PubMed Health⌕ Search

Biomedical subjects

D Sadamitsu

Publications and source records attributed to D Sadamitsu.

At least 19 recordsLinked to original sources
PubMed2001

Apoptotic and necrotic brain lesions in a fatal case of carbon monoxide poisoning.

A 41-year-old man was accidentally exposed to carbon monoxide (CO) gas and found in a state of cardiopulmonary arrest while he took bath. After admission, he was resuscitated and underwent artificial ventilation in a comatose state and died about 19h later. Computed tomography (CT) examination disclosed bilateral low density area in the basal ganglia and the thalamus, a well-known finding in the CO intoxication. Necropsy, histological examination, DNA ladder assay gave the first line of evidence for the presence of apoptosis as well as necrosis in the human case of CO intoxication. TdT-mediated dUTP-biotin nick-end labeling (TUNEL) positive apoptotic cells were more predominant in the CA2 area than in CA1 area. There is general co-relation between the ratio of TUNEL-positive cells and the DNA laddering on the agarose gel. Basal ganglia and thalamus, which showed bilateral low density area in CT, were revealed to be severe edema. The two types of cell death occurred in the cortex, basal ganglia, hippocampus, thalamus, and cerebellum. Hypoxia caused by CO-hemoglobin formation alone cannot explain the phenomena.

Adult↗
PubMed2001

Catalase catalyzes nitrotyrosine formation from sodium azide and hydrogen peroxide.

Sodium azide (NaN3) is known as an inhibitor of catalase, and a nitric oxide (NO) donor in the presence of catalase and H2O2. We showed here that catalase-catalyzed oxidation of NaN3 can generate reactive nitrogen species which contribute to tyrosine nitration in the presence of H2O2. The formation of free-tyrosine nitration and protein-bound tyrosine nitration by the NaN3/catalase/H2O2 system showed a maximum level at pH 6.0. Free-tyrosine nitration induced by peroxynitrite was inhibited by ethanol and dimethylsulfoxide (DMSO), and augmented by superoxide dismutase (SOD). However, free-tyrosine nitration induced by the NaN3/catalase/H2O2 system was not affected by ethanol, DMSO and SOD. NO2- and NO donating agents did not affect free-tyrosine nitration by the NaN3/catalase/H2O2 system. The reaction of NaN3 with hydroxyl radical generating system showed free-tyrosine nitration, but no formation of nitrite and nitrate. The generation of nitrite (NO2-) and nitrate (NO3-) by the NaN3/catalase/H2O2 system was maximal at pH 5.0. These results suggested that the oxidation of NaN3 by the catalase/H2O2 system generates unknown peroxynitrite-like reactive nitrogen intermediates, which contribute to tyrosine nitration.

Animals↗
PubMed2001

Cerebrospinal fluid and plasma concentrations of nitric oxide metabolites in postoperative patients with subarachnoid hemorrhage.

OBJECTIVE: To measure cerebrospinal fluid and plasma concentrations of nitrate and nitrite as indicators of nitric oxide production in adults after subarachnoid hemorrhage (SAH). DESIGN: A prospective, clinical study. SETTING: Multidisciplinary intensive care unit. PATIENTS: Nine patients (three males and six females, aged 29-64 yrs) with aneurysm-induced SAH were studied. Glasgow Coma Scale score on admission ranged from 9 to 15. Ruptured aneurysms were clipped within 72 hrs of ictus, and then conventional hypervolemic, hemodilution, and induced hypertension methods were applied. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Nitrate and nitrite concentrations of patients were examined sequentially by a capillary zone electrophoresis every day for 13 days. As a control group, cerebrospinal fluid was sampled from patients (n = 9, six males and three females, aged 30-60 yrs) without neurologic disorders who underwent spinal taps for spinal anesthesia, and plasma from healthy human volunteers (n = 43, 21 males and 22 females, aged 23-49 yrs). There were no significant differences over time in cerebrospinal fluid nitrate concentrations after SAH. Concentrations of cerebrospinal fluid nitrate after SAH were increased compared with control values. Plasma nitrate concentration was decreased compared with control values, but the value on day 14 was increased significantly (p < .05) compared with those during days 2-11. Plasma and cerebrospinal fluid nitrite concentrations after SAH were similar to those in control subjects. Similar concentrations of nitric oxide metabolite in plasma and cerebrospinal fluid were observed between the patients with and without symptomatic vasospasm. CONCLUSION: The increase of cerebrospinal fluid nitrate after SAH may attribute to the endogenous nitric oxide production in the injured brain.

