R Ando1, C Watanabe. 1. Center for Laboratory Animal Science, Tohoku Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku 981-8558, Sendai, Japan. rando@tohoku-pharm.ac.jp
Abstract
BACKGROUND: In this study we have assessed vascular pain caused by the i.v. anaesthetic agent, propofol, using the flexor reflex response and compared this with that of capsaicin in anaesthetized intact rats. METHODS: Experiments were performed on 133 male Sprague-Dawley rats weighing 280-340 g. The animals were anaesthetized with urethane (1.3 g kg(-1), i.p.), and an arterial cannula was inserted to the level of the bifurcation of the femoral artery. The magnitude of the flexor reflex was examined by recording the electromyogram from the posterior biceps femoris/semitendinosus muscles. RESULTS: Our data show that the flexor reflexes evoked by intra-arterial (i.a.) injection of propofol (1%, 25-100 microl) and capsaicin (0.05-0.2 microg) were dose dependent. An initial i.a. injection of procaine (2%, 200 microl) blocked both responses. Furthermore, the flexor reflex induced by these chemical stimuli were inhibited by morphine (5 mg kg(-1), s.c.) and restored with naloxone (1.5 mg kg(-1), s.c.). Pre-treatment with capsazepine (20 microg, i.a.), a selective VR1 antagonist, inhibited the capsaicin-evoked response, but not that of propofol. Indomethacin (10 mg kg(-1), i.p.), a non-selective cyclo-oxygenase inhibitor, inhibited only the propofol-evoked response and this recovered with arterial PGE2 (5 microg). CONCLUSIONS: Collectively our data suggest that propofol-evoked vascular pain is mainly initiated by prostanoids.
BACKGROUND: In this study we have assessed vascular pain caused by the i.v. anaesthetic agent, propofol, using the flexor reflex response and compared this with that of capsaicin in anaesthetized intact rats. METHODS: Experiments were performed on 133 male Sprague-Dawley rats weighing 280-340 g. The animals were anaesthetized with urethane (1.3 g kg(-1), i.p.), and an arterial cannula was inserted to the level of the bifurcation of the femoral artery. The magnitude of the flexor reflex was examined by recording the electromyogram from the posterior biceps femoris/semitendinosus muscles. RESULTS: Our data show that the flexor reflexes evoked by intra-arterial (i.a.) injection of propofol (1%, 25-100 microl) and capsaicin (0.05-0.2 microg) were dose dependent. An initial i.a. injection of procaine (2%, 200 microl) blocked both responses. Furthermore, the flexor reflex induced by these chemical stimuli were inhibited by morphine (5 mg kg(-1), s.c.) and restored with naloxone (1.5 mg kg(-1), s.c.). Pre-treatment with capsazepine (20 microg, i.a.), a selective VR1 antagonist, inhibited the capsaicin-evoked response, but not that of propofol. Indomethacin (10 mg kg(-1), i.p.), a non-selective cyclo-oxygenase inhibitor, inhibited only the propofol-evoked response and this recovered with arterial PGE2 (5 microg). CONCLUSIONS: Collectively our data suggest that propofol-evoked vascular pain is mainly initiated by prostanoids.
Authors: José A Matta; Paul M Cornett; Rosa L Miyares; Ken Abe; Niaz Sahibzada; Gerard P Ahern Journal: Proc Natl Acad Sci U S A Date: 2008-06-23 Impact factor: 11.205
Authors: Richard E Galgon; Peter Strube; Jake Heier; Jeremy Groth; Sijian Wang; Kristopher M Schroeder Journal: J Anesth Date: 2014-08-06 Impact factor: 2.078