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Takumi Taniguchi

Publications and source records attributed to Takumi Taniguchi.

16 recordsLinked to original sources
PubMed2006

Dose-related effects of direct hemoperfusion using a cytokine adsorbent column for the treatment of experimental endotoxemia.

OBJECTIVE: To clarify the dose-related effects of direct hemoperfusion using a cytokine adsorbent column (CTR) on the mortality and inflammatory responses to endotoxin-induced shock in rats. DESIGN: Prospective and randomized study. SETTING: University research laboratory. SUBJECTS: Male Wistar rats. INTERVENTIONS: Forty-eight rats were injected intravenously with Escherichia coli endotoxin (15 mg/kg over 2 min), and then were randomly allocated to one of the following four groups (n = 12 per group): control group, treated without CTR for 120 min; quarter-dose treatment group, treated with CTR 0.25 ml for 120 min; half-dose treatment group, treated with CTR 0.50 ml; and full-dose treatment group, treated with CTR 1.0 ml. MEASUREMENTS AND RESULTS: Hemodynamics and arterial blood gases were recorded, and mortality and plasma cytokine concentrations were calculated for the 8-h observation period. The mortality rates 8 h after endotoxin injection were 92%, 58%, 42% and 17% for the control column, quarter-dose, half-dose, and full-dose CTR groups, respectively. The increases in plasma cytokine concentrations were smaller in the half-dose and full-dose CTR treatment groups than in the endotoxemic group. CONCLUSIONS: The present study showed that CTR treatment dose-dependently decreased the mortality rate and inhibited inflammatory responses in vivo.

Analysis of Variance↗
PubMed2006

Effects of post-treatment with direct hemoperfusion using a CTR column on mortality and inflammatory responses to endotoxin-induced shock in rats.

BACKGROUND: To clarify the effects of post-treatment with direct hemoperfusion using a CTR column on the mortality and inflammatory responses to endotoxin-induced shock in rats. METHODS: Thirty-six male rats were randomly assigned to 1 of 3 groups (n = 12/group): the endotoxemic group, receiving intravenous Escherichia coli endotoxin (15 mg/kg over 2 min); the control column group, treated without CTR for 120 min at 2 h after endotoxin injection, and CTR-post-treatment group, treated with CTR for 120 min at 2 h after endotoxin injection. Hemodynamics, arterial blood gases, and mortality were recorded for the 8-hour observation period, and plasma cytokine concentrations were measured every 4 h. RESULTS: The mortality rates were 83, 83 and 33% for the endotoxemic, control column, and CTR post-treatment groups, respectively. The increases in IL-6 concentrations were less for the CTR post-treatment group than the other 2 groups. CONCLUSION: The present study shows that CTR post-treatment inhibited hypotension and elevations in IL-6 concentrations, reducing the mortality rate of rats with endotoxin-induced shock.

Animals↗
PubMed2006

A novel adsorbent of circulating bacterial toxins and cytokines: the effect of direct hemoperfusion with CTR column for the treatment of experimental endotoxemia.

OBJECTIVES: The current study examined the ability of a new adsorbent, CTR, to remove enterotoxins, toxic shock syndrome toxin-1 (TSST-1), and cytokines from blood and/or serum in vitro and the effects of the extracorporeal treatment with CTR column on mortality rate and inflammatory responses to endotoxic shock in vivo. DESIGN: Laboratory investigation. SETTING: University and company experimental laboratory. MATERIALS: CTR is composed of porous cellulose beads to which a hydrophobic organic compound with a hexadecyl alkyl chain has been covalently bound to the surface as a ligand. Human/bovine serum and human blood samples in vitro and Male Wistar rats were used. INTERVENTIONS: CTR's ability to adsorb bacterial toxins and cytokines related to sepsis in serum and/or blood was examined with an in vitro batch adsorption protocol. In vivo, male Wistar rats were anesthetized and assigned to one of three groups (n=14 per group): Escherichia coli endotoxin (15 mg/kg intravenously) alone (endotoxemic), apheresis with control column without CTR for 120 mins (control column), or extracorporeal treatment with CTR column for 120 mins (CTR treatment). MEASUREMENTS AND MAIN RESULTS: With use of the CTR adsorbent, the adsorption rates were 50% to 90% for enterotoxins, TSST-1, and cytokines such as TNF-alpha and interleukin (IL)-6 in the batch tests. In vivo, the mortality rates at 8 hrs after endotoxin injection were 92%, 92%, and 14% for the endotoxemic, control column, and CTR treatment groups, respectively. Hypotension and elevated plasma cytokine concentrations and the infiltration of neutrophils of the lungs were less conspicuous in the CTR treatment group than in the other two groups. CONCLUSIONS: CTR, a novel adsorbent, effectively adsorbed small- to middle-sized proteins, such as cytokines, enterotoxins, and TSST-1 in vitro. Direct hemoperfusion apheresis with CTR column reduced mortality and had inhibitory effects on the inflammatory responses during endotoxemia in vivo. These findings suggest that extracorporeal blood purification with CTR column may be available to use for patients with sepsis and/or endotoxemia.

