Search PubMed⌕ Search

Biomedical subjects

N Taenaka

Publications and source records attributed to N Taenaka.

At least 37 records · Page 2Linked to original sources
PubMed1998

The influence of surgical stress on T cells: enhancement of early phase lymphocyte activation.

UNLABELLED: For the control of postoperative infection, it may be important to understand the possible influences of surgical stress on the host immune system. To this end, we examined how the early phase of lymphocyte activation was affected in patients after major surgery (eight patients with esophageal carcinoma and six undergoing cardiac surgery) using a flow cytometric assay based on expression of the early activation antigen, CD69. Freshly isolated T cell in preoperative and postoperative samples did not express CD69. When peripheral blood mononuclear cells were stimulated in vitro, the expression of CD69 was greatly enhanced in both CD4 and CD8 T cells, compared with the preoperative samples. The proportion of de novo CD69-expressing cells in the CD4 subset was approximately 3 times (Postoperative Day 1) and 4 times (Postoperative Days 2, 3, 5, and 7) greater than those preoperatively, whereas the proportion of de novo CD69-expressing cells in the CD8 subset was approximately 1.5 times (Postoperative Days 2 and 5) and 2 times (Postoperative Day 3) greater than those preoperatively. The proportion of CD69+ cells was significantly greater in the CD4+ subset than in the CD8+ subset during the postoperative period. IMPLICATIONS: Our results show that major surgical stress enhances the early phase of lymphocyte activation. The augmentation of activation was greater in CD4 (helper) T cells than in CD8 (cytotoxic) T cells.

Aged↗
PubMed1998

Effects of pressure-support ventilation on recovery from acute diaphragmatic fatigue in rabbits.

OBJECTIVES: To examine the effects of pressure-support ventilation on recovery from acute diaphragmatic fatigue. DESIGN: Prospective laboratory trial. SETTING: Experimental laboratory. SUBJECTS: Twenty-one healthy, adult New Zealand white rabbits. INTERVENTIONS: Diaphragmatic fatigue was induced with 50-Hz phrenic nerve stimulation for 30 mins. Recovery was compared between pressure-support ventilation 0 cm H2O (SB), 10 cm H2O (P10), and 20 cm H2O (P20) for 90 mins immediately after the end of the fatigue inducing procedure. MEASUREMENTS AND MAIN RESULTS: After the fatigue-inducing procedure, pressure-support ventilation reduced transdiaphragmatic pressure and integrated diaphragmatic electromyogram both at P20 and P10, but not in SB. Recovery was assessed by airway occlusion pressure (Poccl) generated by high- (100 Hz) and low- (20 Hz) frequency phrenic nerve stimulation. Poccl at 100 Hz was lower in P10 and P20 than in SB (74.6 +/- 6.2 [SEM] %, 66.9 +/- 3.3%, and 94.8 +/- 3.6% of the baseline at 90 mins for P10, P20, and SB, respectively), while those at 20 Hz showed no differences between the three groups. CONCLUSION: Recovery from acute diaphragmatic fatigue might be disturbed with pressure-support ventilation.

Animals↗
PubMed1998

Circadian secretion patterns of melatonin after major surgery.

Biorhythms, such as regular variation in core body temperature and the pattern of the secretion of melatonin, are thought to be mediated by the same biological clock. Core body temperature is affected by the inflammatory response to major surgery. Apart from the well-known inhibitory effect of bright light on its secretion, melatonin is an exceedingly good marker of one of the central generating systems of circadian rhythms. We sequentially measured the plasma melatonin concentration pattern in patients who had undergone esophagectomy with thoracotomy to elucidate the circadian rhythm after major surgery. From seven patients who had received esophagectomy with thoracotomy for esophageal cancer, plasma concentrations of melatonin were measured using an RIA method. Blood samples were collected via each patient's arterial line at 00.00, 02.00, 04.00, 06.00, 08.00, 12.00, 16.00, 20.00, and 24.00 hr on the first postoperative day for six of the patients, and, for one patient, every 2 hr until the third postoperative day and every 4 hr thereafter until the sixth postoperative day. Four patients out of seven had melatonin concentrations of over 30 pg/ml (mean 34 pg/ml) at 24.00 hr on the first postoperative day. Five patients showed circadian secretion patterns of melatonin during the first postoperative day. One patient whose melatonin concentrations were measured consecutively for 6 days showed a regular circadian secretion pattern through the 6 days of the study. Even the stress caused by extremely invasive surgery did not significantly disturb the melatonin secretion pattern.

