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We assessed the effects of succinylcholine and vecuronium on renal function and on the renal microcirculation in a rodent model. Vecuronium (0.02 mg/kg followed by 0.2 mg.kg-1 x h-1) caused a significant decrease of 16.1% +/- 3.87% in inulin clearance from 0.92 +/- 0.07 to 0.71 +/- 0.05 mL.min-1 x gKW-1 (gram of kidney weight), and a decrease in para-aminohippuric acid clearance by 21.6% +/- 4.69% from 1.58 +/- 0.26 to 1.31 +/- 0.20 mL.min-1 x gKW-1 (P < 0.05), whereas succinylcholine (0.45 mg/kg followed by 2 mg.kg-1 x h-1) altered neither. The effect of these muscle relaxants was also determined on the renal microcirculation in separate experiments using videomicroscopy. Succinylcholine (n = 10; 10(-10) to 10(-6) M) and its parent compound, acetylcholine (n = 10, 10(-10) to 10(-6) M) used as a control, caused a significant vasodilation from baseline diameter in the interlobular, afferent, and efferent arterioles. The vasodilation caused by succinylcholine was significantly less than that observed with acetylcholine. Atropine blocked the response to succinylcholine, indicating the latter has a muscarinic effect. In contrast, vecuronium caused a significant, selective vasoconstriction from baseline diameter in the preglomerular vessels, but not in the postglomerular vessels. The vasoconstriction caused by vecuronium was significantly different than the vasodilation caused by succinylcholine. The preglomerular vasoconstriction observed with vecuronium may contribute to the decrease in renal plasma flow and glomerular filtration rate observed experimentally. The choice of a neuromuscular blocking drug can therefore have the potential to influence renal function by altering the renal microcirculation.

Median nerve somatosensory evoked responses (MnSSERs) were recorded in nine neurologically normal adult cardiac patients before and during the administration of high-dose fentanyl. MnSSERs were recorded prior to induction and at t = 20 min and t = 45 min postinduction. Fentanyl was administered as a slow bolus (53.2 +/- 9.1 micrograms X kg-1), followed by a continuous infusion at 10-20 micrograms X kg-1 X hr-1 (total dose 63.6 +/- 10.1 micrograms X kg-1). All MnSSER waveform components remained recordable and easily identifiable during anaesthesia. The effect of fentanyl was more pronounced on cortical waveform components, leaving subcortical components largely unaffected. There was a significant increase in the latency of the cortical MnSSER at t = 20 min, e.g., for the initial negative cortical wave, N1, the latency was 21.18 +/- 1.55 ms preinduction versus 22.18 +/- 1.42 ms at t = 20 min. There was also a significant decrease in the amplitude of the cortical response at t = 20 min, i.e., 2.04 +/- 1.30 microV preinduction versus 1.31 +/- 0.74 microV at t = 20 min. However, the degree of change was quite variable (range = 0-65 per cent). No further changes occurred at t = 45 min. The authors conclude that MnSSERs can be consistently and reliably monitored during high-dose fentanyl anaesthesia. However, fentanyl produces modest but significant changes in the MnSSER which should be taken into account lest they be misinterpreted as neurologic injury in evolution.

The effect of pH-adjustment of three per cent 2-chloroprocaine (2-CP, Nesacaine MPF) on the onset, duration, and spread of epidural analgesia and anaesthesia was studied in patients undergoing lower extremity surgery. Forty ASA physical status I and II patients were randomized to two groups. In a double-blinded fashion, patients in both groups received an epidural injection of 15 ml of local anaesthetic (LA) solution via a Tuohy needle at the L3-4 interspace. Local anaesthesia for Group I was prepared by adding 3 mEq NaHCO3 to 27 ml three per cent 2-CP and for Group II was prepared by adding 3 ml 0.9 per cent NaCl to 27 ml three per cent 2-CP. Both solutions contained epinephrine (1:200,000). The pH of commercially prepared Nesacaine MPF was 3.19 +/- 0.02. The pH of the solutions used for Group I and Group II patients were 7.32 +/- 0.01 and 3.27 +/- 0.02, respectively. Times to analgesia and anaesthesia at the L2 dermatome were significantly decreased in Group I patients by 2.5 and 6.6 minutes, respectively. Likewise, pH-adjustment accelerated the attainment of maximum level of block by 2.8 min. No statistical differences were found between groups in the maximum level of epidural block, or in time to 2-segment regression. No precipitation of LA was observed in pH-adjusted solutions of 2-CP after 24 hours. We recommend the use of pH-adjusted three per cent 2-CP (Nesacaine MPF) to accelerate the onset of epidural block.