Adult↗
PubMed2000

Angiotensin-converting enzyme inhibitor inhibits dehydration-enhanced fever induced by endotoxin in rats.

It has been reported that a host develops a marked fever under dehydrated conditions compared with normally hydrated conditions (11). The present study was carried out to investigate whether ANG II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. The results showed that intravenous injection of bacterial endotoxin produced a fever in dehydrated rats (rats deprived of water for 24 h) that was significantly greater than that seen in normally hydrated rats. In contrast, dehydration had no effect on the fever induced by intravenous interleukin-1beta (IL-1beta). Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1beta fever was not. These results suggest that the dehydration-induced enhancement of endotoxin fever is due, at least in part, to the action of ANG II, which elicits an increased production of pyrogenic cytokines such as IL-1.

Analysis of Variance↗
PubMed2000

Cerebral circulation and prognosis of the patients with hypoxic encephalopathy.

Recent progress in cardiopulmonary resuscitation techniques improved the survival rate of patients with acute cardiopulmonary disturbances. However, severe cerebral complications remained frequently in patients who survived the acute stage. Early prediction of cerebral prognosis is important to optimize the management of these patients. We examined the relations between radiological findings (Xe-CT and MRI) and cerebral prognosis. Patients included in this study were selected from all patients with hypoxic encephalopathy admitted to our hospital. There were 11 men and 10 women. Causes of hypoxic encephalopathy were heart disease (11 cases), suffocation (4 cases), CO intoxication (2 cases), asthma (1 case), pneumothorax (1 case), anaphyraxy shock (1 case) and electric shock (1 case). Xe-CT and MRI were carried out 3 weeks after the onset. Cerebral blood flow (CBF) of the patients was measured at rest and 15 minutes after intravenous administration of acetazolamide (1 g). The prognosis was evaluated 3 months after the onset in accordance with Glasgow Outcome Scale (GOS). Low hemispheric CBF (30 ml/100 g/min), poor reactivity of acetazolamide challenge test (10 ml/100 g/min), presence of hyperintensity areas in the basal ganglia in T1 weighted images (T1WI) and T2 weighted images (T2WI) are the factors associated with poor outcome in hypoxic encephalopathy.

Acetazolamide↗
PubMed1999

Nitric oxide release from coronary vasculature before, during, and following cardioplegic arrest.

Nitric oxide (NO) is known as a vasodilatory molecule synthesized by vascular endothelium. The NO-dependent vasodilatory response of coronary artery is impaired after ischemia and reperfusion. In the present study, the release of NO from coronary vasculature was evaluated before and during cardioplegic arrest and after reperfusion. Nine patients undergoing heart surgery were studied. Multidose crystalloid cardioplegics were used for myocardial protection. The coronary affluent and effluent were obtained simultaneously before cardioplegic arrest, at each cardioplegic administration, and after reperfusion; and the levels of nitrite and nitrate, the stable end-products of NO, were measured. The NO release from the coronary vasculature was determined as the difference in the levels of nitrite and nitrate between the coronary effluent and affluent. The level of nitrite/nitrate release from coronary vasculature was 6.8 +/- 3.7 microM before cardioplegic arrest. During cardioplegic arrest the nitrite/nitrate release decreased, reaching 1.3 +/- 1.3 microM (p < 0.05, vs. before cardioplegic arrest) at the fourth administration of the cardioplegic. At 3 to 5 minutes after reperfusion, nitrite/nitrate release further decreased to 0.36 +/- 0.34 microM (p < 0.05, vs. before cardioplegic arrest). During cardioplegic arrest the NO release decreased and reached significance at approximately 70 minutes of cardioplegic arrest compared to that before cardioplegic arrest. After reperfusion, NO release was further reduced, with statistical significance compared to that before cardioplegic arrest. Our data may indicate that cardioplegic arrest and reperfusion cause endothelial dysfunction.

