Spinal analgesia with morphine and clonidine.
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Analgesia↗
Biomedical subjects
L M Kitahata
Publications and source records attributed to L M Kitahata.
Fentanyl suppression of nociceptive neurons in the superficial dorsal horn of the cat.
This study was designed to examine the influence of spinally administered fentanyl on the spontaneous and noxiously evoked activity of high threshold (HT) and wide dynamic range (WDR) neurons in the superficial layers (lamina I and II) of the dorsal horn of cats made decerebrate and in which the spinal cord had been transected. Single unit activity was recorded using extracellular microelectrode recording techniques. Neuronal activity was evoked by the presentation of noxious radiant heat (51 degrees C) to the cells' receptive fields on the hind paws. Evoked activity of WDR neurons was monitored, both before and after the spinal administration of either 10 micrograms (n = 9) or 25 micrograms (n = 10) of fentanyl. HT neurons were examined before and after either 25 micrograms (n = 7) or 50 micrograms (n = 7) of spinally administered fentanyl. In all cases 31 min after fentanyl administration naloxone (0.1 mg) was administered intravenously (iv), and its antagonistic effect on the fentanyl suppression was determined. All doses of fentanyl tested suppressed both spontaneous and evoked activity of both types of neurons. Within 30 minutes 10 and 25 micrograms of fentanyl reduced the mean evoked activity of WDR neurons to 61% and 19% of control values, respectively, and 25 and 50 micrograms of fentanyl reduced the mean evoked activity of HT neurons to 70% and 47% of control values, respectively. Naloxone reversed the suppression seen in all cells studied. The results of the present study demonstrate that HT neurons are significantly less suppressed by the spinal administration of fentanyl than WDR neurons located in the same superficial layers of the dorsal horn.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of halothane on medullary inspiratory neurons of the cat.
The effect of halothane on the electrical activity of inspiratory neurons of the nucleus tractus solitarius (NTS) was studied in decerebrate, paralyzed, mechanically ventilated cats. Simultaneous recording of the activity of the neurons of the NTS and the phrenic nerve was done to identify the inspiratory neurons. Cells whose firing activity was synchronous with that of the phrenic nerve were considered inspiratory neurons. Administration of 1% and 1.5% halothane in oxygen induced a dose-dependent depression of the cell activity (spikes/s) with the cervical vagi intact or severed. Five and ten minutes after inhalation of 1% halothane, the cell activity (mean +/- SE) expressed as per cent of the control was 55.3 +/- 9 and 27 +/- 7, respectively (P less than 0.001), before bilateral cervical vagotomy. The corresponding values for 1.5% halothane were 25 +/- 10.1 and 5.6 +/- 3, respectively. Upon termination of halothane administration, the cell activity gradually returned toward the control level. The cell response to halothane was not affected by bilateral cervical vagotomy. Hypercapnia produced by inhalation of 5% CO2 increased the cell activity, but halothane caused profound depression of the cells even in the presence of hypercapnia. Based on these results, it may be concluded that: halothane has inhibitory effects on the activity of the inspiratory neurons of the NTS; and halothane-induced respiratory depression has a central component and that the NTS may serve as a site of action of halothane for its respiratory depressant effect.
Animals↗
Spinal sufentanil effects on spinal pain-transmission neurons in cats.
The ability of sufentanil to suppress noxiously evoked activity of wide dynamic range (WDR) neurons was studied in decerebrate, spinal-cord-transected cats. Sufentanil, 2.5 micrograms (n = 7) or 5.0 micrograms (n = 7), when administered spinally, produced a significant, dose-dependent suppression of noxiously evoked (51 degrees C radiant heat stimulus) activity of WDR neurons in the dorsal horn of the spinal cord. Spontaneous recovery from sufentanil suppression was not seen for up to 2 h. Reversal following intravenous naloxone, 0.12 mg, although present, was not as complete as that seen following other spinal opiates. Intravenous sufentanil, 5.0 micrograms/kg (n = 4), produced significant but short-lasting depression of noxiously evoked WDR neuron activity. A comparison of the results of this study with data from a previous fentanyl study suggests that sufentanil may be more appropriate than fentanyl for spinal or epidural administration because of a possible longer duration of action. However, the lesser degree of naloxone reversal seen in this study may suggest that, clinically, reversal of sufentanil effects may be more difficult.
Animals↗
A comparison of the effects of alfentanil applied to the spinal cord and intravenous alfentanil on noxiously evoked activity of dorsal horn neurons in the cat spinal cord.
