerve activity in healthy humans.

To determine how the baroreflex control of sympathetic nerve activity is affected by aging, muscle sympathetic nerve activity (MSNA) from the tibial nerve was monitored using microneurography, and heart rate and blood pressure were recorded during the pressor or depressor responses to intravenous injections of phenylephrine or nitroglycerin in 39 healthy humans, aged 16 to 56 years. Although the baroreflex slope for heart rate showed attenuation with aging, the baroreflex slope for MSNA was not affected by aging. These data suggest preservation of the baroreflex control of sympathetic nerve activity despite attenuation of the baroreflex control of parasympathetic nerve activity by aging in humans.

Adolescent↗

Effect of metoclopramide on muscle sympathetic nerve activity in humans.

The aim of this study was to determine the effect of metoclopramide on the sympathetic nervous system. Muscle sympathetic nerve activity was increased in two stages after metoclopramide injection. The initial increase in sympathetic nerve activity may result from the unloading of arterial baroreceptors because there was a negative correlation between mean blood pressure and muscle sympathetic nerve activity. The later increase in muscle sympathetic nerve activity may be attributed to the central activation of the sympathetic nervous system because there was a positive correlation between mean blood pressure and muscle sympathetic nerve activity. These results suggest that metoclopramide activates the sympathetic nervous system by two different mechanisms.

Adrenergic Fibers↗

Procaine microinjection into the lower midbrain increases brown fat and body temperatures in anesthetized rats.

A tonic inhibitory mechanism on heat production was studied by microinjecting procaine into various regions of the brain while recording temperature changes of the interscapular brown adipose tissue (IBAT) and rectum in urethane-anesthetized rats at room temperature of 23-25 degrees C. Procaine microinjected bilaterally (10%, 1.0 mu l/site, 1.5 mm to midline) into the midbrain and the upper- to mid-pontine area of the reticular formation increased temperatures of the IBAT and rectum. The highest temperature rise (1.02 +/- 0.11 degrees C for IBAT, 0.64 +/- 0.06 degrees C for rectum) with the shortest onset latency (1.5 +/- 0.3 min for IBAT, 4.6 +/- 1.1 min for rectum) was observed when procaine was injected into the lower midbrain (the area between 6 and 7 mm posterior to the bregma, and 6.5 to 8.5 mm deep from the cortical surface). These regions include the retrorubral field, pedunculopontine tegmental nucleus, and rubrospinal tract. Procaine-induced IBAT and rectal temperature increases were dose-dependent, and reproduced reliably from the same injection site of the same animal. Intravenous indomethacin, a prostaglandin H synthase inhibitor, did not affect procaine-induced temperature rise, and propranolol, a beta-blocker, completely blocked it. These results suggest that microinjected procaine exerts its local anesthetic effect and release a tonic inhibition resulting in a disinhibition-induced temperature increase through the enhanced central sympathetic outflow. They support the hypothesis that a bilateral tonic inhibitory mechanism on heat production exists in the lower midbrain.

Adipose Tissue, Brown↗

A comparison of four infrared tympanic thermometers with tympanic membrane temperatures measured by thermocouples.

PURPOSE: To compare measurements made with four infrared tympanic thermometers (Genius, Thermopit, Quickthermo, and Thermoscan) with those recorded from thermocouples positioned in the contralateral ear. METHODS: Four tympanic thermometers were evaluated in 50 healthy volunteers (12 female and 38 male). Temperatures were measured, in random order, at the right tympanic membrane four times and the highest temperature was considered to be the true value measured by each thermometer. The control temperature was measured at the left tympanic membrane using Mon-a-Therm thermocouples. RESULTS: The tympanic membrane temperature measured by Genius correlated best with the Mon-a-therm measurement (TM) (r = 0.74). The tympanic membrane temperatures measured by Thermopit, Quickthermo, and Thermoscan correlated moderately with TM (r = 0.56, 0.63, and 0.58, respectively). Mean differences between TM and each temperature (TG, TTP, TQ, and TTS) were -0.3, 0.73, 0.42, and -0.3 degrees C, respectively. Likewise standard deviations were 0.33, 0.37, 0.35, and 0.35. CONCLUSION: We conclude that all but the Thermopit (TTP) are similarly useful for the management of patients during anaesthesia.

Adult↗