Biomedical subjects

Takehiko Iijima

Publications and source records attributed to Takehiko Iijima.

10 recordsLinked to original sources

PubMed2006

Neuroprotective effect of propofol on necrosis and apoptosis following oxygen-glucose deprivation--relationship between mitochondrial membrane potential and mode of death.

Mitochondrial membrane potential (MMP) appears to play an important role in apoptotic cascade and has been proposed as an index for apoptosis or necrosis. We examined the neuroprotective effect of propofol on mode of death, focusing on MMP. Hippocampal cell culture was divided into three groups: control, oxygen-glucose deprivation for 30 min (30OGD), 90 min (90OGD). Propofol was added to each culture group at a concentration of 0 microM (Vehicle), 0.1 microM (Pro0.1) or 1.0 microM (Pro1.0). MMP was expressed as normalized JC-1 fluorescence. ATP content was assayed using the luciferin-luciferase reaction. Neuronal viability and appearance of apoptosis were also assessed. ATP content was decreased after OGD (0.276 +/- 0.115 microM/microg (control), 0.172 +/- 0.125 microM/microg (30OGD) and 0.096 +/- 0.092 microM/microg (90OGD)). Propofol did not alter ATP content. MMP was hyperpolarized after 30OGD (1.26 +/- 0.23 (vehicle), 1.29 +/- 0.13 (Pro0.1) and 1.18 +/- 0.06 (Pro1.0)) but was depolarized after 90OGD (0.77 +/- 0.04 (vehicle), 0.89 +/- 0.04 (Pro0.1), but Pro1.0 prevented depolarization (1.03 +/- 0.15 (P < 0.05)). Viability of cells significantly decreased to 50.3 +/- 5.7% (vehicle), 46.1 +/- 7.5% (Pro0.1), but Pro1.0 significantly salvaged neurons 65.1 +/- 6.2% (higher than vehicle and Pro0.1 value, P < 0.05) after 90OGD. At 24 h after OGD, TUNEL-positive cells were increased to 34.5 +/- 6.2% (vehicle), 26.7 +/- 7.9% (Pro0.1) and 30.4 +/- 7.1% (Pro1.0) in the 30OGD group. No pharmacological effect of propofol on the incidence of apoptosis was found. Propofol inhibited acute neuronal death accompanied with the maintenance of MMP but did not prevent subsequent apoptosis. Propofol induces a moratorium on neuronal death, during which pharmacological intervention might be able to prevent cell death.

Analysis of Variance↗

PubMed2006

Mitochondrial membrane potential and ischemic neuronal death.

Mitochondria are intracellular organelles in which high energy phosphate is produced. Ischemia causes depletion of the materials necessary to produce this phosphate and strongly affects the electron transport chain. Apoptosis commences during and after ischemia. As such, it is likely that a significant relationship exists between inactivation of electron transport and apoptosis. Mitochondrial membrane potential (MMP) reflects performance of the electron transport chain and can indicate a pathological disorder of this system. In an experimental setting, oxygen-glucose depletion (OGD) in neuronal cell culture has been employed to simulate an ischemic condition. The relationship between MMP and subsequent neuronal death during and after OGD has been examined. MMP dissipation and concomitant neuronal death have been reported, but recent studies have demonstrated mitochondrial hyperpolarization preceding neuronal death. The direction of MMP polarization depends on the extent of OGD. Long OGD results in depolarization, while shorter OGD induces hyperpolarization. Neurons are still viable during hyperpolarization, but the process may switch on the apoptotic cascade. Meanwhile, dissipation of MMP seems to be a consequence of severe energy deficit, leading to necrosis. MMP may be a marker of subsequent apoptosis, although a causal relationship remains to be determined.

Animals↗

PubMed2006

Perioperative circulating blood volume analysis in management of a 13-year-old female patient with an extraadrenal pheochromocytoma and refractory ventricular tachycardia: a case report.

