GABAA receptor partially mediated propofol-induced hyperalgesia at superspinal level and analgesia at spinal cord level in rats
Abstract
AIM:
To observe effects of propofol on nociceptive response at superspinal and spinal level in rats.
METHODS:
Two hundreds and fifty-eight Sprague-Dawley male rats were randomized into thirty-two groups. Propofol and bicuculline were microinjected into lateral ventricle (icv), ventrolateral periaqueductal gray (vlPAG), intrathecal (ith), and intraperitoneal (ip). The noxious responses were evaluated by hot plate and formalin test.
RESULTS:
In hot-plate test, systemic and superspinal administration of propofol (40 mg.kg(-1) ip, 100 microg in 10 microL, icv, and 4 microg in 0.4 microL vlPAG microinjection) produced hyperalgesia (P<0.01). Hyperalgesia induced by vlPAG microinjection of propofol was significantly antagonized by 69.8 %, 71.2 %, 98.8 % at 10, 20, and 30 min by microinjection of bicuculline (10 ng in 0.4 microL, vlPAG) (P<0.01). Analgesia induced by ith propofol (100 microg.10 microL(-1)) was antagonized about 81.3 %, 54.8 %, 80.8 %, and 97.4 % at 10, 20, 30 and 40 min by ith bicuculline (P<0.05). In formalin test, systemic and superspinal administration of propofol (40 mg.kg(-1) ip, 4 microg in 0.4 microL, vlPAG) also produced hyperalgesia (P<0.01). The increased formalin pain scores were antagonized about 57.1 % by bicuculline (10 ng, vlPAG) (P<0.05) at 60 min after formalin injection. The decreased formalin pain scores induced by ith propofol (100 microg in 10 microL) were antagonized about 66.7 % at 30 min by ith bicuculline (P<0.05) after formalin injection. Hyperalgesia produced by ip propofol in both hot plate and formalin test could not be antagonized by vlPAG administration of bicuculline.
CONCLUSION:
GABAA receptor partly mediated propofol-induced hyperalgesia at superspinal and analgesia at spinal cord in rats.
Keywords:
To observe effects of propofol on nociceptive response at superspinal and spinal level in rats.
METHODS:
Two hundreds and fifty-eight Sprague-Dawley male rats were randomized into thirty-two groups. Propofol and bicuculline were microinjected into lateral ventricle (icv), ventrolateral periaqueductal gray (vlPAG), intrathecal (ith), and intraperitoneal (ip). The noxious responses were evaluated by hot plate and formalin test.
RESULTS:
In hot-plate test, systemic and superspinal administration of propofol (40 mg.kg(-1) ip, 100 microg in 10 microL, icv, and 4 microg in 0.4 microL vlPAG microinjection) produced hyperalgesia (P<0.01). Hyperalgesia induced by vlPAG microinjection of propofol was significantly antagonized by 69.8 %, 71.2 %, 98.8 % at 10, 20, and 30 min by microinjection of bicuculline (10 ng in 0.4 microL, vlPAG) (P<0.01). Analgesia induced by ith propofol (100 microg.10 microL(-1)) was antagonized about 81.3 %, 54.8 %, 80.8 %, and 97.4 % at 10, 20, 30 and 40 min by ith bicuculline (P<0.05). In formalin test, systemic and superspinal administration of propofol (40 mg.kg(-1) ip, 4 microg in 0.4 microL, vlPAG) also produced hyperalgesia (P<0.01). The increased formalin pain scores were antagonized about 57.1 % by bicuculline (10 ng, vlPAG) (P<0.05) at 60 min after formalin injection. The decreased formalin pain scores induced by ith propofol (100 microg in 10 microL) were antagonized about 66.7 % at 30 min by ith bicuculline (P<0.05) after formalin injection. Hyperalgesia produced by ip propofol in both hot plate and formalin test could not be antagonized by vlPAG administration of bicuculline.
CONCLUSION:
GABAA receptor partly mediated propofol-induced hyperalgesia at superspinal and analgesia at spinal cord in rats.