Inhibition of HMGB1 by deep ocean water attenuates endotoxin-induced sepsis.
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Animals↗
Biomedical subjects
Hideo Iwasaka
Publications and source records attributed to Hideo Iwasaka.
Effect of Ulinastatin, a human urinary trypsin inhibitor, on the oleic acid-induced acute lung injury in rats via the inhibition of activated leukocytes.
BACKGROUND: The acute respiratory distress syndrome (ARDS) is often caused by fat tissue embolism. One of the most common animal models of ARDS is produced by direct administration of oleic acid (OA). Activated leukocytes are critically involved in the pathological mechanism in this model. Human urinary trypsin inhibitor (UTI) is known to inhibit production of tumor necrosis factor (TNF)-alpha, which potently stimulates leukocyte activation. The purpose of this study was to clarify whether UTI improves OA-induced lung injury in rats by inhibiting activated leukocytes via TNF-alpha production. MATERIALS AND METHODS: Rats were subjected to a single intravenous administration of OA into the pedicle vein. Acute lung injury was evaluated by arterial blood gases and histological changes in lungs. Pulmonary vascular permeability, accumulation of neutrophils, and the levels of TNF-alpha in lung tissues were also examined. Rats were divided into four experimental groups: a sham operated, OA, OA + UTI, and OA + nitrogen mustard (NM)-induced leukocytopenia group. UTI was intravenously administered 30 min before OA administration. Leukocytopenia was induced by the administration of NM. RESULTS: UTI significantly improved the OA-induced histological changes for 4 h after OA administration. The OA-induced reduction of PaO2, the increase of pulmonary vascular permeability, and the levels of MPO activity and TNF-alpha in lung tissues were significantly improved in rats administrated UTI. The effects in the leukocytopenia group were similar to those in the UTI-administered group. CONCLUSION: Leukocytes play a critical role in the development of OA-induced lung injury. It was suggested that UTI contributed to the reduction in the OA-induced lung injury by inhibiting TNF-alpha and thereby suppressing leukocyte.
Acute Disease↗
[Landiolol does not affect bispectral index scale in off-pump coronary artery bypass surgery in patients under fast-track cardiac anesthesia].
BACKGROUND: We evaluated the effect of landiolol, a novel ultra-short-acting receptor-selective blocker, on bispectral index scale (BIS). METHODS: Ten patients scheduled for off-pump coronary artery bypass (OPCAB) surgery under fast-track cardiac anesthesia were analyzed. Anesthesia was maintained with appropriate additional administration of fentanyl (total dose: 10-15 microg x kg(-1)) and vecuronium under inhalation of a mixture of oxygen, air and sevoflurane (less than 2%). Landiolol was administered continuously for 5 min, when the heart rate (HR) was 80 or more per minute and the BIS values were kept between 40-60. HR, mean arterial pressure (MAP), cardiac index (CI) and BIS values were recorded at 4 time points (after induction of anesthesia, before administration of landiolol, immediately before comple- tion of administration, and 15 minutes after completion of administration). RESULTS: HR decreased significantly by landiolol administration, but there were no significant changes in MAP, CI and BIS. CONCLUSIONS: This study suggests that landiolol does not affect BIS in OPCAB surgery patients under fast-track cardiac anesthesia.
Adrenergic beta-Antagonists↗
[Colforsin daropate does not affect the cerebral blood-flow in cardiac surgery patients under cardiopulmonary bypass].
BACKGROUND: Cerebral blood flow partly plays a pivotal role in cerebral complications among cardiac surgery patients. We evaluated the effect of colforsin daropate (colforsin) on cerebral blood flow in cardiac surgery patients under cardiopulmonary bypass (CPB) by transcranial Doppler sonography (TCD). METHODS: Eighteen patients scheduled for coronary artery bypass surgery under CPB were assigned randomly to two groups:colforsin group (n=9) and control group (n=9). We assessed cardiac function by measuring cardiac index (CI) and systemic vascular resistance index (SVRI). Cerebral blood flow was evaluated by measuring the peak systolic blood flow velocity (Vs), end-diastolic blood flow velocity (Vd) together with mean blood flow velocity (Vm), and calculated the pulsatility index (PI) in the left carotid siphon by TCD. After baseline measurement, the colforsin loading dosage was increased from 0.25 to 0.5 microg x kg(-1) x min(-1) in colforsin group every 60 minutes. RESULTS: Colforsin significantly increased CI and decreased SVRI compared with pre-levels. In both groups there were no significant changes in Vs, Vd, Vm and PI. CONCLUSIONS: We have demonstrated that colforsin is effective for hemodynamics without cerebral blood flow change in cardiac surgery patients under cardiopulmonary bypass.
Aged↗
[Th1/Th2 balance in systemic inflammatory response syndrome (SIRS)].
The activation of a pro-inflammatory cascade after infection, major surgery, burn or trauma appears to be important in the development of subsequent immune dysfunction, susceptibility to sepsis and multiple organ failure. It is well known that T-cell plays a critical role in the systemic response to infection. Distinct patterns of cytokines are produced by two different types of T-helper cells (Th). Th1 lymphocytes produce IFN-gamma and IL-2, favoring cell mediated immunity; Th2 cells secrete IL-4, IL-5, IL-10, IL-13, favoring humoral immunity. Cytokines produced in systemic inflammatory response syndrome (SIRS) may effect Th subset predominance and subsequent immune responses. We measured Thl/Th2 balance in patients with severe sepsis, SIRS patients with non sepsis, and healthy subjects by flow cytometry. In patients with severe sepsis, Th2 antibody mediated (humoral) immune responses predominate. We believe that severe sepsis clearly induce polarization of T-helper lymphocyte activity with a clear shift in Th2 direction. This type of response may lead immunosuppression. Modulation of Th cell subset predominance may present a novel therapeutic option in the treatment of severe sepsis.