This report describes the use of discrete real-time monitoring of blood volume (BV) and cardiac index (CI) by a dye densitography analyzer before, during, and after removal of a pheochromocytoma. The BV expanded by about 1.1 L and CI increased by about 2.2-fold after the tumor was removed. In lieu of a rapid catecholamine determination, the hemodynamic data were used to choose a supplemental catecholamine to stabilize the patient during and after the protracted surgery. This case demonstrates the importance of hemodynamic monitoring (BV and CI) to predict or detect cardiac and other complications, particularly in young patients with catecholamine-secreting tumors.

Adolescent↗

PubMed2006

[Questionnaire survey of anesthesiologists' opinion regarding the Japanese guidelines for transfusion].

BACKGROUND: Anesthesiologists' opinions regarding the Japanese guidelines for transfusion were surveyed. METHODS: From December 28, 2004 to January 28, 2005 a questionnaire survey was performed in 958 hospitals registered with the Japanese Society for Anesthesiologists. Queries regarding the guidelines for packed red cells, fresh frozen plasma, platelet concentrates, autologous blood transfusions, and other miscellaneous subjects were sent to these hospitals. RESULTS: A total of 537 hospitals (56.1%) responded to the survey. The guidelines for packed red cells were complied with and widely accepted. The trigger value of hemoglobin concentration was 7-9 g x dl(-1). Although 54.4% of the anesthesiologists used the coagulation disorder as the triggering factor for transfusion of fresh frozen plasma, only 19.6% of the hospitals monitored coagulopathy. In most hospitals, the trigger value of hemorrhage for use of fresh frozen plasma was the bleeding amount of less than 3000 ml, which is less than 70% of the recommended triggering value (bleeding exceeding 100% of circulating blood volume). The guideline for platelet concentrate transfusions for elective surgery was somewhat accepted (77.1%), but the triggering value; 3 x 10(4) x l(-1) for cardiopulmonary bypass surgery was considered too strict (41.4%). CONCLUSIONS: These guidelines for transfusions appear to be widely accepted. The most dominant complaint was the inadequacy of the guidelines for rapid massive bleeding.

Anesthesiology↗

PubMed2005

Determination of the standard value of circulating blood volume during anesthesia using pulse dye-densitometry: a multicenter study in Japan.

PURPOSE: The standard value for circulating blood volume (BV) during anesthesia was determined by a multicenter study in Japan. The significance of BV on the reduction of blood pressure after the induction of anesthesia was also examined. METHODS: The study included 184 patients from eight university hospitals. After the induction of anesthesia, pulse dye-densitometry was performed according to a uniform protocol. Factors contributing to reduced blood pressure after induction of anesthesia were examined by multiple logistic regression analysis. RESULTS: The mean and standard deviation of BV was 80.0 +/- 13.9 ml x kg(-1); for females and 84.2 +/- 15.3 ml x kg(-1) for males (P > 0.05). There was no age difference in terms of BV. After adjusting for the effects of height, weight, and age, the factors predisposing to a reduction in blood pressure of >20 mmHg after induction of anesthesia were found to be age (P < 0.01) and BV (ml x kg(-1)) (P < 0.001). CONCLUSION: We determined the BV of anesthetized patients before surgery in Japan using pulse dye-densitometry. It is suggested that age is not a factor regarding BV, and that blood pressure tends to be reduced in hypovolemic patients after induction of anesthesia.

Adult↗

PubMed2005

Pulse total-hemoglobinometer provides accurate noninvasive monitoring.

