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Bladder volume measurement with electrical impedance analysis in spinal cord-injured patients.

The purpose of the study contained herein was to determine the usefulness of electrical impedance for measurement of bladder volume in spinal cord-injured patients, with an assessment of the relationship between electrical impedance and bladder volume exclusively. The study was performed during urodynamic studies to match the exact bladder volume. Thirteen patients with complete spinal cord injuries were recruited. We used silver-silver chloride compound electrodes composed of one pair of current and amplitude electrodes to minimize the influence of superficial skin impedance. Each compound electrode was attached on the lower abdomen bilaterally after skin cleansing. Constant current (60 kHz-1.0 mA), converted from 9 V of direct current, was applied, and corresponding electrical impedance (omega) was measured at "pre" (before urodynamic empty bladder), "full" (with a urodynamic filled bladder), and "post" (after urodynamic empty bladder) status. Electrical impedance at the full status was definitely lower than that at the pre and post statuses in all subjects, with a statistically significant difference (P < 0. 001). The correlation between electrical impedance and bladder volume was negative (r = -0.7988), and the fact of how much the variation in electrical impedance could be explained by variation in bladder volume was estimated (r2 = 0.6381). From these findings, we have determined that the electrical impedance analysis technique can be an alternative measure of bladder volume indirectly.

Adult↗

Clinical uses of electrically evoked auditory nerve and brainstem responses.

PURPOSE OF REVIEW: The purpose of this review is to summarize current thinking relative to clinical applications for the electrically evoked compound action potential and the electrically evoked auditory brainstem response with the focus on works published between 1998 and 2003. RECENT FINDINGS: During the period of this review, a considerable body of research has been published describing how the electrically evoked compound action potential can be measured and how the electrically evoked compound action potential may be used in the clinical treatment of cochlear implant patients. During this same period, there has been a decline in the number of studies reporting potential clinical applications for the electrically evoked auditory brainstem response. Perhaps the strongest clinical application for the electrically evoked compound action potential today is as a tool to facilitate the process of fitting the speech processor of the cochlear implant. This is particularly important for pediatric patients who may not be able to be programmed using traditional behavioral techniques. The accuracy of these predictions is discussed in addition to the limitations of the studies reviewed. SUMMARY: The introduction of cochlear implants with the capability of measuring the response of the auditory nerve to electrical stimulation from an intracochlear electrode has tremendous potential to impact clinical practice. Research into how best to use this information is ongoing.

Action Potentials↗

Mapping the VIIIth cranial nerve by electrical stimulation: methods for differentiating auditory from vestibular responses.

HYPOTHESIS: The goal of this study was to map the VIIIth cranial nerve by electrical stimulation. Specifically, the authors sought to 1) characterize auditory and vestibular evoked responses elicited by electrical stimuli delivered directly to the exposed surface of the VIIIth cranial nerve and 2) compare electrically evoked responses elicited in brainstem nuclei with extracranially recorded far-field potentials. BACKGROUND: Intraoperative monitoring of auditory brainstem responses is useful during cerebellopontine angle surgery. Identification of the vestibular portion of the VIIIth cranial nerve, which traditionally has been performed by physical characteristics and some electrophysiologic properties, is important because the vestibular subdivision in humans is indistinct in approximately 25% of cases. Positive identification of evoked responses emanating from the vestibular nerve would constitute a marked improvement over existing intraoperative techniques that use acoustic stimuli only. METHODS: Experiments were performed on 12 anesthetized cats. Electrical pulse stimuli were delivered using a bipolar electrode placed directly on the surface of the exposed VIIIth cranial nerve at several sites. Computer-averaged evoked responses were recorded from far-field electrodes placed on the scalp and from near-field electrodes stereotaxically positioned in or near the inferior colliculus and abducens nucleus. RESULTS: Latencies and morphologies of waves recorded in brainstem nuclei were compared with those of waves recorded extracranially. Direct electrical stimulation of the cochlear nerve elicited a four-wave, auditory brainstem response-like extracranial response, strong activity in the inferior colliculus, and weak activity in the abducens nucleus. Direct stimulation of the vestibular nerve produced a two-wave extracranial response, weak inferior colliculus activity, and strong abducens activation. Stimulation at the border of the cochlear and vestibular nerves produced intermediate responses that possessed both cochlear and vestibular characteristics. CONCLUSION: Direct electrical stimulation of the cochlear and vestibular subdivisions elicits evoked responses with distinctly different wave morphologies. Obtaining electrically evoked responses intraoperatively is feasible and may be of substantial value in the unambiguous identification of VIIIth cranial nerve subdivisions.