The purpose of this study was to examine the effects of alfentanil applied to the surface of the spinal cord and the effects of intravenously administered alfentanil on noxiously evoked activity of dorsal horn neurons. Extracellular single neuron recordings were obtained from wide dynamic range neurons in 26 decerebrate cats with transected spinal cords. Spinally administered alfentanil, 25 micrograms or 50 micrograms, caused 36 and 86% suppression of noxiously evoked activity, respectively. Maximum mean suppression was achieved at 24 and 21 min after 25 micrograms, and 50 micrograms, respectively. Intravenous naloxone, 0.1 mg, when tested, completely reversed the suppression. Spontaneous recovery to control values occurred within 2 hr. Intravenously administered alfentanil, 12.5 micrograms/kg or 25 micrograms/kg, produced suppression of 43 and 89%, respectively, with maximum mean suppression observed at the 6- and 3-min time points, respectively. Complete recovery after intravenous administration was seen within 30 min. This study, using a sensitive neurophysiologic assay, demonstrates the important differences in onset and duration of drug effects that must be considered when comparing the responses of spinal cord neurons to intravenously administered narcotics and narcotics applied directly to the surface of the spinal cord.
Alfentanil↗
Fentanyl and alfentanil suppress brainstem pain transmission.
The effects of intravenously administered fentanyl (25 micrograms/kg, n = 9; 50 micrograms/kg, n = 5) and alfentanil (12.5 micrograms/kg, n = 5; 25 micrograms/kg, n = 7) on the noxiously evoked, single-unit activity of cells in the nucleus reticularis gigantocellularis (NRGC) were studied in decerebrate cats. Only cells of the NRGC excited exclusively by supramaximal electrical stimulation of A delta fibers (noxious stimulation) of the superficial radial nerve were studied. The noxiously evoked activity of all cells in the NRGC was suppressed by the administration of opioids (by 58 and 88% for fentanyl, 25 micrograms/kg and 50 micrograms/kg, respectively; by 35 and 78% for alfentanil 12.5 micrograms/kg and 25 micrograms/kg, respectively). Fentanyl and alfentanil effects were antagonized by the intravenous administration of naloxone. These results indicate that opioid suppression of noxiously evoked activity is seen in neurons located in the brainstem, and thus suppression of brainstem neurons may be important in the production of fentanyl and alfentanil analgesia.
Alfentanil↗
Direct opioid application to peripheral nerves does not alter compound action potentials.
The identification of opiate receptors on primary afferent fibers near the dorsal root ganglia suggests that opiates may be able to affect conduction in primary afferent nerve fibers. We examined the effect of directly applied, preservative-free morphine sulfate (0.1 mg/kg) and fentanyl citrate (25 micrograms/kg) on the A beta, A delta, and C components of the compound action potential of the superficial radial nerve in decerebrate cats (n = 18). Neither drug caused any significant change in the area under the curve of any of the compound action potentials studied. These data indicate that systemically administered opiates are unlikely to cause changes in primary afferent nerve conduction.
Action Potentials↗
Interactions of lidocaine and calcium in blocking the compound action potential of frog sciatic nerve.
The exact role of calcium in nerve conduction in neurons that have been blocked by local anesthetics remains controversial. Recently, attention has been drawn to the importance of examining both frequency-dependent and nonfrequency-dependent conduction block, since it is felt that frequency-dependent block provides a model that more closely approximates the normal physiologic state. The present study was designed to examine the effects of calcium on both the nonfrequency-dependent and frequency-dependent components of lidocaine nerve block. Desheathed, whole sciatic nerves from frogs were placed in a sucrose gap chamber and stimulated by trains of 20 impulses at frequencies from 3 to 90 Hz at supramaximal intensity for activation of the compound action potential. After control studies, the nerve was bathed by a frog Ringer's solution containing calcium concentrations, which increased from 0.0 mM to the physiologic value of 2.0 mM with or without 0.5 mM lidocaine. Compound action potentials were measured, and both frequency-dependent block and nonfrequency-dependent block were compared in each solution. Low calcium concentrations significantly enhanced both nonfrequency- and frequency-dependent lidocaine block. The effect of low concentrations of calcium was greater at higher frequencies of stimulation.
Action Potentials↗
Spinally administered epinephrine suppresses noxiously evoked activity of WDR neurons in the dorsal horn of the spinal cord.
