ELUCIDATION OF PATHOGENESIS OF ANAPHYLACTIC SHOCK AND DEVELOPMENT OF ITS SPECIFIC TREATMENT
| Project/Area Number |
09470336
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | JUNTENDO UNIVERSITY |
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Principal Investigator |
MITSUHATA Hiromasa Juntendo University, Lecturer, 医学部, 講師 (70108934)
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| Co-Investigator(Kenkyū-buntansha) |
SAITOH Jin Jichi Medical School, Assistant, 医学部, 助手 (20260838)
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| Project Period (FY) |
1997 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥12,200,000 (Direct Cost: ¥12,200,000)
Fiscal Year 2000: ¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1999: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1998: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1997: ¥3,300,000 (Direct Cost: ¥3,300,000)
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| Keywords | ANAPHYLAXIS / 3-AMINOBENZAMIDE / PHOPHODIESTERASE 4 AND 1 / ENDOTHELIN / PROPFOL / SEVOFLURANE / SHOCK / アナフィラキシー / 気管支けいれん / プロポフォール / セボフルレン / ショック / エンドセリン / 病態 / phosphodiesterase inhibitor / アナフィラキシ- / PARS / 一酸化窒素 |
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| Research Abstract |
1. The PARS inhibitor 3-aminobenzamide does not improve cardiac depression or bronchospasm provoked by systemic aggregated anaphylaxis in rabbits in vivo, implying that the pathophysiological changes associated with systemic anaphylaxis may not be related to activation of an energy-consuming DNA repair cycle trigged by PARS.These results, along with the lack of improvement in survival rates in PARS inhibitor-treated animals, imply that PARS may not play an important role in anaphylaxis, although direct proof of activation of PARS is lacking in this study.
2. The administration of an inhibitor of PDEs 4 and 1, KF19514, either before or after antigen challenge, improved bronchoconstriction induced by systemic anaphylaxis in rabbits with minimal concomitant cardiovascular side effects compared with aminophylline, suggesting that PDE 4 inhibitors may be useful in the treatment of systemic anaphylaxis.
3. The production of ET-1 rises rapidly during anaphylactic shock, suggesting that ET-1 may have a pathophysiological role during anaphylactic shock. The purpose of the present study was to investigate the role of ET-1 in the cardiovascular depression and bronchospasm provoked by anaphylaxis in vivo. In addition, to determine whether inhibition of ET-1 would improve cardiovascular and bronchospasm in anaphylaxis, we administered BQ610, an ETA receptor antagonist, to fentanyl anesthetized rabbits before the induction of anaphylaxis. In conclusion, ET-1 and ETA receptor does not play an important role in anaphylactic shock.
4. Propfol is as effective as sevoflurane in attenuating bronchoconstriction associated with anaphylaxis in rabbits. Propofol may be a useful alternative to sevoflurane or isoflurane in the treatment of bronchospasm in asthma or anaphylaxis.
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Report
(5 results)
Research Products
(5 results)