Aged↗
PubMed1998

High frequency oscillatory ventilation attenuates the activation of alveolar macrophages and neutrophils in lung injury.

BACKGROUND: Recent investigations have shown that leukocyte activation is involved in the pathogenesis of ventilator-associated lung injury. This study was designed to investigate whether the inflammatory responses and deterioration of oxygenation in ventilator-associated lung injury are attenuated by high-frequency oscillatory ventilation (HFO). We analyzed the effects of HFO compared with conventional mechanical ventilation (CMV) on the activation of pulmonary macrophages and neutrophils in 10 female rabbits. RESULTS: After surfactant depletion, the rabbits were ventilated by CMV or HFO at the same mean airway pressure. Surfactant-depletion followed by 4 h mechanical ventilation hindered pulmonary oxygenation in both groups. Impairment of oxygenation was less severe in the HFO group than in the CMV group. In the HFO group the infiltration of granulocytes into alveolar spaces occurred more readily than in the CMV group. Compared with CMV, HFO resulted in greater attenuation of beta2-integrin expression, not only on granulocytes, but also on macrophages. CONCLUSIONS: In the surfactant-depleted lung, the activation of leukocytes was attenuated by HFO. Reduced inflammatory response correlated with decreased impairment of oxygenation. HFO may reduce lung injury via the attenuation of pulmonary inflammation.

Journal Article↗
PubMed1997

Inhalation anesthetics suppress the expression of c-Fos protein evoked by noxious somatic stimulation in the deeper layer of the spinal cord in the rat.

The effects of inhalation anesthetics, nitrous oxide (N2O) and halothane, on the expression of c-Fos protein evoked by formalin injection were studied in the spinal cord in the rat. The expression of c-Fos protein was detected by immunocytochemistry following the injection of formalin (5%, 100 microliters) into the plantar surface of the left hindpaw. After 15 min of halothane (F) anesthesia, the anesthetics was switched to 40% or 70% of N2O, 0.5% or 1.5% of F or room air (for control) immediately following the formalin injection. Two hours later the rats were sacrificed and perfused. Sections of the L4 level of spinal cord were immunostained with anti c-Fos antibody. We counted the number of Fos-like immunoreactive (FLI) cells in every specific lamina as follows: superficial layer (laminae I and II), nucleus proprius (laminae III and IV), neck of the dorsal horn (laminae V and VI) and ventral gray (laminae VII-X). Then we compared the results of each category of sample. Both N2O and halothane suppressed the expression of c-Fos in the neck of the dorsal horn and ventral gray in a dose-dependent manner, but no effects were seen at the superficial layer or nucleus proprius. Suppression of c-Fos expression was greater under N2O than halothane anesthesia. This finding suggests that N2O had a stronger analgesic effect than halothane. The current study indicates that inhalation anesthetics do not act equally on every kind of spinal neurons. Both N2O and halothane have effects on spinal neurons in the deeper layers but not on the neurons existed in laminae I-II, some of which directly receive noxious inputs. Pretreatment with 2 mg/kg of naloxone, which completely reversed the effects of morphine, did not alter the effect of 70%N2O, suggesting that the analgesic effect of N2O is not mediated by an intrinsic opioid mechanism at the spinal cord level.

Analgesia↗
PubMed1997

Ocular surface disorders in the critically ill.

