• K Hirota, T Sato, S F Rabito, E K Zsigmond, and A Matsuki.
• Department of Anesthesiology, University of Illinois at Chicago, College of Medicine, 60612, Chicago, IL, USA.
• J Anesth. 1996 Mar 1;10(1):55-7.

AbstractRecent studies indicate that not only inflammatory cells but also neural mechanisms by which tachykinins such as substance P (SP) and neurokinin A (NKA) are released from vagal afferent C-fiber contribute to asthma. Although ketamine (K) has been used in the anesthetic management of asthmatic patients, the mechanism by which K relaxes the airway smooth muscle is still uncertain, and no information exists on any differential effect of K and its isomers. We determined the spasmolytic effect of racemic [R(±)]K and its isomers S(+) K and R(-) K on SP and NKA-induced contraction of tracheal smooth muscle in guinea pigs. Strips of guinea pig trachea were mounted in an organ bath filled with Tyrode's solution at 37°C bubbled with 95% O2/5% CO2. Strip tension was measured isometrically with a force displacement transducer. Strip contraction was elicited with SP 10(-6) M or NKA 5×10(-7) M.R(±), R(-), or S(+) K (4.5-18.0×10(-4)M) was cumulatively administered into the bath. The calculated ED50 values (the concentration that relaxed the contraction by 50%) of R(±), R(-) and S(+) K were 7.6±0.5, 7.8±0.6, and 7.6±0.5 (10(-4)M), respectively, when the contraction was elicited with SP, and 8.0±1.0, 8.2±1.2, and 7.9±1.3 (10(-4)M), respectively, when NKA was used. We concluded that K and its isomers have equipotent spasmolytic effects on airway smooth muscle precontracted with tachykinins.

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