Aged↗
PubMed1999

Nonclostridial gas gangrene due to Streptococcus anginosus in a diabetic patient.

Streptococcus anginosus was recently identified as a distinct species from the other members of Streptococcus milleri group (Streptococcus constellatus, Streptococcus intermedius). We report a rare case of nonclostridial gas gangrene caused by S. anginosus. A 62-year-old diabetic woman was admitted with gas gangrene of the perineal area. She had been taking her oral hypoglycemia medication regularly for 10 years, but the diabetes was inadequately controlled. She was treated with surgical debridement of the necrotic tissue, insulin injection, and antibiotic therapy, and had a satisfactory clinical course.

Diabetes Mellitus, Type 2↗
PubMed1999

Glucocorticoid enhances interleukin-1-induced pressor response in freely moving rats through its effect on nitric oxide release.

We investigated whether changes in nitric oxide (NO) release might be responsible for the modulation by glucocorticoids of the pressor response to i.p. injection of interleukin-1beta (IL-1beta) in freely moving rats. In such rats, IL-1beta (10 microgram/kg) induced a biphasic pressor response, with a rise in the plasma concentration of NOx (NO2(-) and NO3(-): metabolites of NO) during the second phase. Systemic pretreatment with an exogenous glucocorticoid, dexamethasone (0.5 mg/kg), enhanced the second phase of the pressor response and completely suppressed the increase in plasma NOx. Treatment with Nomega-nitro-L-arginine methyl ester (L-NAME, a nonspecific NO synthase inhibitor), enhanced the pressor response while attenuating the increase in plasma NOx. After bilateral adrenalectomy, IL-1beta induced a smaller pressor response, but a larger increase in plasma NOx; dexamethasone reversed these changes. Our results suggest that endogenous NO moderates the pressor response to IL-1beta in freely moving rats, and that glucocorticoids enhance the IL-1beta-induced pressor response at least in part by reducing endogenous NO release.

Adrenalectomy↗
PubMed1999

[Diagnosis of malaria by allele-specific PCR].

Malaria is relatively rare in Japan. Of 13 patients referred to our laboratory for malarial screening in the past 4 years, malarial parasites were detected in 8. Conventional screening procedures commonly detect hepatic dysfunction, thrombocytopenia, elevated LDH activity, and increased CRP levels in malaria patients. More notably, the 8 malaria patients identified by our laboratory also demonstrated reactive lymphocytosis. In the absence of additional clinical information, reactive lymphocytosis alone may be enough to warrant laboratory blood smear tests on the suspicion of malaria. Conventional microscopic methods have often proved inconclusive in identifying malarial parasite species or detecting mixed infections. However, by combining the methods of DNA analysis with those of microscopy, we were able to conclusively diagnose all cases of suspected malaria. As a test of their skills, 9 laboratory technicians relatively inexperienced with malarial parasites were asked to screen 6 samples: 3 containing malarial parasites, and 3 that were malaria-free. Although none of the technicians were able to accurately identify the samples without additional clinical information, 4 accurately identified all malarial samples when that information was provided. Experience is a crucial determinant of ability to detect malarial parasites by microscopic methods alone. Nonetheless, the findings of our study suggested the diagnostic accuracy of laboratory screening procedures for malaria can be significantly improved if combined with minimal clinical data and the techniques of DNA analysis.

Adult↗
PubMed1998

Long-term heart rate fluctuations in postoperative and brain-dead patients.

