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Biomedical subjects

Mayuki Aibiki

Publications and source records attributed to Mayuki Aibiki.

11 recordsLinked to original sources

Serum albumin levels anticipate antithrombin III activities before and after antithrombin III agent in critical patients with disseminated intravascular coagulation.

Elevated thrombin-antithrombin complex (TAT) or decreased serum albumin levels suggest heightened vascular permeability in disseminated intravascular coagulation (DIC). In such a situation, plasma antithrombin III (AT-III) may decrease because of the leakage. We thus examined whether AT-III activity before and after administration of an AT-III agent changed depending on plasma TAT and/or serum albumin levels in 20 consecutive patients with DIC. We also analyzed the pharmacokinetics for AT-III using a two-compartment model. Serum albumin levels before AT-III administration correlated with preadministered and postadministered AT-III activity, but TAT levels did not. Regardless of TAT levels, AT-III trough activity on the third day increased significantly. In patients with albumin levels of 2.5 g/dL or less, AT-III trough levels on the third day were significantly lower than those with higher levels of albumin. The half-life of the distribution phase for AT-III agent in the patients was shortened to less than one third the value reported in congenital AT-III deficiency, suggesting increased vascular permeability in the acute state patients here. The distribution volume of the agent increased remarkably compared with the previous control. We report here for the first time that in critical patients with DIC, plasma AT-III levels before and after AT-III administration could be predicted by preadministered serum albumin levels, but not by TAT. These findings could be explained by the pharmacokinetic profile, increased vascular permeability and distribution volume, observed in critical patients.

Adult↗

Time related changes in reversible MRI findings after prolonged hypoglycemia.

Diffusion weighted magnetic resonance images (DWI) in hypoglycemic coma show more definite and earlier findings than do T1-weighted images, or even fluid-attenuated inversion recovery (FLAIR). However, there has been limited information on the time related changes of such MRI images. We report here the time related changes of MRI findings after prolonged hypoglycemia in a diabetic 62-year-old man without hypoxia. We found in the patient that hyperintensities in DWI, T2-weighted and FLAIR images disappeared on the 14th day along with normalization of the apparent diffusion coefficient (ADC). Single photon emission computed tomography (SPECT) showed no low perfusion findings throughout the course. Since the day when the hyperintensities disappeared, the patient became to open his eyes in response to verbal command. This paper demonstrates serial alterations in reversible DWI findings after prolonged hypoglycemia and we need to define its mechanisms in the future.

Brain↗

Elevated serum beta-D-glucan level and depressed neutrophil phagocytosis in a heatstroke patient.

Endotoxemia has been reported as a mechanism for the fatal sequela after heatstroke. Subsequent disseminated fungal infection in a heatstroke patient has been also described. Beta-D-glucan, a constituent of the fungal cell wall, is an early diagnostic measure for fungal infection. In a heatstroke case, we examined for the first time levels of serum beta-d-glucan and endotoxin. A 34-year-old man with a body temperature of 43.5 degrees C was admitted in a state of shock. Prior to the development of disseminated intravascular coagulopathy (DIC), a remarkable elevation of serum beta-D-glucan level to 116 pg/mL (normal level<6.0 pg/mL) was revealed on the first day of admission. However, serum endotoxin was not detected when using a method that excluded beta-D-glucan contamination from endotoxin measurement (normal level<1.0 pg/mL). This change of beta-D-glucan level was accompanied by a depressed neutrophil function, especially in phagocytosis of 34% (normal range 70-90%) but not in bacterocidal function (81% versus a normal range of 70-100%). After intensive care including continuous hemodiafiltration, the patient regained consciousness but remained ataxic due to cerebellar infarction, which might have resulted from DIC, and subsequent bilateral fungal oculitis were revealed 45 days after admission. This case report demonstrates the elevation of serum beta-D-glucan but normal endotoxin levels after heatstroke, which may prompt further study to re-examine the serum levels of endotoxin in such catastrophic insults.

