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Articles by J Kato
Total Records ( 2 ) for J Kato
  J Kato , Y Ogawa , W Kojima , K Aoki , S Ogawa and K. Iwasaki

The low and moderate doses of dexmedetomidine reduce arterial pressure and heart rate (HR), suggesting attenuation of sympathetic activity and dominance of cardiac-vagal activity. These autonomic responses under dexmedetomidine sedation may attenuate cardiovascular reflex responses to temporal reduction in arterial pressure, inducing a severe hypotension. We therefore investigated the effects of dexmedetomidine on cardiovascular reflex responses to temporal reduction in arterial pressure induced by the thigh cuff method.


Twelve healthy men received placebo, low-dose (loading 3 µg kg–1 h–1 for 10 min; maintenance 0.2 µg kg–1 h–1 for 60 min), and moderate-dose (loading 6 µg kg–1 h–1 for 10 min; maintenance 0.4 µg kg–1 h–1 for 60 min) dexmedetomidine infusions in a randomized, double-blind, crossover study. After 70 min of drug infusion, systolic arterial pressure (SAP) and HR responses after thigh cuff deflation were evaluated as indices of cardiovascular reflex.


Reduction in SAP (SAP) [placebo 8 (4), low 12 (4), moderate 19 (5) mm Hg] after thigh cuff deflation was significantly greater in dexmedetomidine than placebo infusions, in a dose-dependent manner. The change in HR (HR), HR/SAP, and the percentage restoration of SAP were lower with dexmedetomidine compared with placebo.


The present results indicated that dexmedetomidine weakens arterial pressure preservation and HR responses after thigh cuff deflation, suggesting attenuated cardiovascular reflexes. Therefore, it must be cautioned that dexmedetomidine can lead to further and sustained reduction in arterial pressure during transient hypotension induced by postural changes, haemorrhage, and/or other stresses.

  K Kawa , H Tsutsui , R Uchiyama , J Kato , K Matsui , Y Iwakura , T Matsumoto and K. Nakanishi

Hyper-coagulation, hypothermia, systemic inflammatory responses and shock are major clinical manifestations of endotoxin shock syndrome in human. As previously reported, mice primed with heat-killed Propionibacterium acnes are highly susceptible to the action of LPS to induce tumour necrosis factor (TNF)- and to that of TNF- to trigger lethal shock. Here we investigated the mechanisms underlying the P. acnes-induced sensitization to LPS and TNF- and the development of individual symptoms after subsequent challenge with LPS or TNF-. Propionibacterium acnes-primed wild-type (WT) mice, but not naive mice, exhibited hyper-coagulation with elevated levels of thrombin–antithrombin complexes and anti-fibrinolytic plasminogen activator inhibitor 1 in their plasma, hypothermia, systemic inflammatory responses and high mortality rate after LPS or TNF- challenge. Propionibacterium acnes treatment reportedly induces both Th1 and Th17 cell development. Propionibacterium acnes-primed Il12p40–/– and Ifn–/– mice, while not Il17A–/– mice, evaded all these symptoms/signs upon LPS or TNF- challenge, indicating essential requirement of IL-12–IFN- axis for the sensitization to LPS and TNF-. Furthermore, IFN- blockade just before LPS challenge could prevent P. acnes-primed WT mice from endotoxin shock syndrome. These results demonstrated requirement of IFN- to the development of endotoxin shock and suggested it as a potent therapeutic target for the treatment of septic shock.

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