Animals↗

Field distributions in the rat tibia with and without a porous implant during electrical stimulation: a parametric modeling.

Expeditious post-operative ingrowth of bone is necessary for clinically successful fixation of porous joint prostheses. Electrical or electromagnetic fields to stimulate bone growth into porous implants have been used; however, they produced nonconvincing data. This was partially attributable to the lack of quantification of the localized electric fields produced in the pores of the implants. Therefore, this study set out: i) to quantify the local electric field values induced into the surface pores of nonconducting implants by "capacitive" coupling and to determine the magnitude of the macroscopically applied capacitively coupled electrical currents to induce specific electric field amplitudes in the pores, ii) to identify the important dielectric properties of the implant-tissue interface, and iii) to create the basis for successfully applying electrical fields in an animal model to stimulate bone ingrowth. A finite element method was used to calculate the electric field gradients and current densities present in a rat tibia modeled with a porous intramedullary implant when capacitively stimulated. Results indicated that while the current density in the pores are reduced in comparison to the region just outside the pore by about one order of magnitude, a significant current density still exists in the pore region. Furthermore, the presence of the implant increases the current densities in the trabecular bone while decreasing these values in the cortical bone. Replacing the trabecular bone in the pore by saline increases the current density in the pore by three-fold, but decreases the voltage gradient by a similar factor.

Animals↗

Diffuse electrical injury: a study of 89 subjects reporting long-term symptomatology that is remote to the theoretical current pathway.

Historically, tissue damage from electrical contact was thought to arise from resistive heating of tissues along the current pathway. The modern view has accepted that tissue damage can result from cellular rupture (electroporation) induced by the presence of an electric field. There remain electrical injuries that defy explanation by either theory. In rare electrical contacts, diffuse symptomatology arises that is neither proportionate to the electrical contact nor does it occur along the theoretical linear pathway of the current from entry point to exit point. Disproportionate, remote electrical injury is most notable when the contact voltage is low (120 and 240 V). Symptoms occur, absent diagnostic evidence, that defy explanation as organic injury. A Web-based interactive survey was used to locate and query individuals suffering from rarely occurring responses to electrical contact. The results of the study suggest that there is a common symptomatology that is neither linked to voltage nor loss of consciousness at the time of contact.

Accidents↗

Todd, Faraday, and the electrical basis of epilepsy.

PURPOSE: To consider the origins of our understanding of the electrical basis of epilepsy in the light of the Lumleian lectures to the Royal College of Physicians in London for 1849, "On the pathology and treatment of convulsive diseases," by Robert Bentley Todd (1809-1860). METHODS: I have reviewed Todd's neglected Lumleian lectures and his observations and concepts of the electrical basis of epilepsy in relation to the influence of Michael Faraday (1791-1867), his contemporary in London, and in relation to later nineteenth century writings on the subject by Jackson, Ferrier, and Hitzig, all of whom overlooked Todd's lectures. RESULTS: Todd was a clinical scientist as well as Professor of Physiology and Morbid Anatomy, with a special interest in the nervous system, at King's College, where he came into contact with Michael Faraday, the greatest electrical scientist of all time, at the nearby Royal Institution. On the basis of his own clinical and experimental studies and his cutting-edge knowledge of neuroanatomy, neurophysiology, neuropathology, and electrical science, Todd brilliantly developed his concepts of the electrical basis of brain activity and of epilepsy in particular. With his microscope, he perceived each nerve vesicle and its related fibres (neurone in later terminology) as distinct entities for the generation of nervous polarity (force) and its transmission in the white nerve fibres throughout the nervous system by unknown molecular mechanisms. In epilepsy, an increase in electrical tension, especially in the grey matter of the hemispheres, led to periodic, sudden explosive discharges, based on Faraday's concept of disruptive discharges. CONCLUSIONS: Todd was the United Kingdom's first outstanding neurologist and neuroscientist before these disciplines existed. Influenced by Faraday, he proposed and confirmed the electrical basis of nervous discharges in epilepsy more than 20 years ahead of Jackson, Ferrier, and Hitzig, who did not refer to his priority, although Ferrier also worked at King's College, and Jackson also gave his own famous Lumleian lectures on the same subject in 1890. Todd deserves the credit for laying the foundations of our modern understanding of epilepsy.