Adult↗

Biphasic concentration change during continuous midazolam administration in brain-injured patients undergoing therapeutic moderate hypothermia.

OBJECTIVE: To define the pharmacokinetics of midazolam, a probe for monitoring cytochrome (CYP) 3A 4 activity, during moderate hypothermic therapy. DESIGN: A prospective randomized study. SETTING: The intensive care unit of a medical university hospital. PATIENTS AND INTERVENTIONS: In 15 consecutive brain-injured patients, midazolam concentrations were measured serially using high-performance liquid chromatography (HPLC). Under continuous administration of the agent, eight patients underwent moderate hypothermia of 32-34 degrees C (hypothermia group) and seven received normothermic therapy (normothermia group). A one-compartment model was selected for pharmacokinetic analyses for the continuous administration. Data represent +/-S.D. Statistical analysis was performed using ANOVA followed by Scheffe's F-test or the Mann-Whitney U-test ( P<0.05 ). MEASUREMENT AND MAIN RESULTS: Serum midazolam concentrations in the hypothermia group increased linearly until the body temperature (BT) reached 35 degrees C without plateauing, even during continuous administration, after which the levels decreased remarkably when BT rose to 36 degrees C. However, the concentrations in the normothermia group remained on a plateau, which lasted until the end of the study. In the hypothermia group, elimination rate constant (k(e)) and clearance (CL) in the phase below 35 degrees C BT were much lesser than those above 35 degrees C BT, whereas distribution volume (V(d)) during the hypothermic phase was greater than that during the period above 35 degrees C BT. CONCLUSION: This study has demonstrated for the first time that midazolum concentration changes biphasically even during continuous infusion in hypothermic therapy. The mechanisms for the change are unclear. Thus, further studies including confirmation of cytochrome 3A 4 activity are required, while monitoring for the development of undesirable effects from over-dosing is also needed.

Adolescent↗

Hypothermia.

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Blood Pressure↗

Non-specific hyperamylasemia in shosin beri-beri.

Several reports demonstrate non-specific hyperamylasemia in cardiac surgery or diabetic ketoacidosis. We report here for the first time non-specific hyperamylasemia in a cardiovascular beri-beri case who showed shock with severe metabolic acidosis. Her echocardiography revealed hyperkinetic wall motion of the small left ventricle. Despite intravascular volume expansion in parallel with dopamine administration, her blood pressure did not recover. Abdominal computed tomography (CT) did not reveal pancreatic swelling or any other signs of acute pancreatitis. Her history suggested a possibility of cardiovascular beri-beri due to chronic alcoholism. Thiamine administration dramatically reversed her haemodynamic derangements, metabolic acidosis and even relieved her abdominal pain. Isozyme examinations for hyperamylasemia showed that most of the serum amylase consisted of salivary type. This case report expands our information on non-specific hyperamylasemia encountered in the emergency setting.

Acidosis↗

Neuroprotective effects of hyperthermic preconditioning on infarcted volume after middle cerebral artery occlusion in rats: role of adenosine receptors.

