Miura K, Yamanaka S, Ebara T, Okumura M, Imanishi M, Kim S, Nakatani T, Iwao H
Department of Pharmacology, Osaka City University Medical School, Osaka, Japan.
Jpn J Pharmacol. 2000 Mar;82(3):261-4. doi: 10.1254/jjp.82.261.
The present experiments were conducted to clarify the mode of cardiovascular action of carboxy-2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), a nitric oxide (NO) scavenger, during rat endotoxic shock by determining cardiac output and systemic arterial tone simultaneously. Lipopolysaccharide (LPS) (10 mg/kg, i.v.) decreased systemic blood pressure and cardiac output with transient increases in hematocrit and total vascular resistance. Administration of carboxy-PTIO (1.7 mg x kg(-1) x min(-1), i.v. for 60 min) at 90 min after LPS attenuated further decline in blood pressure and cardiac output without affecting changes in hematocrit or total vascular resistance. It is concluded that carboxy-PTIO attenuates endotoxin-induced hypotension predominantly by maintaining cardiac output in rat experimental endotoxic shock.
本实验旨在通过同时测定心输出量和体动脉张力,阐明一氧化氮(NO)清除剂羧基-2-苯基-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物(羧基-PTIO)在大鼠内毒素休克期间的心血管作用模式。脂多糖(LPS)(10mg/kg,静脉注射)降低了体循环血压和心输出量,同时血细胞比容和总血管阻力短暂升高。在LPS注射90分钟后给予羧基-PTIO(1.7mg·kg⁻¹·min⁻¹,静脉注射60分钟),可减轻血压和心输出量的进一步下降,而不影响血细胞比容或总血管阻力的变化。得出的结论是,在大鼠实验性内毒素休克中,羧基-PTIO主要通过维持心输出量来减轻内毒素诱导的低血压。