This study was designed to determine if spinally administered epinephrine is capable of suppressing noxiously evoked activity of wide dynamic range (WDR) neurons in the dorsal horn of the spinal cord. Extracellular activity was recorded from single WDR neurons in the dorsal horn of decerebrate, spinal cord-transected (T-12) cats. Activity was evoked by the presentation of a noxious radiant heat stimulus (51 degrees C) to the cells' receptive fields on the hind paws. Evoked activity was monitored both before and after the spinal administration of either 50 micrograms (n = 6) or 100 micrograms (n = 6) epinephrine. Both doses of epinephrine produced a significant suppression of noxiously evoked activity, which was dose-dependent. In addition, the 100-microgram dose produced a suppression that was of longer duration than that seen following the 50-microgram dose. Recovery from suppression was recorded following both the 50- and 100-microgram dose. These results indicate that spinally administered epinephrine is capable of suppressing noxiously evoked activity of WDR neurons in the dorsal horn of the spinal cord. Since WDR neurons have been identified as cells of origin for the spinothalamic tract, such an action may block the central transmission of afferent pain information. This may be a mechanism by which spinally administered epinephrine enhances the duration or intensity of spinal anesthesia produced by local anesthetics and may also explain spinal analgesia resulting from the spinal administration of adrenergic agonists. Interactions between spinally administered epinephrine and spinally administered opioids also were studied.(ABSTRACT TRUNCATED AT 250 WORDS)
Afferent Pathways↗
Magnesium enhances local anesthetic nerve block of frog sciatic nerve.
The present study was designed to examine the effects of increased magnesium concentration on the nerve block produced by lidocaine, benzocaine, and QX 572 (a quaternary derivative of lidocaine). Desheathed whole sciatic nerves from northern Rana pipiens frogs were placed in a sucrose gap chamber and stimulated at various frequencies at supramaximal intensity for the activation of the compound action potential. After control studies, the nerve was bathed by a calcium-free frog Ringer's solution containing magnesium concentrations of 3.0, 10.0, or 20.0 mM with or without 0.5 mM lidocaine, 0.5 mM benzocaine, or 0.75 mM QX 572. Compound action potentials were measured, and nonfrequency and frequency dependent blocks were compared in each solution. Increased magnesium ion concentration, in the absence of local anesthetics, enhanced the nonfrequency dependent block but did not change the frequency dependent block. All three local anesthetics enhanced both types of block. Increased magnesium concentrations enhanced only the nonfrequency dependent benzocaine block. In contrast, increased magnesium enhanced both types of block produced by QX 572 and lidocaine. These results suggest a potentially important interaction between high magnesium concentrations and local anesthetic nerve blocks.
Action Potentials↗
Alpha-chloralose suppression of neuronal activity.
Alpha-chloralose, an anesthetic agent widely used in neurophysiologic studies, caused a significant and long-lasting suppression of single neuron activity recorded from two areas of the central nervous system in decerebrate cats. A 50 mg/kg dose (an average anesthetic dose used in many neurophysiologic studies) caused suppression of spontaneous and evoked activity of neurons in the dorsal horn of the spinal cord and greater suppression of neurons in the nucleus reticularis gigantocellularis (NRGC) of the medial medullary reticular formation. Many researchers are of the opinion that alpha-chloralose causes less suppression of the central nervous system (CNS) than other commonly used anesthetic agents. The neuronal suppression recorded in this study appears similar in many ways to suppression caused by other anesthetic agents in the same two areas of the CNS. The results of the present study suggest that alpha-chloralose may be capable of producing significant suppression of neurons in the dorsal horn of the spinal cord and NRGC. Its ability to influence other areas of the CNS should not be inferred from these results, but the data do indicate the importance of evaluating the effects of anesthetics upon neurophysiologic systems under study.
Animals↗
Epidural morphine does not affect the duration of action of epidural 2-chloroprocaine following Caesarean section.
The effect of epidural morphine on the duration of action of epidural 2-chloroprocaine was studied in a double-blind fashion in 30 patients following elective Caesarean section. When compared to epidural saline controls (n = 15), patients (n = 15) who received epidural morphine (4.0-5.0 mg) did not experience a prolongation or reduction in the duration of the somatic or sympathetic nervous system blockades produced by epidural 2-chloroprocaine.
Anesthesia, Epidural↗
Suppression of noxiously evoked WDR dorsal horn neuronal activity by spinally administered morphine.
The present study was carried out in order to examine the ability of spinally administered morphine to suppress noxiously evoked activity of wide-dynamic-range (WDR) neurons in the dorsal horn of the spinal cord in decerebrate, spinal cord-transected cats. All cells (n = 25) responded maximally to high-intensity noxious heat stimulation (51 degrees C) and were classified as wide dynamic range neurons. The spinal administration of 0.1 mg of morphine caused a significant reduction of noxiously evoked activity but did not significantly change spontaneous activity. The 0.25-mg dose caused a significant reduction of both types of activity. Thirty minutes after spinal administration, 0.1 mg of morphine caused a 27% reduction of spontaneous activity and a 43% reduction of noxiously evoked activity. The 0.25-mg dose reduced spontaneous activity by 44% and the evoked activity by 70%. Naloxone partially reversed the morphine-induced neuronal suppression. In addition, in the four neurons in which it was tried, spinally administered epinephrine was found to further suppress the remaining neuronal activity following the spinal morphine effect. These results demonstrate for the first time that spinally administered morphine is capable of suppressing noxiously evoked activity of wide-dynamic-range neurons in the dorsal horn of the spinal cord. They also demonstrate the dose-dependent nature of this effect and the potential importance of the interaction between morphine and adrenergic agonists in blocking information about noxious events. This information provides a probable mechanism of action for spinal opiate analgesia.