Abnormalities of the cornea and conjunctiva occur in association with neurological diseases, nocturnal lagophthalmos, coma, infection, and mechanical ventilation. We investigated the incidence and causes of ocular surface disorders in critically ill patients. In a retrospective study, the presence of conjunctivitis and corneal erosion was determined by reviewing the medical charts of 143 mechanically ventilated patients (intensive care unit [ICU] stay > or =7 days). In the subsequent prospective study, 15 patients who had sedatives or muscle relaxants administered continuously for more than 48 h in the ICU were investigated. Corneal erosion was examined using a slit lamp once a day. Ocular surface disorder was found in 28 of the 143 patients (20%) whose ICU stay exceeded 7 days. The incidence increased with continuous sedation (35% vs 15%). The incidence also increased with continuous neuromuscular blockade (39% vs 11%). In the prospective study, nine patients (60%) developed corneal erosion. A patient's inability to fully close his or her eyes increased the incidence (P < 0.01) of corneal erosion. Protective eyelid taping was effective in preventing and treating the corneal erosion. In conclusion, the critically ill often develop ocular surface disorders, especially when sedated and immobilized. A close relationship was observed between these conditions and the inability to close one's eyes.

Adolescent↗
PubMed1997

Tension pneumopericardium following tracheoplasty for congenital tracheal stenosis.

Tension pneumopericardium is a rare complication of mechanical ventilation following tracheoplasty for congenital tracheal stenosis. This case report describes fatal tension pneumopericardium in a three-month-old male infant some 24 hours following tracheoplasty for this condition. Because of persisting stenosis of the left main bronchus, ventilation pressures of PIP 23 cm H2O and PEEP 5 cm, progressing to PIP 28 cm and PEEP 7 cm were needed to maintain adequate respiratory exchange. Partial relief of the pneumopericardium was achieved by vigorous cardiac massage, but three days later the infant died of massive airway haemorrhage.

Acidosis, Respiratory↗
PubMed1996

Ketamine inhibits nitric oxide production in mouse-activated macrophage-like cells.

We have investigated the effects of ketamine on nitric oxide produced by activated macrophages using a murine macrophage-like cell line, J774. Cells were incubated for 18 h under stimulation with lipopolysaccharide and interferon-gamma or lipoteichoic acid and interferon-gamma, with various concentrations of ketamine (6-600 mumol litre-1). Nitric oxide production was assessed by measuring nitrite, a stable by-product of nitric oxide breakdown, in the medium. Other N-methyl-D-aspartate receptor antagonists, MK-801 (150 mumol litre-1) and dextromethorphan (150 mumol litre-1) were also tested. In addition, we studied the effects of ketamine on production of tumour necrosis factor-alpha by activated macrophages. Ketamine inhibited nitrite production dose-dependently with both lipopolysaccharide- and lipoteichoic acid-activated macrophages by up to approximately 65% at the highest ketamine concentration (600 mumol litre-1). Neither MK-801 nor dextromethorphan had an inhibitory effect. Ketamine also suppressed production of tumour necrosis factor-alpha. The data show that ketamine inhibited nitric oxide production by activated macrophages probably, in part, via inhibition of production of tumour necrosis factor-alpha, an autocrine stimulatory factor for nitric oxide production, but not via the NMDA receptor pathway, which is involved in neuronal nitric oxide production.

Anesthetics, Dissociative↗
PubMed1996

Fucoidin, a potent inhibitor of leukocyte rolling, prevents neutrophil influx into phorbol-ester-induced inflammatory sites in rabbit lungs.

The polysaccharide fucoidin, a homopolymer of sulfated L-fucose, is known, by interfering with the function of L-selectin, to inhibit leukocyte rolling, which is an early and essential step in the process of leukocyte extravasation into inflamed sites. We tested the inhibitory effect of fucoidin on neutrophil accumulation in lung inflammation induced by phorbol myristate acetate and peritoneal inflammation induced by thioglycollate in rabbits. Pretreatment (10 mg/kg) followed by continuous administration (10 mg/kg/h) of fucoidin dramatically reduced the number of neutrophils recruited into the lungs (determined by neutrophil counts in bronchoalveolar lavage fluid; 97.7 +/- 0.52% reduction) and peritoneal cavity (determined by neutrophil counts in peritoneal lavage fluid; 98.4 +/- 1.29% reduction). Fucoidin treatment also increased the systemic neutrophil count. These results suggest that the inhibition of leukocyte rolling, which may be a primary function of fucoidin, leads to a reduction of neutrophil accumulation at inflammatory sites, which may be beneficial for attenuating neutrophil-mediated tissue injury.