Adsorption↗
PubMed2006

Effects of extracorporeal treatment with Lixelle on the mortality and inflammatory responses to endotoxin-induced shock in rats.

Endotoxemia and endotoxic shock are common problems in intensive care units and are associated with a very high mortality. Several previous studies have shown that Lixelle, which absorbs beta2-microglobulin for the treatment of dialysis-related amyloidosis, is also useful for the adsorption of inflammatory cytokines and endotoxins. The current study examined the use of Lixelle and its effects on the mortality and inflammatory responses to endotoxin-induced shock in rats. Male Sprague-Dawley rats were anesthetized and assigned to one of four groups (N = 13 per group): Escherichia coli endotoxin (15 mg/kg, i.v.) alone (endotoxemic); direct hemoperfusion apheresis without Lixelle for 120 min (direct hemoperfusion (DHP) alone); Lixelle treatment with Lixelle for 120 min immediately after endotoxin injection (Lixelle treatment); or Lixelle treatment with Lixelle for 120 min 2 h after endotoxin injection (Lixelle post-treatment). Hemodynamics and plasma lactate and cytokine concentrations were measured during observation. Mortality was assessed up to 8 h after the endotoxin injection. The mortality rates at 8 h after endotoxin injection were 92%, 85%, 23% and 46% for the endotoxemic, DHP-alone, Lixelle treatment, and Lixelle post-treatment groups, respectively. Elevated plasma cytokine concentrations were less conspicuous in the Lixelle treatment group than in the other three groups. Thus, Lixelle treatment drastically reduced the high mortality and the inflammatory responses in endotoxin-exposed rats. Moreover, Lixelle post-treatment also suppressed hypotension and a high mortality, although the inflammatory responses were the same as for endotoxin alone. These findings indicate that Lixelle treatment might be an effective therapy for endotoxemia and endotoxic shock.

Adsorption↗
PubMed2005

Sevoflurane pretreatment inhibits endotoxin-induced shock in rats.

UNLABELLED: We examined the effects of sevoflurane pretreatment on mortality and inflammatory responses during endotoxin-induced shock. Rats were allocated randomly to 1 of 4 groups (n = 12 per group): an endotoxemia group, receiving IV Escherichia coli endotoxin (15 mg/kg over 2 min); a saline control group, receiving 0.9% saline (1.0 mL/kg); a sevoflurane-only group, receiving 2.4% sevoflurane for 30 min immediately before injection of 0.9% saline; and a sevoflurane pretreatment group, receiving 2.4% sevoflurane for 30 min immediately before injection of endotoxin. Hemodynamic variables, arterial blood gases, and plasma concentrations of tumor necrosis factor-alpha and interleukin-6 were measured. The 8-h mortality rate was determined. Systolic arterial blood pressure and acid-base balance improved with sevoflurane pretreatment before induction of endotoxemia. Mortality rates 8 h after endotoxin injection were 83%, 8%, 0%, and 25% for the endotoxemia, saline control, sevoflurane-only, and sevoflurane pretreatment groups, respectively. Plasma cytokine concentrations were significantly larger in the endotoxemia group than in the other groups. Sevoflurane pretreatment inhibited inflammatory responses and decreased mortality in rats exposed to endotoxin. IMPLICATIONS: Sevoflurane pretreatment decreased mortality rate, severity of hypotension, and acidosis, and inhibited cytokine responses in rats injected with endotoxin, suggesting that sevoflurane may be an anesthetic of choice in endotoxemic states.

Anesthetics, Inhalation↗
PubMed2005

Anti-inflammatory effects of intravenous anesthetics on endotoxemia.

