- 作者: Gau-Jun Tang a, You-Lan Yang b, Yu Ru Kou b
- 作者服務機構: a Department of Anesthesiology and Surgical CriticalCare, Veterans General Hospital-Taipei ,b Institute of Physiology, School of Medicine, National Yang-Ming University ,Taipei , Taiwan , ROC
- 中文摘要: --
- 英文摘要: 96,345. The plasma extravasation was largely attenu-ated by CP-96,345 and/or SR-48,968. We conclude that(1) endogenous tachykinins play an important role inproducing changes in lung mechanics and airway micro-vascular leakage during the early phase of endotoxemiaand (2) activation of tachykinin NK receptors is responsi-ble for the former response, while activation of bothtachykinin NK and NK receptors is involved in the latterresponse.We investigated the role of tachykinins in airway neuro-genic responses occurring in the early phase of endotox-emia. Forty-eight anesthetized guinea pigs were evenlydivided into six groups pretreated with either saline vehi-cle, CP-96,345 (a tachykinin NK receptor antagonist),SR-48,968 (a tachykinin NK receptor antagonist) or CP-96,345 and SR-48,968 in combination. Animals then re-ceived an intravenous injection of either saline (the vehi-cle for endotoxin) or endotoxin (30 mg/kg). Total lungresistance (R ) and dynamic lung compliance (C ) werecontinuously measured before and 30 min after adminis-tration of saline or endotoxin. Airway microvascularleakage was assessed at the end of the observation peri-od. Endotoxin significantly increased R and decreasedC 10 min after intravenous endotoxin injection. Plas-ma extravasation significantly increased in the trachea,main bronchi and intrapulmonary airways with endotox-in administration. These changes in lung mechanicswere abolished by SR-48,968, but were unaffected by CP-
- 中文關鍵字: --
- 英文關鍵字: Tachykinins, Endotoxin, Microvascular permeability