Long-term heart rate fluctuations in postoperative and brain-dead patients were investigated. Heart rates were monitored continuously, and the data were stored, edited, and interpolated to allow for data lost during calibration and disconnection of the sensors for various treatments. Heart rate power spectra were calculated using the fast Fourier transform method. The power spectra of the patients who recovered showed that the heart rate fluctuated and produced a 1/f relationship, termed 1/f fluctuations, whereas those of patients who died in the intensive care unit (ICU) consisted of white-noise-like signals. The power spectra in brain-dead patients showed a 1/f relationship under steady-state conditions, while the power density and variation of the frequency distribution were lower than those in a normal subject. Therefore, 1/f fluctuations appear to be universal and occur independent of the central nervous system.

Blood Pressure↗
PubMed1998

[Spinal cord stimulation therapy at an early stage for unresponsive patients with hypoxic encephalopathy].

Recently, spinal cord stimulation (SCS) has been used for the treatment of patients in prolonged coma. However, the results of SCS in unresponsive patients with hypoxic encephalopathy at the chronic stage have not been satisfactory. Considering these circumstances, we began SCS from one month after the onset of hypoxic encephalopathy and evaluated its effect. Twelve patients (5 males and 7 females) with hypoxic encephalopathy, ranging in age from 7 to 72 years, were treated with SCS. The causes of hypoxia were acute cardiac failure in 4, automobile exhaust gas poisoning in 2, and asthma, pneumothorax, anaphylaxis, asphyxia, drowning and hypotension during aortic surgery in one patient each. One month after the onset, an electrode for electrical stimulation was implanted in the epidural space at the C2-C4 level under general anesthesia. The spinal cord was stimulated for 8 hours each day, starting on the day after implantation, and was continued for 3 months. Magnetic resonance imaging (MRI), cerebral blood flow (CBF) measurement using xenon-computed tomography (Xe-CT), and measurement of auditory evoked potential (AEP) and somatosensory evoked potential (SEP) were carried out 3 weeks after the onset for presurgical evaluation. Among the 12 patients, 7 (58%) showed clinical improvement, beginning within two weeks after starting stimulation. They were able to communicate with others and to express their emotion. However, disturbance of writing, picture drawing and calculation were not improved by stimulation. From presurgical evaluation, cases in which SCS therapy was effective had the following features: 1) No hemorrhagic infarction in the basal ganglia was demonstrable by MRI. 2) Mean hemispheric CBF measured by the Xe-CT method exceeded 25 ml/100 g per min. 3) The mean increase in hemispheric CBF 20 min after acetazolamide administration exceeded 5 ml/100 g per min. 4) An N20 peak was evident on the median nerve SEP, SCS appears to be an effective supplementary for unresponsive patients with hypoxic encephalopathy at the subacute stage, in addition to rehabilitation and drug therapy.

Adolescent↗
PubMed1997

Effects of mild hypothermia on nitric oxide synthesis following contusion trauma in the rat.

The exact mechanism of hypothermic cerebroprotection after traumatic brain injury (TBI) is not fully understood. The present study was conducted to investigate the effects of mild hypothermia on trauma-induced synthesis of nitric oxide (NO), which has been implicated in the pathogenesis of ischemic brain damage associated with glutamate neurotoxicity. Cerebral contusion was created in the rat parietal cortex by a weight-drop method, and extracellular concentrations of the NO end products nitrite and nitrate were measured using in vivo brain microdialysis and capillary electrophoresis under normothermic (37 degrees C) and mild hypothermic (32 degrees C) conditions. In normothermic animals, the level of NO end products increased markedly 10 min after contusion, reaching a maximum level at 20 min. In the hypothermic rats, such increases were absent. Although it is unknown whether endothelial NO synthase, neuronal NO synthase, or both caused the elevation of the NO end products seen in the normothermic animals, the present results indicate that inhibition of NO synthesis may play a part in hypothermic cerebroprotection following TBI.

