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T Kasaba

Publications and source records attributed to T Kasaba.

At least 37 records · Page 2Linked to original sources

[Effects of rectal premedication and the mother's presence on induction of pediatric anesthesia].

The effects of the rectal premedication and the mother's presence on induction of anesthesia were studied with 67 children between the ages of 1 and 6 years. All children were induced with mask using nitrous oxide-oxygen-halothane. Children's emotional states during induction were categorized as excellent, good or fair. Rating of excellent or good was considered to indicate satisfactory induction. Forty-seven children were accompanied by their mother. Twenty-two of them were premedicated with rectal bromazepam (3 mg), while another twenty-five children were not premedicated. Satisfactory induction after premedication was performed on 78% of the 1-3 year olds and 100% of the 4-6 year olds, whereas without rectal premedication, satisfactory induction was achieved in 42% of the 1-3 year olds and 69% of the 4-6 year olds. Rectal premedication was important for satisfactory induction. Another twenty of all children were premedicated with rectal bromazepam (3 mg) and induced without mother presence. Satisfactory induction was performed on 38% of the 1-3 year olds and 100% of the 4-6 year olds. Mother's presence tended to lead to satisfactory induction. Furthermore, we sought feedback from the mothers about their presence during induction of anesthesia. Almost all of the mothers said they appreciated the opportunity to be present, with the exception of four mothers (8.5%) who reported feeling of some anxiety to be in an operating room.

Administration, Rectal↗

[Effects of intravenous lidocaine administration on median nerve somatosensory evoked potentials].

The effect of lidocaine on the median nerve somatosensory evoked potential (SSEP) was investigated in 14 neurologically normal patients. Lidocaine 1.5 mg.kg-1.min-1 was injected intravenously over a 5 min period immediately followed by a continuous infusion of lidocaine 60 micrograms.kg-1.min-1. The peak latencies (N1, P2, N2) and amplitudes (N1-P2, P2-N2) of the SSEP response over the sensory cortex were recorded before and after lidocaine infusion. The peak latencies in the control group and in the experimental group after lidocaine infusion of N1, P1, N2 were 19.4 +/- 1.0 msec, 19.7 +/- 1.0 msec (N1), 24.6 +/- 1.4 msec, 25.0 +/- 1.5 msec (P2), 32.5 +/- 2.5 msec, and 33.3 +/- 2.8 msec (N2), respectively. The amplitudes in the control group and in the experimental group after lidocaine infusion of N1-P2, P2-N2 were 9.0 +/- 4.3 microV, 10.3 +/- 4.7 microV (N1-P2), 7.2 +/- 3.6 microV, 8.6 +/- 3.9 microV (P2-N2), respectively. Peak latencies of all components (N1, P2, N2) increased after lidocaine infusion compared with control values. Amplitude of N1-P2 and P2-N2 increased significantly following lidocaine infusion compared with control values. The data obtained in this study suggested that the changes in peak latencies and amplitude after epidural anesthesia with lidocaine were due to the systemic effect of lidocaine absorbed intravenously from the epidural space.

Aged↗

[The effects of thiamylal, ketamine and nicardipine on the hippocampal theta waves produced by cerebral ischemia in cats].

Spontaneous hippocampal electroencephalogram (EEG) was recorded in the pyramidal cell layer (PCL) and dentate gyrus (DG) during and after ischemia produced by bilateral clamping of the common carotid arteries in cats. Hippocampal theta waves, approximately 180 degree out of phase in PCL and DG, appeared within 4.3 +/- 2.3 seconds after the onset of bilateral carotid artery occlusion and continued for more than 60 minute. These hippocampal theta waves disappeared 34.2 +/- 10.2 seconds after 4 vessel occlusion. We could not find the clear difference between the two areas in the appearance and disappearance of the hippocampal theta waves. We further investigated the effects of thiamylal, ketamine and nicardipine on the hippocampal theta waves during bilateral carotid artery occlusion. Thiamylal changed the two hippocampal theta waves to a similar pattern of EEG, which has irregular slow and fast waves, in both PCL and DG. Ketamine changed the two theta waves to irregular complex pattern of fast and slow waves and spike activity, which is independent at two areas. Nicardipine, a Ca antagonist, changed the theta waves to irregular slow waves which were similar to the pattern of EEG observed before carotid artery occlusion. These results indicate that thiamylal, ketamine and nicardipine have different effects on the ischemia of hippocampus.

