Katsutoshi Wakita

Suppressant effects of midazolam on responses of spinal dorsal horn neurones in rabbits.

Recordings of noxious intra-arterial bradykinin (BK)-induced chemonociceptive and spontaneous activity from 30 single spinal lamina V neurones of the dorsal horns in non-anaesthetized and decerebrated rabbits, were performed with tungsten microelectrodes. Intravenous injection of midazolam (0.2 mg/kg; 7 neurones) depressed BK-induced neural discharges by 55.0 +/- 6.2% (P less than 0.05) and 57.9 +/- 8.4% (P less than 0.05) 5 and 25 min after administration, respectively. Treatment with flumazenil (0.2 mg/kg, i.v.; 7 neurones), administered 20 min after midazolam, completely reversed the inhibition by midazolam of the BK-induced spinal lamina V neural responses and spontaneous neuronal activity. In contrast, a large dose of naloxone (1.0 mg/kg, i.v.; 6 neurones), administered 20 min after midazolam, failed to alter the midazolam-induced depressant effects on the nociceptive responses, at the spinal dorsal horn. Treatments with flumazenil (5 neurones) and naloxone (5 neurones) did not influence either the spontaneous or the BK-induced neuronal discharges, recorded in spinal lamina V cells. Midazolam depressed the nociceptive responses probably through its agonistic activity on the binding to the GABA-benzodiazepine-barbiturate system in the spinal dorsal horn.

Naloxone and flumazenil fail to antagonize the isoflurane-induced suppression of dorsal horn neurons in cats.

Effects of naloxone and flumazenil on isoflurane activities were examined on dorsal horn neurons in cats. Isoflurane suppressed bradykinin-induced nociceptive responses in transected feline spinal cords. The bradykinin-induced neuronal firing rates were significantly suppressed by 60.0%, 35.3% and 32.2% at 10, 20 and 30 min after isoflurane administration, respectively. The 32.2% suppression on bradykinin-induced neuronal responses at 30 min after isoflurane administration was not reversed 5 min after administration of naloxone (36.4% suppression). The suppressive effects of isoflurane were not reversed by naloxone (0.2 mg·kg−1, i.v. Similarly, the benzodiazepine antagonist, flumazenil (0.2 mg·kg−1 i.v., did not affect the suppressive effects of isoflurane. Failure of naloxone and flumazenil to reverse the suppressive effects of isoflurane suggests that isoflurane interacts with neither opioid nor benzodiazepine receptors in producing its suppressive action on nociceptive responses in dorsal horn neurons of the feline spinal cord.

Yohimbine and flumazenil: effect on nitrous oxide-induced suppression of dorsal horn neurons in cats

PurposeThe purpose of this study was to determine the mechanisms of nitrous oxide (N2O) antinociception at the spinal level with yohimbine (an α2-adrenergic antagonist) and flumazenil (a specific benzodiazepine antagonist) using chemonociceptive stimuli in spinal dorsal horn neurons in the cat.MethodsA lumbar laminectomy extending from L4 to L6 was performed to allow insertion of a extracellular recording device via a microelectrode. Additional laminectomy was performed at the T12 level to transect the spinal cord. As a noxious stimulus, bradykinin (BK) was injected via the cannula inserted into the femoral artery. Animals were divided into four treatment groups for subsequent experiments: N2O+flumazenil, N2O+yohimbine, flumazenil (alone), and yohimbine (alone).ResultsN2O suppressed BK-induced nociceptive responses in transected feline spinal cords. The BK-induced neuronal firing rates were significantly suppressed: to 69.2%, 61.8%, and 52.2% of the baseline firing rate at 10, 20, and 30 min, respectively, after N2O administration. The 47.8% suppression on BK-induced neuronal responses at 30 min after N2O administration was reversed 5 min after administration of yohimbine (25.2% suppression). Similarly, N2O suppression (42.5%) on chemically induced neuronal responses was reversed by flumazenil (24.9% suppression) at identical postadministration intervals.ConclusionThese data imply that N2O suppresses the nociceptive responses in part probably through its agonistic binding activity to the α2-adrenergic, γ-aminobutyric acid (GABA)-benzodiazepine, or both receptor systems in dorsal born neurons of the feline spinal cord.

Suppressive action of enflurane on dorsal horn neurons in rabbits

The neurophysiologic mechanism of the suppressive action of enflurane on spinal nociceptive transmission was examined in rabbits with intact and with transected spinal cords. Enflurane suppressed nociceptive responses in both intact and transected spinal cord groups. The suppressive effects of enflurane were significantly greater in the intact group than in the transected group. The suppressive effects of enflurane were not reversed by the addition of 0.2 mg·kg−1 of naloxone. These results suggest that enflurane suppresses nociceptive responses by activating descending inhibitory systems and directly suppressing activity at the spinal level. This suppressive action of enflurane does not interact with the opioid receptor.

Anesthesia in Shy-Drager syndrome

The Shy-Drager syndrome (SDS) is characterizes by autonomic dysfunction, accompanied by additional central neurologic symptoms. The main clinical manifestations of the autonomic dysfunction include orthostatic hypotension, vesicorectal dysfunction, hydrohidrosis and extrapyramidal syndrome. During anesthesia, the cardiovascular instability due to autonomic dysfunction represent a potential danger. The present paper reports the anesthetic course of a patient with SDS undergoing abdonimal surgery.

Recurrent coronary artery spasm during a non-cardiac surgical procedure

Coronary artery spasm is often reported in the perioperative period1 ll • Myocardial ischemia caused by coronary artery spasm as characterized by ST-segment elevation occurs suddenly and is not preceded by an increase in blood pressure or heart rate. This may frequently result in premature contractions, atrioventricular block, severe hypotension and even cardiac arrest. We report a case of coronary artery spasm occurred 4 times during a noncardiac surgical procedure.

The effects of composition of subarachnoid gas space and anesthetic gas mixture on cerebrospinal fluid pressure changes during cisternography for transsphenoidal craniectomy

The effects of gas composition in the subarachnoid space (injection of air or N2O) and in an anesthetic gas mixture (inhalation with or without N2O) on cerebrospinal fluid pressure were studied in 22 patients with pneumocisternography for transsphenoidal craniectomy. N2O (66%) anesthesia for 10 min increased cerebrospinal fluid pressure by up to 150% in 7 patients who were intrathecally injected with air. Withdrawal of N20 from the anesthetic gas mixture for sixty minutes reduced cerebrospinal fluid pressure to the initial pressure. A second N2O administration to the anesthetic gas mixture did not elevate cerebrospinal fluid pressure by as much as the first N20 administration. In 7 patients receiving subarachnoid air injection, replacing 66% N2O with 66% nitrogen prevented the change in cerebrospinal fluid pressure throughout the operation. In 8 patients N20 anesthesia and N20 intrathecal injection failed to eliminate the rise in cerebrospinal fluid pressure in 8 patients. Withdrawal of N20 from the anesthetic gas mixture for 60 min is recommended to prevent an extreme increase in cerebrospinal fluid pressure during pneumocisternography.