Complex effects of general anesthesia on sensory processing in the spinal dorsal horn.

A chronic animal preparation allowed us to compare activity of the same single, spinal dorsal horn neurons in the physiologically intact, awake, drug-free state and in the anesthetized state. The inhalation anesthetic enflurane produced profound, and at times, opposite effects on spinal dorsal horn neuron responses to non-noxious and noxious receptive field stimulation. Some effects would not have been predicted, based upon current understanding of anesthetics.

Cutaneous responsiveness of lumbar spinal dorsal horn neurons is reduced by general anesthesia, an effect dependent in part on GABAA mechanisms.

Extracellular activity was recorded from single spinal dorsal horn neurons in both chronic cat and acute rat models. This was done to define the effects of anesthesia on the processing of sensory information elicited by nonnoxious tactile stimulation of peripheral receptive fields (RFs). In the chronic cat model, baseline data were obtained in physiologically intact, awake, drug-free animals before anesthetic administration (halothane 1.0-2.0%). This made it possible to compare and contrast activity of each cell in the drug-free and anesthetized state. Halothane effects were confirmed in the acute rat model (anesthetized, spinally transected, and in some cases decerebrate). In addition, the gamma-aminobutyic acid-A (GABAA)-receptor antagonist picrotoxin (2 mg/kg) was administered intravenously to verify that the observed halothane effect on spinal dorsal horn neurons was mediated by an interaction with GABAA-receptor systems. Halothane effects on three separate measures of response to nonnoxious tactile stimuli were observed in the chronic cat model. Halothane produced a significant, dose-dependent reduction in the low-threshold RF area of the neurons studied. Halothane also caused a significant reduction in neuronal response to RF brushing (dynamic stimulus) and to maintained contact with the RF (static stimulus). A dose dependency was not observed with these latter two effects. Neurons with a predominant rapidly adapting response seemed to be less susceptible to halothane suppression than slowly adapting cells. In the acute rat model an increase in halothane caused a reduction in neuronal response similar to that seen in the cat. The intravenous administration of 2 mg/kg of picrotoxin by itself caused no significant change in RF size or response to brushing. However, the same amount of picrotoxin did cause a 50% reversal of the halothane-induced reduction in RF size without causing a significant change in the halothane effect on response to RF brushing. In contrast to work recently reported in a chronic sheep model, halothane causes a significant reduction in spinal dorsal horn neuronal response to tactile stimulation of peripheral RFs. This effect is caused by, in part, but not exclusively, to GABAA-neurotransmitter systems. However, the relative influence of GABAA systems may vary with the nature of the stimulus.

[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.

[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.

[Cardiac arrest during anesthesia--a case of effective open chest massage].

A 58-year-old man suffering from esophageal cancer was scheduled for radical resection and reconstruction of the esophagus. Immediately after the start of the operation, with the patient under general anesthesia, cardiac arrest occurred. The operation was immediately discontinued and closed chest heart massage was started. As the patient did not respond, open chest massage was initiated. Cardiac arrest can be caused by any one of a number of factors. This case was suspected to have had a coronary artery spasm. It took a total of 100 minutes to resuscitate the patient. But resuscitation was successful without any resulting neurological damage. This was attributed to appropriate open chest massage. If a case of cardiac arrest due to any coronary artery disease does not respond to the usual cardiopulmonary resuscitation, we should consider open chest massage.

[Effects of lumbar epidural anesthesia on brainstem auditory response].

Auditory brainstem responses (ABR) are used increasingly to monitor the integrity of neural pathways in anesthetized patients. To evaluate the effect of epidural anesthesia on the central nervous system, we studied the effects of lumbar epidural anesthesia with lidocaine on the ABR in 10 patients. The seven peak latencies (waves I-VII) and amplitudes (waves I-VII) of the ABR were recorded before and 15 min after epidural anesthesia. Peak latencies of waves III, IV, V, VI, VII increased after epidural anesthesia compared with control values. Amplitude of waves II only decreased significantly following epidural anesthesia compared with control values. We further compared the interpeak latencies to investigate the brainstem transmission. Interpeak latencies (I-II, II-III, III-IV, IV-V, V-VI, VI-VII) were unchanged from the control values except waves VI-VII interval. Interpeak latencies of every second peak (II-IV, IV-VI, V-VII), of every third peak (II-V, III-VI, IV-VII), of every forth peak (I-VI, II-VII), of every fifth peak (I-VII) increased after epidural anesthesia compared with control values. The data obtained in the study demonstrated that lumbar epidural anesthesia with lidocaine prolonged the interpeak latencies of ABR. Considering that the waves of ABR are related to anatomically distinct sites in the auditory pathway (I; Acoustic nerve, II; Cochlear nucleus, III; Superior olivary complex, IV; Lateral lemniscus, V; Inferior colliculus, VI: Medial geniculate body, VII; Auditory radiation), the delay in the latencies of ABR seems to be present in the time intervals which involve more than two or three synaptic transmissions.

[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.

Changes in pulmonary function during continuous epidural bupivacaine with or without morphine following upper abdominal surgery.

To assess the effect of postoperative continuous thoracic epidural infusion of bupivacaine on pulmonary function, a prospective randomized study was conducted in patients undergoing upper abdominal surgery (UAS). Sixteen patients, divided into two treatment groups, received continuous epidural infusion of 0.25% bupivacaine at a rate of 2-5 ml.hr(-1), or that of a combination of 0.125% or 0.25% bupivacaine and 0.0025% or 0.005% morphine at a rate of 2-4 ml.hr(-1). One, 4, 10, 16, 24 and 40 hr postoperatively, the following indices were measured: visual analogue scale score, modified Prince Henry pain scale score, arterial Pa(O)(2) and Pa(CO)(2), functional residual capacity (FRC), and tidal volume (TV). There was no difference in pain scores between the two groups except for significantly less pain at 40 hr in the combination group. Postoperative measurements of pulmonary function revealed a significant fall in Pa(O)(2), FRC and TV, indicating a reduction of 15-25% as compared with the preoperative values, and no significant differences between the two groups. The authors conclude that postoperative continuous epidural infusion of bupivacaine combined with morphine is highly effective in alleviating pain and improving pulmonary function in patients following USA.