SummaryWe examined the antinociceptive effect of intrathecally administered magnesium sulphate (MgSO 4 ) in rats, using acute pain models including mechanical pressure, heat and subcutaneous formalin injection. According to the locomotion test 10 ml of 6.2% MgSO 4 did not produce motor paralysis. At the same dose, responses to pressure and heat were intact, compared with controls given saline. MgSO 4 produced depression of pain responses only after the first 10 min in the formalin test. Our studies indicated that MgSO 4 did not show remarkable antinociceptive effects in acute pain models.
The NMDA receptor and the NK-1 receptor are important determinants of the MAC of isoflurane, exerting this influence by inhibition of pain transmission in the spinal cord, while mGlu and AMPA receptors have no effect on the MAC of isoflurane.
SummarySomatosensory evoked potential, locomotion and vocalisation upon tail pinch in rats was studied in order to determine whether intrathecal magnesium sulphate administration causes spinal anaesthesia. In Wistar rats with indwelling intrathecal catheters, cortical somatosensory evoked potential was recorded following stimulation via electrodes inserted into the hind paw under chloral hydrate anaesthesia before and after intrathecal administration of 10 ml of either magnesium sulphate (12.3% or 24.6%) or lignocaine (4% or 8%). Locomotion and vocalisation after tail pinch were tested following intrathecal administration of the same two drugs in conscious rats. Somatosensory evoked potential amplitude was diminished after administration of lignocaine (p < 0.05) but did not change after magnesium sulphate. Latency of P1 was increased by lignocaine and by magnesium sulphate 12.3% (p < 0.05). Although lower extremity paralysis was observed in both groups, its duration with magnesium sulphate was much longer than with lignocaine. Vocalisation was recognised after magnesium sulphate 12.3%, but was not observed after lignocaine 8% during paralysis (p < 0.05). We believe that magnesium sulphate caused motor paralysis, but not complete analgesia.
Intrathecal neurokinin-1 receptor antagonist reduces isoflurane MAC in ratsPurpose: To study the effects of intrathecal administration of a neurokinin-l(NK-l) receptor antagonist (CP96,345) on the minimum alveolar anaesthetic concentration (MAC) of isoflurane in anaesthetized rats, and on the locomotive activity of conscious rats.Methods: Wlstar rats (n=36) were fitted with indwelling intrathecal catheters, and the MAC of isoflurane was determined following the intrathecal administration of saline (control group) or the NK-I receptor antagonist CP96,345 (CP) at I, I 0 and I00 #g. Subsequently a reversal dose of intrathecal Substance P (SP) at I, I 0 and 100Hg was administered and MAC isoflurane was redetermined. Conscious rats (n=3S) were also examined for the presence of locomotor dysfunction following intrathecal administration of CP and SP. Animals were randomly assigned to each treatment group and the investigators were blinded.Results: CP at I 0 and 100~g reduced MAC isoflurane by 9.9% and 15.3%, respectively (P < 0.05). Intrathecal administration of SP reversed the decreases in MAC by CP; however, locomotive activity was not changed.Conclusion: These results suggest that the NK-I receptor plays an important role in determining the MAC of isoflurane by inhibition of pain transmission in the spinal cord.
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