Animals↗
PubMed1996

Nitric oxide concentrations in the follicular fluid and apoptosis of granulosa cells in human follicles.

To study the relationship between follicular atresia, apoptosis, and nitric oxide (NO) generation in follicular development, steroidogenesis, NO levels in follicular fluid and apoptosis were analysed in the various sized follicles of women receiving ovarian stimulation with human menopausal gonadotrophin (HMG)-human chorionic gonadotrophin (HCG) treatments for in-vitro fertilization (IVF)-embryo transfer. The follicles were divided into three groups by diameter: large follicle, > or = 18 mm; medium follicle, > or = 12 and < or = 15 mm; small follicle, < or = 10 mm. Follicular fluid was obtained from 20 women 34 h after HCG administration, and the concentrations of oestradiol, progesterone and testosterone, and nitrite, nitrate, arginine and citrulline were measured. Granulosa cells obtained from each group of follicular fluid were stained with Hoechst dye, and nuclear morphology was examined by a fluorescence microscopy. Oestradiol and progesterone concentrations in large follicles were significantly (P < 0.01) higher than those in medium or small follicles, and testosterone concentrations in small follicles were significantly (P < 0.01) higher than those in large follicles. There were no significant differences in the concentrations of nitrite, nitrate, arginine and citrulline among three groups. The percentage of apoptotic cells with nuclear fragmentation was significantly (P < 0.01) higher in small follicles than in large follicles. The present results suggested that small follicles with poor response to HMG may undergo atresia through apoptosis. No significant difference in the follicular NO level between large and small follicles led us to speculate on a different responsiveness to NO in these two types of follicles.

Adult↗
PubMed1996

Effect of intravenous magnesium sulfate on cardiac arrhythmias in critically ill patients with low serum ionized magnesium.

Magnesium affects cardiac function, although until the recent development of a new ion-selective electrode no method existed for measuring the physiologically active form of magnesium, free ions (iMg2+), in the blood. We investigated the antiarrhythmic effect of magnesium sulfate administered to critically ill patients with cardiac arrhythmias and reduced iMg2+ as determined using the ion-selective electrode. Eight patients with a low iMg2+ level (less than 0.40 mmol/L) were given intravenous magnesium sulfate (group L). Magnesium sulfate was also administered to patients with a normal iMg2+ level (more than 0.40 mmol/L) but who did not respond to conventional antiarrhythmic drugs (group N). Intravenous magnesium sulfate significantly increased the iMg2+ level in patients in group L from 0.35 +/- 0.06 mmol/L (mean +/- SD) to 0.54 +/- 0.09 mmol/L (p < 0.01), and had an antiarrhythmic effect in 7 of the 8 patients (88%). However, in group N patients, intravenous magnesium sulfate had an antiarrhythmic effect in only 1 of the 6 patients (17%) (p < 0.05 vs group L). These results suggest that intravenous magnesium sulfate may be effective in the acute management of cardiac arrhythmias in patients with a low serum iMg2+ level.

Aged↗
PubMed1995

The determination of nitrite and nitrate in human blood plasma by capillary zone electrophoresis.

The determination of nitrite and nitrate in human blood plasma by capillary zone electrophoresis (CZE) is described. Electrophoresis was carried out in a 65 cm long, 75 microns wide silica capillary, using 750 mM sodium chloride containing 5% NICE-Pak OFM Anion-BT (an additive reversing the electroosmotic flow) as running buffer, at a potential of 20 kV, with on-column UV detection at 214 nm. Under these conditions, the two anions migrated in the order of nitrite and nitrate, completely resolved from each other. Forty-one samples of ultrafiltered blood plasma of healthy volunteers were analyzed. The concentrations of nitrite and nitrate were 0.15 +/- 0.07 mg/L and 3.2 +/- 1.6 mg/L (mean +/- SD), respectively, with a linear correlation in the range of 0.1-50 mg/L. The within-day and between-day coefficients of variation (CVs) for nitrite and nitrate were lower than 5% and 8%, respectively. The recovery was 97-114%. The estimated plasma volume needed for each determination was 108 nL.