Animals↗
PubMed1995

NOC, a nitric-oxide-releasing compound, induces dose dependent apoptosis in macrophages.

The ability of exogenous nitric oxide (NO) to induce apoptosis in macrophages was analyzed using NOC, a NO-releasing compound, as a source of NO. Exogenous NO was shown to induce apoptosis in a dose dependent manner. Quantitative analysis revealed that the amount of NO required to induce apoptosis in more than half of macrophages exposed was 100 times larger than that for endogenous NO-induced apoptosis. NOC proved to be a convenient and useful tool for investigation of apoptosis related to NO.

Animals↗
PubMed1995

Thoracic epidural anesthesia attenuates halothane-induced myocardial sensitization to dysrhythmogenic effect of epinephrine in dogs.

BACKGROUND: The autonomic nervous system plays a critical role in the central modulation of cardiac dysrhythmias. Because sympathetic blockade by thoracic epidural anesthesia has been documented to protect patients from various stress responses, the authors speculate that epidural anesthesia can attenuate the dysrhythmogenic interaction between halothane and epinephrine. METHODS: In adult mongrel dogs anesthetized with halothane, the dysrhythmogenic dose (DD) of epinephrine, defined as the smallest dose producing four or more premature ventricular contractions within a 15-s period, was determined in the presence of thoracic epidural mepivacaine or saline. To address the effect of circulating mepivacaine after epidural administration, the authors examined the DD of epinephrine in the presence of intravenous mepivacaine. They also investigated the effect of thoracic epidural anesthesia in bilaterally vagotomized dogs. RESULTS: Epidural mepivacaine significantly increased the DD of epinephrine compared with epidural saline. However, intravenous mepivacaine did not affect the DD of epinephrine, even when the plasma concentration of mepivacaine during the dysrhythmias was twice that in the epidural mepivacaine group. The beneficial effect of epidural mepivacaine was not seen in bilaterally vagotomized dogs. CONCLUSIONS: Thoracic epidural anesthesia attenuated the myocardial sensitization by halothane, and vagal activity had an essential role in this action.

Anesthesia, Epidural↗
PubMed1995

A comparative evaluation of pressure-triggering and flow-triggering in pressure support ventilation (PSV) for neonates using an animal model.

The triggering system in pressure support ventilation needs to respond rapidly, especially in neonates. The aim of this study was to compare the effects of flow-triggered and pressure-triggered pressure support ventilation on neonatal mechanical ventilation using an animal model. Respiratory flow, airway pressure, oesophageal pressure, and diaphragmatic electromyogram were measured during pressure support ventilation in five anaesthetized rabbits. The animals were connected to a VIPBIRD (Bird, U.S.A.) (CPAP mode, pressure support ventilation, 5 cm H2O and PEEP 0 cm H2O). Flow-triggering sensitivity was set at 0.2l/min, 0.5l/min, 1.01l/min, or 1.5l/min. Pressure-triggering sensitivity was set at -1.0 cm H2O. Shorter trigger delay and longer pressure support time were observed in flow-triggering. There was also less diaphragmatic activity in flow-triggering as evidenced by the amplitude of integrated diaphragmatic electromyogram and negative deflection of oesophageal pressure. The findings suggest that flow-triggering will prove superior to pressure-triggering in pressure support ventilation for neonates.

Animals↗
PubMed1994

Comparative evaluation of diaphragmatic activity during pressure support ventilation and intermittent mandatory ventilation in animal model.