Action Potentials↗
Dose-response suppression of noxiously evoked activity of WDR neurons by spinally administered fentanyl.
The present study examined the influence of spinally administered fentanyl on the spontaneous and noxiously evoked activity of wide dynamic range (WDR) neurons in the dorsal horn of decerebrate, spinal cord-transected cats. This work was performed in order to evaluate the dose-response relationship, time course, and naloxone reversibility of fentanyl suppression of neurons that are involved with the transmission of information about pain. Extracellular single neuron recordings were obtained from 18 WDR neurons in the lumbar enlargement. These neurons were activated by a radiant heat stimulus on the footpads of the hindpaw. Fentanyl (10, 15, 25 micrograms in 0.5 ml of physiologic saline) was placed on the spinal cord following control studies of each neuron and the effect was observed. In 12 cats, 31 min after fentanyl administration, naloxone (0.1 mg) was administered intravenously, and its effect on the fentanyl suppression was determined. All three doses of fentanyl suppressed both the spontaneous and evoked activity of all the neurons studied. Thirty minutes after fentanyl the mean evoked activity was reduced to 47, 23, and 11% of control values by 10, 15, and 25 micrograms, respectively. The spontaneous activity was reduced to similar levels. Intravenous naloxone (0.1 mg) caused a significant reversal of the fentanyl suppression. The results of the present study indicate that fentanyl causes a naloxone-reversible, dose-dependent suppression of noxiously evoked WDR neuron activity. Such results support the concept that fentanyl is acting through a specific drug-receptor interaction. The onset of neuronal suppression occurred more rapidly, and the duration of the suppression was longer following fentanyl than that seen following spinal morphine. The onset and duration of this suppression correlates well with human clinical data, providing further evidence that alterations of WDR neuronal activity may be important in the production of spinal opioid analgesia.
Action Potentials↗
Excision of pheochromocytoma under isoflurane anesthesia. A case report.
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Adrenal Gland Neoplasms↗
Use of isoflurane during resection of pheochromocytoma.
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Adrenal Gland Neoplasms↗
Serum morphine levels in cats during dorsal horn neuron suppression by spinally administered morphine.
The degree of serum uptake of morphine following spinal morphine administration was measured in cats. Total serum morphine levels (free plus conjugated) were determined during suppression of noxiously evoked wide dynamic range neuron activity by spinally administered morphine and compared with total serum morphine levels following i.v. administration of similar doses. The serum levels at 30 minutes after spinal application of morphine (a time at which there was significant suppression of noxiously evoked neuronal activity) were low; after 0.1 and 0.25 mg the levels were 6.5 (n=6) and 12.5 (n=5) ng/ml respectively. In contrast, intravenous administration of the same doses (0.1 and 0.25 mg) produced levels at 30 minutes of 24 and 36 ng/ml respectively, while an intravenous dose commonly used in earlier neurophysiologic studies (2 mg/kg) produced serum levels in excess of 400 ng/ml. These results indicate that although there is systemic uptake following spinal administration of morphine, the serum levels achieved are much lower than those following intravenous administration of a comparable dose, and are insufficient to explain the resultant suppression of wide dynamic range neurons.
Animals↗
Thiopental suppression of neurons of the nucleus reticularis gigantocellularis of the cat.
The effects of sodium thiopental on the single-unit activity of cells in the nucleus reticularis gigantocellularis (NRGG) were examined in decerebrated cats. Only cells in the NRGC that responded exclusively to electrical stimulation of A-delta fibers (noxious stimulation) in the superficial radial nerve were studied. Sodium thiopental caused a significant, dose-dependent suppression of spontaneous and evoked neuronal activity of cells in the NRGC. Spontaneous activity was suppressed by 66% and 98% after intravenous administration of sodium thiopental, 2.5 mg/kg and 5.0 mg/kg, respectively. Evoked activity was suppressed by 65% and 79%. These findings, when added to previous reports of the suppressive effects of nitrous oxide, morphine sulfate, ketamine hydrochloride, and halothane, suggest the involvement of the NRGC in nociception and provide evidence that sodium thiopental significantly modifies the neuronal message about a noxious stimulus as recorded at the level of the NRGC.
Action Potentials↗