Electrophoresis, Capillary↗
PubMed1995

Qualitative comparison of carbon dioxide-induced change in cerebral near-infrared spectroscopy versus jugular venous oxygen saturation in adults with acute brain disease.

OBJECTIVE: To compare carbon dioxide-induced changes in cerebral oxy- and deoxyhemoglobin, measured by near-infrared spectroscopy, with those changes in jugular venous oxygen saturation in adult patients with acute brain disease. DESIGN: A prospective study. SETTING: The medical and surgical intensive care unit of a university hospital. PATIENTS: Nine patients with head trauma (n = 4), cerebrovascular disease (n = 3), and meningitis (n = 2). A total of ten measurements were done, while PaCO2 was increased from hypocapnia toward normocapnia in the nine patients. INTERVENTIONS: Arterial and jugular bulb catheterization, and intracranial pressure monitoring were performed as a part of the clinical intervention. An increase in PaCO2 was obtained by inhalation of CO2 and, if necessary, by reducing the ventilator rate. MEASUREMENTS AND MAIN RESULTS: In each patient, the position of the jugular bulb catheter was ascertained by skull roentgenography. Near-infrared spectroscopic values for oxy- and deoxyhemoglobin were set at zero at the beginning of the study. An increase in PaCO2 from 29 +/- 1 (SEM) torr (3.9 +/- 0.2 kPa) to 39 +/- 2 torr (5.2 +/- 0.3 kPa) was accompanied by a significant increase in jugular venous oxygen saturation from 63 +/- 3% to 76 +/- 3%; a significant increase in oxyhemoglobin of 3.5 +/- 0.9 mumol/L (of the brain tissue); and a significant decrease in deoxyhemoglobin of 1.5 +/- 0.4 mumol/L. In nine of ten measurements, the slopes of changes in oxyhemoglobin against the slopes of change in jugular venous oxygen saturation were very similar. In one patient, oxyhemoglobin changed negligibly while jugular venous oxygen saturation increased by 20%. CONCLUSIONS: Jugular venous oxygen saturation consistently demonstrates cerebrovascular responsiveness to CO2. The direction and magnitude of changes in cerebral oxyhemoglobin, measured by near-infrared spectroscopy, were similar to those changes in jugular venous oxygen saturation in most of our cases. Interpretation of a negligible change in oxyhemoglobin in one patient, despite an obvious increase in jugular venous oxygen saturation, requires further study comparing near-infrared spectroscopy with standard techniques.

Acute Disease↗
PubMed1993

[Safety applications in apnea test].

Apnea test for brain death determination is able to perform easily with the method written in Japanese criteria (Brain death study group, Ministry of Health and Welfare, 1987) (Figure 3). PaCO2 is increased to more than 60 mmHg, by which respiratory center in the brain stem is stimulated enough. Hypoxemia may occur and is the most serious complication during apnea test. We examined O2 delivery methods either by a thin cannula inserted to near tracheal carina (Ordinary method, 6 l/min) or by constant flow using a ventilator (6 l/min, or 20 l/min). During 10 minutes apnea test, PaO2 and PaCO2 changed significantly from 429 to 264 mmHg and 43 to 90 mmHg, respectively. But there was no significance between the methods. During apnea test, we have to distinguish spinal reflex movement from spontaneous respiratory movement. It is better to keep body temperature near 37 degrees C, because low body temperature requires much longer duration to reach required PaCO2, 60 mmHg (y = 0.54x - 15.2, where x is body temperature, degrees C and y is delta PaCO2, mmHg/min). Hypoxemia during apnea test must be prohibited, because it may cause farther organ damage. Maintenance of oxygenation during apnea test is difficult in patients who have severe respiratory failure. Oxygenation is kept much higher by adding positive airway pressure (10 cm H2O) and continuous monitoring of oxygenation by a pulse oxymeter prepares much safer apnea test in these patients.

Apnea↗