Fourteen patients whose posterior tibial nerve somatosensory cortical-evoked potentials (SCEPs) were monitored for spinal surgery, underwent sequential recordings at different stimulus rates (6.1, 5.1, 4.1, 3.1, 2.1, and 1.1 Hz), after induction of anesthesia and patient positioning but before the incision was made. A markedly detrimental influence of higher (5.1 and 6.1 Hz), yet commonly used, stimulus rates on the amplitude of the evoked potential waveform was noticed. This tendency was most pronounced in patients with an antecedent spinal cord injury. In three patients with severe incomplete cord injuries, the amplitude of the cortical-evoked potential was sufficiently attenuated to preclude reliable intraoperative monitoring when stimulus rates of 5.1 Hz and greater were used. By contrast, evoked potentials could be monitored reliably in all patients when stimulus rates of 1.1 or 2.1 Hz were used. Six of seven patients (87%) whose evoked response amplitude showed a major reduction with higher stimulus frequencies had either a discrete sensory level or bilateral lower extremity weakness or both. Only two of seven patients (29%) whose evoked potential remained minimally affected by the stimulus rate had similar neurologic impairment. The authors conclude that, particularly in the setting of severe incomplete spinal cord injuries, the higher rates of stimulus presentation commonly used may result in failure to obtain waveforms that are adequate for intraoperative SCEP monitoring. The use of unconventionally low stimulus rates may greatly facilitate SCEP monitoring in such situations.

We present an algorithm that permits automated acquisition, display, and disk storage of single or dual channel sensory evoked potential waveforms using a Pathfinder II evoked response monitor. Once initiated, data acquisition and storage continue at user-specified intervals without additional user input. A cascade screen display provides trend monitoring. The file for data storage is established and searched using standard Pathfinder commands. The algorithm is written in MECOL, the Pathfinder specific programming language. This programming code imposed a number of limitations that had to be overcome to create a versatile and user friendly algorithm. During clinical use in our operating rooms, the program has been found effective and easy to use by both veteran and novice Pathfinder operators. The "hands-off" trend monitoring permitted by this algorithm has reduced the labor-intensive aspect of sensory evoked potential monitoring.

Brain stem auditory (BAERs) and median nerve somatosensory evoked responses (MnSSERs) were recorded from normal neural pathways during the induction of pentobarbital coma in six patients undergoing elective excision of complex arteriovenous malformations. Each patient received a 33-minute infusion of pentobarbital at a rate of 0.6 mg/kg (total dose. 19.8 mg/kg). This regimen resulted in burst suppression or isoelectricity of the electroencephalogram in all patients. Although statistically significant changes in latency and amplitude occurred, both BAERs and MnSSERs were readily recordable in all patients throughout the infusion. For the BAER, there were significant increases in the latencies of Waves III and V. However, these increases are sufficiently small that misinterpretation of these changes as an evolving neurological injury is unlikely, e.g., Wave V latency increased from 6.25 ± 0.25 (SD) to 6.58 ± 0.16 ms (P < 0.006). For the MnSSER, changes of greater potential clinical relevance were observed. There were substantial increases in the latencies of the early components of the primary cortical response and in the central conduction time (e.g., CCT of 6.1 ± 0.6 ms preinduction vs. 7.7 ± 1.1 ms at t = 33 min, P < 0.003), and the amplitude of the early cortical response (N20-P25) decreased by a mean of 45% (P < 0.02). By contrast, subcortical components of the MnSSER (brachial plexus, upper cervical spine) were only minimally affected. We conclude that, in patients who are initially neurologically intact, BAERs and MnSSERs can be monitored effectively during pentobarbital coma and that the loss of these responses should not be ascribed to the effects of this drug alone. However, the interpretation of evoked response changes, particularly MnSSER changes, that occur during pentobarbital administration should take into account the dose-related changes in latency and amplitude that we have observed.

This study was undertaken to define the effect of acute hypocapnia on intraoperatively recorded somatosensory evoked potentials (SSEPs). Median nerve SSEPs were studied in ten anesthetized neurologically normal adult patients undergoing elective nonneurologic surgery. End-tidal carbon dioxide tension (ETCO2) was allowed to stabilize for 15 min before SSEP recordings were obtained during normocapnia (N) (ETCO2 = 39.9 +/- 1.45 mm Hg), hypocapnia (H) (ETCO2 = 20.6 +/- 1.07 mm Hg), and after return to normocapnia (NR). Although a trend toward a reduction in the latencies of all SSEP components was evident, only the cervical (CII), and cortical (N1 and P1) latencies decreased significantly with H when compared to N. Mean latencies for CII, N1, and P1 (+/- SD) were, respectively, 14.80 +/- 1.14, 20.93 +/- 1.50, and 25.17 +/- 2.88 msec during N, and 14.50 +/- 1.13, 20.25 +/- 1.49, and 24.23 +/- 2.52 msec during H. On return to normocapnia, latencies were unchanged from N. Cortical latencies were affected to a greater extent than subcortical ones. Aside from a small but statistically significant increase in CII amplitude at H (2.05 +/- 0.55 microV vs 1.83 +/- 0.49 microV at N), SSEP amplitudes were unaffected by hypocapnia. The authors conclude that acute hypocapnia in neurologically normal patients results in a small reduction of SSEP latencies. The magnitude of the change is such that it is unlikely to interfere with recording or interpretation of intraoperative SSEPs.