OBJECTIVE: Rapid noninvasive measurement of total hemoglobin would be extremely useful for various clinical situations. This study determined the clinical accuracy and utility for a pulse total-hemoglobinometer using four wavelengths: 660 nm (reduced hemoglobin), 805 nm (isosbestic point), 940 nm (oxygenated hemoglobin), and 1300 nm (water density). DESIGN: Clinical trial. SETTING: University school of medicine. PATIENTS: Patients were 122 individuals (age, 18-82 yrs; 49.4 +/- 16.0 yrs [mean +/- SD]), including 71 healthy volunteers, 24 patients undergoing surgery, and 27 patients undergoing hemodialysis. INTERVENTIONS: The hemoglobinometer probe, which simultaneously indicated peripheral oxygen saturation, pulse rate, and hemoglobin, was placed on the fingertip similarly to a regular pulse oximeter. The hemoglobin values were compared with those obtained by the co-oximeter or the sodium lauryl sulfate-methemoglobin method. Those hemoglobin values were assigned to either the training set or the validation set for statistical evaluation. MEASUREMENTS AND MAIN RESULTS: Multiple regression analysis including the ratio of the pulsatile optical density (phi(ij)) derived from the four wavelengths and other factors demonstrated that the mean value of the normalized pulse wave obtained from the photodiode at 805 nm (DC805) and the ratios of DC940 and DC1300 (DC940/DC1300) were the pivotal factors in the hemoglobinometer's increased accuracy in the clinically useful range. The coefficient of determination between both methods was r2 = .81 (p < .0001) in the training set and r2 = .75 (p < .0001) in the validation set. When the cutoff value of anemia was set at 10 g/dL, and anemia was defined as <10 g/dL, the respective sensitivity and specificity of hemoglobinometer values to detect anemia in intraoperative patients were 84.3% and 84.6% (n = 20). CONCLUSIONS: The data demonstrated the necessity for consideration of light scattering in red blood cells for pulse-spectrophotometric hemoglobin measurement. This was accomplished with additional factors, such as DC805 and DC940/DC1300. With these improvements, the pulse hemoglobinometer provided noninvasive, clinically acceptable measurement of hemoglobin. The pulse hemoglobinometer is a versatile tool that might be useful for routine health checkups of neonates and young children, intraoperative monitoring of bleeding, and emergency care.

Adult↗

PubMed2004

An increased circulating blood volume does not prevent hypotension after pheochromocytoma resection.

PURPOSE: Pulse dye-densitometry, a novel monitor that measures circulating blood volume (CBV) and cardiac output (CO), was used in patients with pheochromocytoma to determine the relationship between CBV and post resection hypotension. METHODS: Case control study. An alpha blocker was administered for approximately two weeks, and its effect on the expansion of CBV was quantified. CBV was monitored in seven patients admitted for resection of suspected pheochromocytoma before preoperative alpha-blocker therapy, after alpha-blocker therapy and three times during the operation. Relationships between the CBV and blood pressure after resection of the tumour were examined. RESULTS: CBV increased from 72.0 +/- 10.0 mL.kg(-1) to 83.4 +/- 12.2 mL.kg(-1) after alpha blockade. (P < 0.001). We found a significant inverse relationship between the increase in CBV after alpha-blocker therapy and blood pressure after resection of the tumour. CONCLUSIONS: Expansion of the CBV by alpha-blocker therapy was related to lower blood pressures after resection of the pheochromocytoma. Expansion of the CBV by an alpha blocker may have increased the elastance of blood vessels. Preoperative blood volume expansion does not preclude hypotension after tumour resection. Although the CBV value itself is not a predictor for hypotension after tumour resection, pulse dye-densitometry provides values of CO and CBV simultaneously, assisting in the management of volume resuscitation and/or the need for catecholamines.

Adrenal Gland Neoplasms↗

PubMed2003

Mitochondrial hyperpolarization after transient oxygen-glucose deprivation and subsequent apoptosis in cultured rat hippocampal neurons.