Endotoxemia and endotoxin shock are common problems in the intensive care unit and carry a very high mortality rate. Endotoxemia increases production of endogenous cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), IL-6, and IL-8. Not only endotoxin but also cytokines have been implicated as important factors in the pathophysiology of endotoxic shock and the development of cardiovascular dysfunction in endotoxemia. Recently, it has been shown both in vitro and in vivo that several intravenous anesthetics have anti-inflammatory effects. Thiopental and ketamine inhibit the endotoxin-induced TNF-alpha, IL-1 and IL-8 responses and increase IL-10 release in vitro. Ketamine prevent the pro-inflammatory cytokine (TNF-alpha, IL-1, and IL-6) responses to endotoxemia in vivo. Moreover, thiopental and ketamine suppress the activation of nuclear factor-kappa B induced by endotoxin. Propofol have been proven its anti-inflammatory effects on endotoxemia both in vitro and in vivo, but several studies have shown that propofol does not have any anti-inflammatory effects and deteriorates the inflammatory response to endotoxemia. This article reviews the anti-inflammatory effects of intravenous anesthetics on endotoxemia and endotoxic shock.

Anesthetics, Intravenous↗
PubMed2005

[Role of anesthesiologists is the education of cardiopulmonary resuscitation in local hospitals].

BACKGROUND: In Japanese local hospitals there are not many persons who can give speedy and exact medical treatment in emergency. We investigated a role of anesthesiologists in the education of cardiopulmonary resuscitation (CPR) in local hospitals. METHODS: A total of 3 doctors and 30 nurses completed the questionnaire about the education of CPR after training of advanced cardiac life support (ACLS) in a local hospital. RESULTS: It showed that all doctors and nurses have had some anxiety about the emergency treatment of patients and could understand the importance of CPR. Moreover, most of them answered that they wanted to learn ACLS more, and that the training of ACLS simulation was the most impressive. CONCLUSIONS: It is important for anesthesiologists to teach ACLS and to promote the spread of ACLS in local hospitals.

Anesthesiology↗
PubMed2004

Effects of dexmedetomidine on mortality rate and inflammatory responses to endotoxin-induced shock in rats.

OBJECTIVES: The aim of this study was to document the effects of a new sedative agent, dexmedetomidine, on the mortality rate and inflammatory responses to endotoxin-induced shock in rats. DESIGN: Randomized laboratory study. SETTING: University experimental laboratory. SUBJECTS: Fifty-seven male rats. INTERVENTIONS: The animals were randomly assigned to one of four groups. The endotoxemic group (n = 16) received intravenous Escherichia coli endotoxin (15 mg/kg over 2 mins). The saline control group (n = 10) was given saline alone. The dexmedetomidine alone group (n = 15) was treated identically to the control group but also received dexmedetomidine (infusion at 5 microg.kg(-1).hr(-1)) immediately after the injection of 0.9% saline. The dexmedetomidine-endotoxin group (n = 16) was treated identically to the endotoxemic group with the additional administration of dexmedetomidine (infusion at 5 microg.kg(-1).hr(-1)) immediately after endotoxin injection. MEASUREMENTS AND MAIN RESULTS: Hemodynamics and arterial blood gases were recorded and plasma cytokine concentrations measured during the observation. The mortality rate was assessed up to 8 hrs after endotoxin or saline injection. In addition, microscopic findings of lung tissue for each group were obtained at necropsy. Mortality rates 8 hrs after endotoxin injection were 94%, 10%, 0%, and 44% for the endotoxemic, saline control, dexmedetomidine alone, and dexmedetomidine-endotoxin groups, respectively. Hypotension and increases in plasma cytokine (tumor necrosis factor-alpha and interleukin-6) concentrations and infiltration of neutrophils in the airspace or vessel walls of the lungs were less in the dexmedetomidine-endotoxin group than in the endotoxemic group. CONCLUSIONS: Dexmedetomidine reduced mortality rate and had an inhibitory effect on inflammatory response during endotoxemia. These findings suggest that dexmedetomidine administration may inhibit the inflammatory response.

Animals↗
PubMed2004

The antiinflammatory effects of ketamine in endotoxemic rats during moderate and mild hypothermia.