Animals↗

[Effects of lumbar or thoracic epidural anesthesia on median nerve somatosensory evoked potentials].

Somatosensory evoked potentials (SSEP) are used increasingly to monitor the integrity of neural pathways in anesthetized patients. To evaluate the influence of epidural anesthesia on the central nervous system, we studied the effects of lumbar or thoracic epidural anesthesia with lidocaine on the median nerve SSEP in 9 patients. The peak latencies (N1, P2, N2) and amplitudes (N1-P2, P2-N2) of the SSEP response over the sensory cortex were recorded before and 15 min after epidural anesthesia. The peak latencies of control and post epidural anesthesia of N1, P1, N2 were 19.2 +/- 1.7 msec, 19.6 +/- 1.6 msec (N1), 24.7 +/- 2.3 msec, 25.7 +/- 2.0 msec (P2), 32.8 +/- 2.8 msec and 34.6 +/- 2.5 msec (N2), respectively. The amplitude of control and post epidural anesthesia of N1-P2, P2-N2 were 4.5 +/- 2.9 microV, 5.9 +/- 6.6 microV (N1-P2), 4.4 +/- 3.2 microV and 5.6 +/- 5.2 microV (P2-N2), respectively. Peak latencies of all components (L1, P2, N2) increased after epidural anesthesia compared with control values. Amplitude of N1-P2 increased significantly following epidural anesthesia compared with control values. The data obtained in this study were contrary to the previous concept that anesthetic agents generally increase the latency of SSEP and decrease their amplitude.

Adult↗

[A comparative study of the depressive effects of halothane and isoflurane on medullary respiratory neurons in cats].

The depressive effects of halothane (H) and isoflurane (I) on the same respiratory neuron were studied in cats. Using a tungsten microelectrode, activities of medullary inspiratory neurons were recorded around nucleus ambiguus. The number of spikes (Spike) of each respiratory cycle and inter-spike interval (ISI) were measured. At 1 MAC, in 9 units out of 11, Spike was significantly fewer with I than with H. In 2 units out of 11, Spike was not significantly different between H and I. These results indicate that each respiratory neuron shows different sensitivity to H and I at 1MAC concentration. With increasing depth of anesthesia, Spike showed a concentration-related depression. During the course of respiratory depression, the spikes were 75.9 (1MAC), 63.3 (1.5MAC), 48.0 (2MAC), 24.2 (2.5MAC), 5.0 (3MAC) with H, and 77.4 (0.5MAC), 51.9 (1MAC), 23.5 (1.5MAC) with I. These spikes were completely depressed at 3.5MAC in H and 2MAC in I. Both H and I increased ISI with increasing depth of anesthesia. The effects of H and I on the phrenic nerve discharges closely resembled their effects on the respiratory neurons. We conclude that the respiratory depression produced by I exceeds that produced by equal MAC of H.

Animals↗

[The effects of intravenous lidocaine on the activity of medullary respiratory neurons in cats].

The effects of intravenous lidocaine on the activity of medullary respiratory neuron were studied in urethane anesthetized cats. Using a tungsten microelectrode, spikes from medullary inspiratory neurons were recorded around nucleus ambiguous. Lidocaine was administered using a constant-rate infusion pump until electrographic seizures appeared. The effect of lidocaine on the activity of respiratory neurons showed two types. In one type, consisting of 7 units out of 10, a sequence of changes was observed: the initial stage was represented by increased duration of the burst and decreased frequency of neural discharge; the second stage by desynchronization with mechanical lung inflation; the third stage by continuous activity and the forth stage by decreased spike activity and electrographic seizures. Blood concentration of the lidocaine was 9.6 +/- 3.5 micrograms.ml-1 at the second stage, 15.3 +/- 4.4 micrograms.ml-1 at the third stage, 26.6 +/- 4.1 micrograms.ml-1 at the fourth stage. In another type, consisting of 3 units out of 10, following administration of lidocaine the number of spikes showed only a concentration related depression. Blood concentration of the lidocaine was 6.9 +/- 2.7 micrograms.ml-1 when the spikes disappeared. These results indicate that intravenous lidocaine influences the respiratory rhythm and produces the respiratory depression working in the central nervous system.