Humans↗
[Pneumothorax during retroperitoneoscopic nephrectomy: a case report].
A 54-year-old female patient was scheduled for retroperitoneoscopic nephrectomy. Anesthesia was induced with propofol and maintained with nitrous oxide/sevoflurane and epidural anesthesia. One hour after the start of the surgery, arterial oxygen saturation suddenly decreased from 99% to 94%. Because her oxygenation gradually improved and hemodynamics was stable, the operation was continued. After the end of the surgery, left pneumothorax was found on a chest X ray. The patient was extubated following thoracocentesis that had improved her pneumothorax and oxygenation. There is no report of pneumothorax in retroperitoneoscopic nephrectomy, as far as we know, although several cases have been reported in laparoscopic nephrectomy. We must be careful of pneumothorax in both laparoscopic and retroperitoneoscopic nephrectomy.
Anesthesia, Epidural↗
Antiviral effects of geranylgeranylacetone: enhancement of MxA expression and phosphorylation of PKR during influenza virus infection.
A cyclic polyisoprenoid compound, geranylgeranylacetone (GGA), has been used as antiulcer drug. GGA is also a potent inducer of heat shock proteins (HSPs). HSPs are considered to induce an antiviral effect; however, the detailed mechanism is unknown. To determine whether GGA might show antiviral activity and what the mechanism is, the effect of GGA against influenza virus (strain PR8) infection in vivo and in vitro was investigated. The results demonstrated that GGA treatment strongly suppressed the deleterious consequences of PR8 replication and was accompanied by an increase in HSP70 gene expression in mice. Results from in vitro analyses demonstrated that GGA significantly inhibited the synthesis of PR8-associated proteins and prominently enhanced expression of human myxovirus resistance 1 (MxA) followed by increased HSP70 transcription. Moreover, GGA augmented the expression of an interferon-inducible double-strand RNA-activated protein kinase (PKR) gene and promoted PKR autophosphorylation and concomitantly alpha subunit of eukaryotic initiation factor 2 phosphorylation during PR8 infection. It is proposed that GGA-induced HSP70 has potent antiviral activity by enhancement of antiviral factors and can clinically achieve protection from influenza virus infection.
Animals↗
Monocarboxylates and glucose utilization as energy substrates in rat brain slices under selective glial poisoning--a 31P NMR study.
We have investigated effects of various energy substrates including glucose, lactate and pyruvate on the recovery of the high energy phosphate levels after high-K+ stimulation in rat brain slices by using 31P NMR. It was found that lactate, pyruvate and glucose almost equally supported the recovery of phosphocreatine (PCr) levels after high-K+ stimulation (60 mM, 8 min) in artificial cerebrospinal fluid (ACSF). In iodoacetic acid (IAA) and fluorocitrate (FC)-pretreated slices, whereas glucose was unable to be utilized, the recovery of the PCr level after high-K+ stimulation in ACSF containing lactate was completely abolished, the recovery of the PCr in ACSF containing pyruvate was unaffected. These results indicate that neurons themselves can utilize pyruvate as an exogenous energy substrate, but not lactate, without glial support. In intact brain, glucose may be metabolized to pyruvate in glial cells and then transported to neurons as an energy substrate. These suggest an astrocyte-neuron pyruvate shuttle mechanism of the brain energy metabolism in vivo. We also investigated the effect of ischemic-preconditioning in FC-pretreated slices, which showed that the PCr levels recovered substantially in ACSF containing lactate after high-K+ stimulation. This indicates that after the preconditioning, such as ischemia, neurons themselves acquired the ability to utilize lactate as an energy substrate.
Animals↗
Lactate utilization as an energy substrate in ischemic preconditioned rat brain slices.
We examined the utilization of lactate as an energy substrate in ischemic preconditioned slices obtained from the rat brain left hemisphere, of which the contralateral middle cerebral artery was occluded 48 h before the slice preparation. The levels of high-energy phosphates in the brain slices were measured using 31P NMR with a time resolution of 4 min at 25 degrees C. When iodoacetic acid-pretreated brain slices were further treated with fluorocitrate, a glial toxin, for 2 h (neuron-rich slices), the recovery of the phosphocreatine (PCr) level in artificial cerebrospinal fluid (ACSF) containing lactate after high-K+ stimulation was completely abolished in intact slices, whereas the PCr level in ischemic preconditioned slices well recovered in otherwise similar conditions. These results indicated that neurons, when preconditioned with ischemia, acquire the ability to utilize lactate as an energy substrate. In parallel experiments, we recorded population excitatory postsynaptic potentials and spikes from granule cells in hippocampal slices. Population spikes of intact slices in ACSF containing lactate were completely abolished in 30 min, but those of the ischemic preconditioned slices were maintained well over 50%. These results show that ischemic preconditioning may induce certain systematic changes in neurons, such as the expression of lactate transporters and/or the activation of lactate dehydrogenase.
Animals↗