Yasuo Ide

Intravenous midazolam suppresses noxiously evoked activity of spinal wide dynamic range neurons in cats.

The effects of intravenously (IV) administered midazolam on noxiously evoked activity of spinal wide dynamic range (WDR) neurons were investigated in decerebrate, spinal-cord-transected cats. Extracellular, single-unit recordings were measured during stimulation by pinching the receptive field on the hind paw and the effect of midazolam at doses of 0.25, 0.5, 1, 2, and 4 mg/kg were measured. Two series of experiments were performed to characterize the analgesic effects of midazolam. In the first, dose-response experiments (n = 59) demonstrated a dose-dependent suppression of the noxiously evoked activity of spinal WDR neurons after midazolam administration. This effect of midazolam was maximal at a dose of 1 mg/kg IV. The second series of experiments (n = 14) demonstrated that a benzodiazepine antagonist, flumazenil (n = 8), promptly reversed the effect of midazolam, while an opioid antagonist, naloxone (n = 6), had no effect on the effect of midazolam. The present study demonstrates that IV administered midazolam suppresses noxiously evoked activity of spinal WDR neurons that is reversible by a benzodiazepine antagonist. This is consistent with an analgesic action of midazolam. (Anesth Analg 1995;80:58-63)

Effects of Acetaldehyde on Action Potentials and Ca2+ Currents in Single Atrial Myocytes from the Bullfrog

Aim: The purpose of the present study was to examine the effects of acetaldehyde on the contractile force and membrane potentials and currents in the bullfrog heart. Methods: Contractile force was recorded using right atrial tissues, and membrane potentials and currents were measured by using whole cell patch clamp methods in right atrial myocytes. Results: Acetaldehyde at 500 µmol/l and 1 mmol/l increased the contractile force significantly. Acetaldehyde at 300 and 500 µmol/l increased the overshoot and the plateau of electrically induced action potentials in a concentration-dependent and reversible manner, while the resting membrane potential did not change. The duration of the action potential (APD90) measured at the 90% repolarization level was shortened. The L-type Ca2+ current (ICa) increased significantly when 300 and 500 µmol/l were applied. The fast transient inward current, the inward rectifying potassium current and the outward delayed-rectifier potassium current were not changed following acetaldehyde application (500 µmol/l or 1 mmol/l). Conclusion: These results suggest that acetaldehyde increased the ICa, thereby increased the contractile force, the overshoot and the plateau of action potentials. The shortening of APD90 may be due to the acceleration of the current decay during the ICa inactivation phase.

Suppressive effect of spinal dorsal-horn neuronal activity by local spinal-cord cooling is reversed by naloxone in cats

AbstractPurpose. The purpose of this study was to assess the effect of local spinal cord cooling on spinal dorsal-horn neuronal activity, with special emphasis on the role of endogenous opioid. Methods. Decerebrate, spinal-cord-transected cats (n= 30) were subjected to local spinal-cord irrigation, using 0.9 N saline solution (15°C; n= 15, and 35°C; n= 15) for 90 min. The extracellular, single-cell activity of spinal dorsal-horn neurons responding to noxious stimulation was recorded. Sixty-one minutes after induction of local spinal-cord irrigation, naloxone (0.1 mg·kg−1) was administered intravenously. Local spinal-cord blood flow was measured using the hydrogen clearance technique. Results. Local spinal cord cooling produced significant suppression of both spontaneous and evoked activity (33.1 ± 7.7% and 31.4 ± 5.5%, respectively; mean ± SE). Naloxone reversed this suppression immediately. Local spinal-cord blood flow was significantly reduced during spinal-cord cooling, but naloxone did not change local spinal-cord blood flow. Conclusion. The results demonstrate that endogenous opioids may play an important role in dorsal-horn neuronal suppression induced by local spinal-cord cooling.

Postherpetic neuralgia as a risk factor for classic heatstroke.

On one of the first hot days of summer (ambient temperature 33°C, relative humidity 78%) in late July, the patient took mianserin and slept as normal, without air-conditioning. Early the next morning, she was taken to the emergency room with an axillary temperature of 40.0°C, as a result of exposure to high ambient temperatures throughout the night. The patient vomited on the way to the hospital, and, on arrival, was found to be dehydrated and confused with the following clinical signs: a rectal temperature of 40.0°C; heart rate, 105/ min; blood pressure, 90/50 mmHg; and Glasgow Coma Scale, 13. From these clinical manifestations, her condition was diagnosed as classic heatstroke. She received external cooling and infusions of Ringer’s lactate solution, and, by afternoon, her body temperature had normalized and she was conscious. Results of laboratory tests were normal except for slight hypokalemia and hypoglycemia. On the third day, she was able to walk unattended. On the tenth day, she was discharged from this hospital without sequelae.

The effect of pentobarbital sodium on the dorsal horn of the spinal cord

The effect of intravenously administered pentobarbital sodium on the activity of single unit in Rexed lamina V of the transected feline lumbar spinal cord was studied using an extracellular microelectrode recording technique. Pentobarbital sodium 1.0 mg·kg−1, 2.5 mg·kg−1, and 5.0 mg·kg−1 administered intravenously suppressed both the spontaneous and the evoked activity in Rexed lamina V cells, known to respond principally to noxious stimuli, in a dose-dependent manner. The maximum depression of cell activity occurred within 5 min after intravenous administration. The recovery of cell activity occurred within 70 min after intravenous administration of pentobarbital sodium. We conclude that pentobarbital sodium intravenously administered has a suppressive effect on single unit activity of cells in Rexed lamina V and probably has an analgesic effect. Its suppressive effect is dose-dependent.