Animals↗

Phrenic nerve and vagal nerve activities during differential lung ventilation in cats.

The effect of differential lung ventilation (DLV) on afferent vagal and efferent phrenic nerve activities was studied in urethane anesthetized cats. One endotracheal tube was inserted into the left bronchus to ventilate its side lung. Another tube was inserted until its tip reached about 1 cm above the carina to ventilate the right lung. Using two respirators, each lung was ventilated independently. Using hooked silver electrodes, the vagal and phrenic nerve activities were recorded. The afferent vagal nerve was activated in concurrence with lung inflation at any ventilation rate. The right and left vagal nerves were activated by right and left lung ventilation, respectively. On the other hand, the right and left efferent phrenic nerves were synchronized, whether the ventilation was discussed or ventilation was achieved by right or left one lung ventilation or even by asynchronous DLV. The phrenic nerve activity was surpressed by one-lung, right or left, ventilation independently, so that the rhythm of the phrenic nerve was disturbed by asynchronous DLV. From these results, to reduce the stress of patients during asychronous DLV, it was considered that patients need heavier sedation than a usual mechanical ventilatory support.

Journal Article↗

The possible role of collateral sprouting in the functional restitution of corticospinal connections after spinal hemisection.

We investigated in monkeys whether the corticospinal fibers increase their connections with lumbosacral neurons after spinal hemisection, using the retrograde horseradish peroxidase (HRP) method. In three monkeys 3.5-38 months after spinal hemisection at the lower thoracic or upper lumbar cord, HRP was injected into the lumbosacral cord unilaterally on the hemisected side at a level caudal to the lesion. Control injections were performed in two intact monkeys and in two other monkeys immediately after hemisection. In all animals, corticospinal neurons in the precentral motor cortex were labeled bilaterally. However, in the chronically spinal hemisected monkeys, the number of the labeled neurons was significantly increased on the side ipsilateral to the lesion. These results suggest that corticospinal connections to lumbosacral motoneurons are newly formed on the side of spinal cord hemisection. This synapse formation may be due to collateral sprouting of intact corticospinal fibers, and it may underlie the mechanisms of motor recovery.

Animals↗

Localization of the spinal accessory motoneurons in the cervical cord in connection with the phrenic nucleus: an HRP study in cats.

The localization of the spinal accessory motoneurons (SAMNs) that innervate the accessory respiratory muscles, the sternocleidomastoid (SCM) and trapezius (TP) muscles, was identified in the cat using the horseradish peroxidase (HRP) method. In the cases of HRP bathing of the transected spinal accessory nerve (SAN), HRP-labeled motoneurons were observed ipsilaterally from the C1 to the rostral C6 segments of the spinal cord. Labeled neurons were located principally in the medial and central regions of the dorsomedial cell column of the ventral horn in the C1 segment, in the lateral region of the ventrolateral cell column in the C2-C4 segments, between the ventrolateral and ventromedial cell columns in the C5 segment and in the lateral region of the ventromedial cell column in the C6 segment. In the cases of HRP injection into either SCM or TP muscles, labeled SCM motoneurons were found in the C1-C3 segments of the spinal cord and labeled TP motoneurons were chiefly localized more caudally within the spinal accessory nucleus. The present study revealed that, in the C5 and C6 segments, the SAMNs have a very similar topographic localization to the phrenic nucleus in the ventral horn. This finding implicated the functional linkage of the SAMNs with the phrenic motoneurons in particular types of respiration.

Accessory Nerve↗

Bupivacaine-induced convulsion is suppressed by MK-801.