Mitochondrial membrane potential (MMP) regulates the production of high-energy phosphate and apoptotic cascade, both occurring after ischemic impact. The timed profile of MMP differing from grading ischemic impact has to be determined. Primary rat hippocampal cultures were exposed to oxygen-glucose deprivation (OGD) for 30, 60, and 90 min and then were reoxygenated. MMP was expressed as a voltage-dependent dye, JC-1 fluorescence, under confocal microscopy. Cell viability was assessed by calcein AM and ethidium homodimer, each at 3 hours and 24 hours after 30, 60, and 90 min of OGD. The appearance of apoptosis was also evaluated by the TUNEL method at 24 hours. Hyperpolarization of MMP (2.31+/-0.94 normalized JC-1 fluorescence ratio between red and green) was observed during reoxygenation after 30 min OGD, while 60 min OGD induced depolarization (0.66+/-0.22, Valinomycin (potassium ionophore)-induced depolarization: 0.53+/-0.19). The fluorescence of mitochondria became weak after 90 min OGD. Most of the neurons were shrunken after 90 min and neurons were TUNEL-positive 24 hours after 30 min OGD, although most neurons were viable at 3 hours. A longer period of OGD induced necrosis, and most neurons remained viable after only 3 hours. Our data present that the short (30 min) OGD induced hyperpolarization of MMP during reoxygenation, while a longer OGD (60 or 90 min) induced depolarization and acute necrosis. Neurons were still viable even during hyperpolarization of mitochondria, but this hyperpolarization appears to be linked to subsequent apoptotic change.

Animals↗

PubMed2003

Mitochondrial membrane potential and intracellular ATP content after transient experimental ischemia in the cultured hippocampal neuron.

Ischemia limits the delivery of oxygen and glucose to cells and disturbs the maintenance of mitochondrial membrane potential (MMP). MMP regulates the production of high-energy phosphate and apoptotic cascading. Thus, MMP is an important parameter determining the fate of neurons. Differences in the time course of MMP according to the grading of the ischemic impact have not been clarified. MMP and intracellular ATP contents were monitored before and after short-term oxygen-glucose deprivation. A primary hippocampal culture seeded in a 35 mm fenestrated dish for fluorescence microscopy was mounted in a sealed chamber for an anaerobic incubation. A continuous flow of 100% nitrogen into the chamber and a replacement of glucose-free medium allowed the condition of oxygen-glucose deprivation (OGD), thereby extrapolating ischemia. MMP was evaluated by the fluorescence of a voltage-dependent dye, JC-1, under fluorescence microscopy. The intracellular ATP content was evaluated in a hippocampal culture seeded in a 96-well plate by the luciferin-luciferase reaction after a designated period of OGD. During OGD, MMP decreased to 0.72+/-0.03 (normalized JC-1 fluorescence), then increased to the hyperpolarized level 1.99+/-0.12 during 60 min reoxygenation after 30 min OGD. MMP after 60 min OGD decreased and recovered occasionally during reoxygenation. After 90 min OGD and reoxygenation, MMP was reduced and never recovered. The intracellular ATP content was 8.1+/-6.6 and 3.2+/-1.9% after 30 min OGD and 30 min reoxygenation following 30 min OGD, respectively; 60 min OGD did not significantly change these levels (7.1+/-5.8, 2.6+/-0.5%). Hyperpolarization after OGD did not accompany ATP production. This observation suggests the inhibition of electron reentry into an inner membrane during reoxygenation and the disturbance of FoF1-ATP synthase. This pathological finding of an energy-producing system after OGD may provide a clue to explain post-ischemic energy failure.

Adenosine Triphosphate↗

PubMed2002

Relationship between oxidation of glutathione and reactive nitrogen species during the early-reperfusion phase of cerebral ischemia.

A timed profile of glutathione oxidation and reactive nitrogen species during reperfusion after cerebral ischemia in rat was obtained. Dialysate was collected every 25 min from a microdialysis probe inserted into the cerebral cortex before and after cerebral ischemia. NO2-, NO3-, and reduced and oxidized glutathione (GSH, GSSG) were detected by high-performance liquid chromatography. GSH and GSSG increased and reached a peak: 3408 +/- 1710% (mean +/- SE) at 25 min of reperfusion (P < 0.0001) and 329 +/- 104% at 50 min of reperfusion (P = 0.06), respectively. Oxidation ratio decreased from 0.82 +/- 0.04 to 0.42 +/- 0.07 (P < 0.0001) at 25 min of reperfusion. NO3- levels significantly decreased (68.3 +/- 9.1%) (P < 0.01) during ischemia and remained lower than the control value during reperfusion. NO2- levels did not significantly change. These data suggest that GSH releases during early phase of reperfusion and that its rapid oxidation contributes to prevent an increase in reactive nitrogen species.

Animals↗