The aim of the present study is a comparative evaluation of the effects of pressure support ventilation (PSV) and intermittent mandatory ventilation (IMV) on diaphragmatic activity in rabbit model of neonate. The animals were divided into a PSV group and an IMV group. In the IMV group, spontaneous breathing and four kinds of IMV rate (5, 10, 15, and 20/min) were applied (Ventilator: Bear BP200, peak inspiratory pressure [PIP]: 12 cm H2O, inspiratory time: 0.6 s). In the PSV group, spontaneous breathing and four levels of PSV (3, 6, 9, and 12 cm H2O) were applied (Ventilator: VIP Bird, flow triggering). Airway pressure (Paw), flow (V), esophageal pressure (Pes), integrated diaphragmatic electromyogram (Edi), and arterial gas data were measured. Amplitudes of Pes and Edi were expressed as percentages (% Edi and % Pes) of the control value during spontaneous breathing to evaluate diaphragmatic activity. Lower IMV rates did not reduce diaphragmatic activity. Approximately half of diaphragmatic activity of control remained even at IMV 15/min. Diaphragmatic activity disappeared at IMV20/min. In contrast, PSV reduced Edi and Pes linearly according to support level. In conclusion, diaphragmatic activity could be reduced more gradually with PSV than IMV by altering ventilatory support level.

Animals↗
PubMed1994

Monitoring of hepatic venous oxygen saturation for predicting acute liver dysfunction after Fontan operations.

Acute liver dysfunction after Fontan operations may result from inadequate hepatic perfusion along with low cardiac output and high central venous pressure. We monitored hepatic venous oxygen saturation in 15 patients after Fontan operations to determine whether oxygen saturation predicts the occurrence and severity of acute liver dysfunction. We measured oxygen saturation from hepatic venous blood samples every 4 to 5 hours for at least 24 hours after the operation and used the mean hepatic venous oxygen saturation value for the first 24 hours after the operation to analyze the relationship between oxygen saturation and hepatic function. As indices of hepatic function, we measured serum alanine aminotransferase, total bilirubin, blood lactate (arterial, hepatic venous, and the difference between them), and the arterial ketone body ratio (the ratio of aceto-acetate to beta-hydroxybutyrate). For alanine aminotransferase and bilirubin, we used the maximal values during the first week in the analysis, and for blood lactate and ketone body ratio, we used the mean values for the first 24 hours after the operation. Significant broken-line regression relationship existed between mean hepatic venous oxygen saturation and hepatic function indices (alanine aminotransferase, total bilirubin, and blood lactate). The interpretation of these relationships is that hepatic indices are constant above the critical mean hepatic venous oxygen saturation values but are correlated with mean hepatic venous oxygen saturation below critical points in the range of 21% to 26%. Thus a hepatic venous oxygen saturation value below about 25% during the first 24 hours after a Fontan operation predicts the occurrence and the severity of acute liver dysfunction. We suggest that monitoring hepatic venous oxygen saturation is useful for management of critically ill patients after Fontan operations.

Adolescent↗
PubMed1992

An initial comparison of intensive care in Japan and the United States.

OBJECTIVE: The objective of this study was to compare the utilization of, and outcome from, critical care services in selected medical centers providing secondary and tertiary care in the United States and Japan. DESIGN: Prospective data collection on 1,292 patients from each of the participating Japanese study hospitals in 1987 to 1989 and compared with the 5,030 patients in the United States 1982 Acute Physiology and Chronic Health Evaluation (APACHE II) database used to develop the APACHE II equation. Detailed organizational characteristics of the participating ICUs and hospitals were also obtained. SETTING: Data collection took place in the ICUs of 13 U.S. hospitals and six Japanese hospitals. PATIENTS: Data were collected on consecutive, unselected patients from medical, surgical, and mixed medical/surgical critical care units, with a spectrum of medical and surgical diagnoses. MEASUREMENTS AND MAIN RESULTS: U.S. and Japanese ICUs have a similar array of diagnostic and therapeutic modalities. Only 2% (range 0.6 to 3.5) of beds in Japanese hospitals were designated to intensive care. The organization of the Japanese and U.S. ICUs varied by hospital. There were significantly fewer women admitted to Japanese ICUs and a substantially lower proportion of low-risk-of-death patients. Despite a rapidly aging population, there were relatively fewer elderly patients with chronic health ailments in the Japanese ICU population (8%) compared with the U.S. cohort (18%). CONCLUSIONS: In this sample of hospitals, similar high-technology critical care is available in the United States and Japan. Variations in utilization between the two countries represent differences in case mix and bed availability. The APACHE II equation stratified patients in the Japanese patient cohort across the full spectrum of increasing severity of illness.

Chi-Square Distribution↗