UNLABELLED: Endotoxemia is a common problem among critically-ill patients. We previously found that ketamine inhibited hypotension, metabolic acidosis, and increase of plasma cytokines during endotoxemia in rats. Although endotoxic patients often develop hypothermia, it has not been determined whether ketamine retains its antiinflammatory effects during hypothermia. We investigated the effects of ketamine on endotoxemic rats subjected to moderate and mild hypothermia. Male Wistar rats (n = 100) were anesthetized intraperitoneally with pentobarbital sodium and assigned to one of two protocols: one representing moderate hypothermia (30 degrees C-32 degrees C) and the other, mild hypothermia (33 degrees C-35 degrees C). Each protocol included 5 equal groups: 1). Escherichia coli endotoxin (15 mg/kg IV) in normothermia, 2). ketamine (10 mg x kg(-1) x h(-1) IV) during and after endotoxin injection in normothermia, 3). saline in hypothermia, 4). endotoxin (15 mg/kg IV) in hypothermia, and 5) ketamine (10 mg x kg(-1) x h(-1) IV) in hypothermia after endotoxin injection. Rats were then warmed or cooled to maintain rectal temperatures as above for 6 h. We assessed hemodynamics, acid-base status, and plasma concentrations of tumor necrosis factor-alpha, and interleukin-6. Endotoxemic rats developed hypotension and metabolic acidosis as well as increased plasma cytokine concentrations. At 6 h after endotoxin injection, the mean systolic arterial blood pressure decreased by 71% in the saline/normothermia/endotoxin group, whereas it decreased by only 6%, 41%, and 29% in the ketamine/normothermia/endotoxin, saline/moderate hypothermia/endotoxin, and ketamine/moderate hypothermia/endotoxin groups, respectively. Ketamine administration to endotoxemic rats with hypothermia, whether moderate or mild, also attenuated hypotension, metabolic acidosis, and cytokine increase, but these effects were not superior to those of hypothermia alone. Our findings suggest that, during hypothermia, ketamine administration may not have additive beneficial antiinflammatory effects. IMPLICATIONS: Although ketamine administration decreased the severity of hypotension and acidosis in endotoxemic rats, ketamine administration may not have additive beneficial antiinflammatory effects during hypothermia.

Anesthetics, Dissociative↗
PubMed2003

Effects of hypothermia on mortality and inflammatory responses to endotoxin-induced shock in rats.

We studied the effects of hypothermia on mortality rate, concentrations of tumor necrosis factor alpha and interleukin 6 in plasma, and the end products of nitric oxide (NO) in endotoxemia. It was found that moderate and mild hypothermia improved the mortality rate and attenuated cytokine responses and the elevation of the end products of NO after endotoxin injection and that these beneficial effects were similar for moderate and mild hypothermia.

Animals↗
PubMed2003

The dose-related effects of ketamine on mortality and cytokine responses to endotoxin-induced shock in rats.

In our previous study, ketamine administration was found to inhibit hypotension, metabolic acidosis, and cytokine responses in endotoxemia. However, only a few studies have indicated whether ketamine has the dose-related beneficial effects after endotoxin injection. Our objective was to clarify the dose-related effects of ketamine on mortality and cytokine responses to endotoxemia in rats. Sixty-five rats were divided at random among five equal groups: Group C was given saline alone. Group E was given endotoxin alone (Escherichia coli endotoxin; 10 mg/kg, IV). Group L received a a low dose of ketamine (5 mg.kg(-1).h(-1), IV), Group M a medium dose of ketamine (10 mg.kg(-1).h(-1), IV), and Group H a high dose of ketamine (20 mg.kg(-1).h(-1), IV), all exposure to endotoxin. After endotoxin injection, hemodynamics, acid-base status, mortality rate, and plasma concentrations of tumor necrosis factor alpha and interleukin 6 were assessed for each of the five groups. Endotoxin injection produced progressive hypotension, metabolic acidosis, and a large increase in plasma cytokine concentrations. Mortality rates 8 h after endotoxin injection were 0% for group C, 92% for group E, 48% for group L, 0% for group M, and 32% for group H. Ketamine administration thus clearly had a beneficial effect on mortality rates, with that for group M lower than for groups L and H (P < 0.05). The cytokine responses to endotoxin were somewhat suppressed in group M but not in group L. Ketamine administration dose-independently inhibited hypotension, metabolic acidosis, and cytokine responses in rats injected with endotoxin.

Animals↗
PubMed2003

Effects of ketamine and propofol on the ratio of interleukin-6 to interleukin-10 during endotoxemia in rats.