BACKGROUND AND OBJECTIVES: Not only the facilitation of inhibitory synapses but also the suppression of excitatory synapses may be effective in treating convulsion induced by local anesthetics. The effects of MK-801, a N-methyl-D-aspartate (NMDA) receptor antagonist, on bupivacaine-induced convulsion and hemodynamic changes were studied. METHODS: Cortex and hippocampal (A4; L5.5; H8) electroencephalogram (EEG), heart rate, and mean arterial pressure were measured in 21 cats anesthetized with urethane. Blood samples were obtained when cats demonstrated arrhythmias, convulsed, and became hypotensive. In the control group (n = 7), bupivacaine was continuously infused until a hypotensive state of 40 mm/Hg was reached. In the MK-801 pretreated group (n = 7), MK-801 (0.5 mg/kg) was injected intravenously 15 minutes before the bupivacaine injection. In the MK-801 treatment group (n = 7), MK-801 (0.5 mg/kg) was injected intravenously at the appearance of convulsive EEG after the bupivacaine injection. RESULTS: Bupivacaine produced convulsion in the control group (17.1 +/- 2.4 microg/mL), but not in the MK-801 pretreated group. In the treatment group, convulsive EEG was suppressed gradually after injection of MK-801. The mean plasma bupivacaine concentrations (microg/mL) reaching arrhythmia and hypotension were 9.5 +/- 2.9 and 23.0 +/- 3.0, respectively, in the control group; 10.9 +/- 3.5 and 22.5 +/- 4.9, respectively, in the MK-801 pretreated group; and 7.5 +/- 1.6 and 21.0 +/- 3.0, respectively, in the MK-801 treatment groups. The mean arterial pressure and heart rate did not differ among the three groups. CONCLUSIONS: These results demonstrated that one mechanism of bupivacaine-induced convulsion is the excitatory neurotransmitter system in central nervous system and that MK-801 is effective in suppressing the convulsion without any effects on hemodynamics.

Anesthetics, Local↗

Effects of levobupivacaine, bupivacaine, and ropivacaine on tail-flick response and motor function in rats following epidural or intrathecal administration.

BACKGROUND AND OBJECTIVES: Commercially available bupivacaine is a racemic mixture of S (-)- and R(+)-enantiomers. Although the S(-)-enantiomers levobupivacaine and ropivacaine are less toxic to the cardiovascular and central nervous systems than bupivacaine, their relative efficacy has not been determined. This study directly compares the dose response of levobupivacaine, ropivacaine, and bupivacaine following epidural and intrathecal administration in the rat. METHODS: The time course of change in tail-flick latency and qualitative motor function was studied in rats following epidural or intrathecal administration of 0.25-0.75% levobupivacaine, ropivacaine, or bupivacaine in blinded, randomized fashion. RESULTS: Levobupivacaine and bupivacaine produced comparable and significantly enduring antinociceptive effects compared with ropivacaine at all test concentrations following both epidural and intrathecal administrations. Duration of motor block at lower local anesthetic concentrations (epidurally and intrathecally) was comparable with levobupivacaine and ropivacaine but significantly shorter than with bupivacaine. Epidural 0.75% levobupivacaine and bupivacaine showed more enduring motor block than ropivacaine. CONCLUSIONS: Levobupivacaine, given epidurally or intrathecally, produces longer lasting antinociceptive action than ropivacaine at equivalent concentrations and similar motor blocking effect at lower concentrations in both epidural and intrathecal administrations. Levobupivacaine-induced prolongation of the tail-flick latency is comparable to that of bupivacaine, as is motor blocking effect at higher concentrations. The possibility of significant differential block with levobupivacaine compared with bupivacaine warrants further study.

Amides↗

Control of the nasal mucosa by the tonic activities of the autonomic nervous system in dogs.

We studied the effects of stimulation and acute denervation of the cervical sympathetic nerve and the vidian nerve on the nasal vascular tone, as measured by intranasal balloon pressure. Significant vasoconstriction was found during electrical stimulation of the cervical sympathetic nerve. When the cervical sympathetic nerve was sectioned, causing a transient vasoconstriction due to the stimulatory effect of the nerve injury, then significant vasodilation was found in 23 out of 30 experiments. Significant vasodilation during electrical stimulation of the vidian nerve and slight but significant vasoconstriction after sectioning of the vidian nerve were also found. In addition, we found spontaneous nerve discharges in the cervical sympathetic nerve trunks. These nerve discharges increased after stopping the respiratory pump. Differences in these sympathetic nerve discharges between the sides of the body were also recognized.

Animals↗