OBJECTIVE: There are still only a limited number of studies regarding the neuroprotective effects of hyperthermic preconditioning on regional brain ischemia or regarding the role of adenosine A1 receptors in such pretreatment. We examined the effects of hyperthermic pretreatment on infarcted volume after middle cerebral artery occlusion (MCAO), as well as the contribution of A1 receptors, to the responses in rats. DESIGN: Prospective, randomized animal study. SETTINGS: An animal research laboratory in a medical university. SUBJECTS: Male Wistar rats (200-250 g). INTERVENTION: All animals were anesthetized with isoflurane during each pretreatment, as well as for MCAO. The animals were assigned as follows: (i) sham-control group (n = 8), which was maintained at normothermia (37 +/- 0.2 degrees C pericranial temperature) for 15 mins, then kept in an awake state for 0.5, 3, 6, 18, 24, or 48 hrs before 2-hr MCAO; (ii) hyperthermia group (n = 8), which was subjected to 42 +/- 0.5 degrees C for 15 mins, and then received the same treatment as the sham group; (iii) DPCPX (a selective central adenosine receptor antagonist)-treated control group, which was given the agent before normothermia pretreatment, then kept for a recovery time of 0.5 or 24 hrs (n = 8 in each group) before MCAO; (iv) DPCPX plus hyperthermia-treated group, which was administered the agent at the same dose as the control before hyperthermic exposure, then selected for each recovery time (n = 8 in each group) before MCAO; (v) DPCPX-ischemic group, to which the agent was administered before MCAO (n = 8); and (vi) vehicle-ischemic group, in which peanut oil as a vehicle, instead of DPCPX, was injected before MCAO (n = 8). Values are expressed as mean +/- se. Statistical analysis was done by analysis of variance, followed by Scheffe's F test, Mann-Whitney U test, or the chi-square test as appropriate (p <.05). MAIN RESULTS: The infarcted volume in hyperthermic animals kept for 18 or 24 hrs before the occlusion procedure was significantly smaller than in the sham controls, but not in rats kept for 0.5, 3.0, 6.0, and 48 hrs. DPCPX partially reversed the reduction in infarcted volume that was induced by hyperthermic preconditioning after focal ischemia, whereas the agent itself did not affect the volume after ischemia. CONCLUSION: These data indicate that hyperthermic pretreatment reduces the effects on MCAO-induced cerebral infarction, possibly via a partial mediation of the central adenosine receptors in the brain. The results also suggest a need for further studies to define the relationship between heat shock proteins and central adenosine receptors in preconditioning.

Animals↗

Differential effects of lowering culture temperature on mediator release from lipopolysaccharide-stimulated neonatal rat microglia.

OBJECTIVE: Therapeutic moderate hypothermia has the potential for neuronal protection against brain injury. Microglia, a type of immune-related cell in the brain, may play a certain role in neuronal damage subsequent to injury. We examined the effects of culture temperature changes from 37 degrees C to 33 degrees C or 30 degrees C on mediator release, including nitric oxide, interleukin-6, and tumor necrosis factor-alpha from lipopolysaccharide-stimulated microglia harvested from neonatal rats. DESIGN: Laboratory study. SETTING: University medical school. SUBJECTS: Microglial cells isolated from primary cultures of rat brains. INTERVENTIONS: The production of nitric oxide was measured by a nitrite accumulation method in a culture medium, whereas cytokines, interleukin-6, and tumor necrosis factor-alpha were measured by enzyme-linked immunosorbent assay. MEASUREMENT AND MAIN RESULTS: At 30 degrees C and 33 degrees C, nitric oxide production stimulated by lipopolysaccharide decreased to 10 and 30% of control (37 degrees C), respectively, 24 hrs after the stimulation, and the decrease was sustained for 48 hrs. Interleukin-6 production at 30 degrees C and 33 degrees C was also reduced to 30% of control 6 hrs after the activation. Such responses lasted throughout the study. However, tumor necrosis factor-alpha release at 30 degrees C and 33 degrees C was depressed for only 6 hrs after stimulation, followed by subsequent elevation to concentrations similar to those at 37 degrees C. Microglial morphologic activation, showing changes from round to bipolar, reached a peak at 6 hrs in the 37 degrees C group, returning to round 12 hrs after lipopolysaccharide application. In 30 degrees C and 33 degrees C, the zenith was detected at 6 hrs, with activation remaining even 12 hrs after the stimulation, suggesting prolongation of the microglial response to lipopolysaccharide, which was inconsistent with changes in tumor necrosis factor release. CONCLUSIONS: Decreasing culture temperature inhibits the production of nitric oxide and interleukin-6 from activated microglia. Differences were found in the degree or time course change between tumor necrosis factor-alpha and the other mediators. Also, the time course of morphologic changes in microglia was dependent on culture temperature. Further studies are required to define the mechanisms for such differences in mediator release from cooled microglia and also to clarify the inconsistency between morphologic change and its function in the cell.

Animals↗