Our previous study reported that the change in the ratio of interleukin (IL)-6 to IL-10 influences the severity of sepsis in patients with systemic inflammatory response syndrome. We evaluated the change in the ratio of IL-6 to IL-10 after administration of ketamine or propofol in endotoxin-exposed rats in order to evaluate the relationship of pro-inflammatory and anti-inflammatory cytokines following ketamine or propofol administration during endotoxemia. We randomly assigned 40 rats to one of four equal groups: endotoxin alone, receiving Escherichia coli endotoxin (15 mg/kg, i.v.); saline control; ketamine (10 mg x kg(-1) x h(-1), i.v.) before and during exposure to endotoxin; and propofol (10 mg x kg(-1) x h(-1), i.v.) before and during exposure to endotoxin. We measured the plasma concentrations of tumor necrosis factor (TNF)-alpha, IL-6, and IL-10 and calculated the ratio of IL-6 to IL-10 in each group. The current study showed that ketamine and propofol administration attenuated the increase in TNF-alpha, IL-6, and IL-10, and ketamine attenuated the increase in the ratio of IL-6 to IL-10, but propofol increased this ratio in rats receiving a single intravenous bolus of endotoxin. While the mechanisms responsible for the inhibitory effects require further investigation, our results suggest that proper use of ketamine as an anesthetic agent may offer certain advantages in the management of patients with endotoxemia.

Anesthetics, Dissociative↗
PubMed2003

[Evaluation of the animal model for endotoxin-induced shock].

BACKGROUND: We evaluated our animal model for endotoxin-induced shock and compared its characteristics with those of clinical endotoxic shock. METHODS AND RESULTS: Male Japanese rabbits anesthetized with urethane and ventilated mechanically were assigned to one of two groups: the endotoxin group, receiving intravenous E. coli endotoxin (0.5 mg.kg-1) via the mesenteric vein; control group, receiving 0.9% saline. After the endotoxin injection, the mean arterial pressure, cardiac output, and systemic vascular resistance decreased progressively. Four hours after the endotoxin injection, the levels of both interleukin (IL)-6 and IL-8 in the endotoxin group were higher than those in the control group. Male Wistar rats anesthetized with pentobarbital and ventilated mechanically were assigned to one of two groups: endotoxin group, receiving intravenous E. coli endotoxin (15 mg.kg-1); and control group, receiving 0.9% saline. After the endotoxin injection, the systolic arterial pressure and heart rate decreased progressively. The plasma tumor necrosis factor alpha and IL-6 increased in the endotoxin group. CONCLUSIONS: We could not observe the hyperdynamic state and multiple organ dysfunctions and did not administer vasopressors and antibiotics in our endotoxin shock models, compared with the characteristics of clinical endotoxin shock. Further refinement of our animal models for endotoxin shock is challenging.

Animals↗
PubMed2002

Effects of posttreatment with propofol on mortality and cytokine responses to endotoxin-induced shock in rats.

OBJECTIVE: To clarify the effects of posttreatment with propofol administration on mortality rate and cytokine responses to endotoxin-induced shock in rats. DESIGN: Randomized prospective laboratory study. SETTING: University laboratory. SUBJECTS: Thirty-three male rats. INTERVENTIONS: Animals were randomly assigned to one of three groups (n = 11 per group): a) endotoxemic group, receiving intravenous Escherichia coli endotoxin (20 mg/kg over 2 mins); b) early posttreatment group, treated identically to the endotoxemic group with the additional administration of propofol (10 mg/kg bolus, followed by infusion at 10 mg x kg(-1) x hr(-1)) 1 hr after the injection of endotoxin; and c) late posttreatment group, treated identically to the endotoxemic group with the additional administration of propofol (10 mg/kg bolus, followed by infusion at 10 mg x kg(-1) x hr(-1)) 2 hrs after the injection of endotoxin. MEASUREMENTS AND MAIN RESULTS: Hemodynamics and arterial blood gases were recorded, and mortality rate and plasma cytokine concentrations were calculated for the 5-hr observation. The mortality rate 5 hrs after endotoxin injection was 73% for the endotoxic, 9% for the early posttreatment, and 36% for the late posttreatment groups. The mortality rate for the early posttreatment group was significantly lower than that for the other groups. The increases in plasma cytokine (tumor necrosis factor-alpha and interleukin-6 and -10) concentrations were less for the early posttreatment group than the other two groups. CONCLUSIONS: The early posttreatment of propofol after endotoxin injection drastically reduced the mortality rate of rats and attenuated their cytokine responses. Moreover, propofol attenuated the production of tumor necrosis factor-alpha. These findings suggest that propofol administration may be beneficial during sepsis.

Animals↗