Electricity↗

Development of electrical rhythmicity in the murine gastrointestinal tract is specifically encoded in the tunica muscularis.

1. Interstitial cells of Cajal (ICCs) have been identified as pacemaker cells in the gastrointestinal (GI) tracts of vertebrates. We have studied the development of ICCs in pacemaker regions and the onset of electrical rhythmicity in the gastric antrum, small bowel and proximal colon of the mouse. 2. ICCs, as detected by c-Kit immunofluorescence, were found during embryogenesis in regions of the GI tract that eventually become pacemaker areas. Prior to birth, these cells were organized into well-structured networks, and by the end of the embryonic period the morphology of ICC networks in pacemaker regions appeared very similar to that observed in adult animals. 3. Electrical rhythmicity was recorded prior to birth (by E18) in the proximal GI tract (stomach and jejunum), and this activity developed to adult-like behaviour within a week after birth. In the ileum and proximal colon rhythmicity developed after birth, and adult-like characteristics were apparent within the first week. 4. Post-junctional responses of smooth muscles to neural inputs could be recorded at birth, and stimulation of intrinsic nerves often led to oscillatory activity resembling slow waves for up to several minutes following brief stimuli. Nerve stimulation augmented spontaneous activity in the proximal portions of the GI tract and elicited rhythmic activity temporarily in quiescent tissues of the distal GI tract. 5. ICCs and rhythmicity developed in an apparently normal manner in tissues isolated at birth and placed in organ culture. These data suggest that the tunica muscularis provides a suitable microenvironment for the development of ICCs and rhythmicity without the need for extrinsic stimuli. 6. Treatment of small intestinal tissues taken from embryos at E15 with neutralizing c-Kit antibodies abolished ICC development and the organization of ICCs into networks that typically occurs during the late embryonic period. Treatment of muscles taken from newborn animals with c-Kit antibodies blocked postnatal development of ICCs, disrupted already established and functional ICC networks, and rendered muscles electrically quiescent. 7. In summary, ICC networks develop in the pacemaker regions of the murine GI tract before birth. Development and organization of ICCs of the myenteric plexus region into networks precedes the development of electrical rhythmicity. Post-natal development of electrical rhythmicity is mainly characterized by enhancement of the amplitude and frequency of slow waves. The development of ICCs and electrical rhythmicity persists in vitro. ICCs appear to be necessary for the initiation of electrical rhythmicity. These findings provide further evidence for the pacemaker role of ICCs.

Animals↗

The role of Na(+)-Ca2+ exchange current in electrical restitution in ferret ventricular cells.

1. The mechanisms underlying electrical restitution (recovery of action potential duration after a preceding beat) were investigated in ferret ventricular cells. The time to 80% recovery (t80) of action potential duration was approximately 204 ms. 2. At a holding potential of -80 mV, the Ca2+ current (ICa) reactivated and the delayed rectifier K+ current (IK) deactivated very rapidly (t80: approximately 32 and approximately 93 ms, respectively). The kinetics of both currents are too fast to account for electrical restitution alone. 3. The putative inward Na(+)-Ca2+ exchange current (INa-Ca) produced by the Na(+)-Ca2+ exchanger in response to the intracellular Ca2+ transient reprimed (t80: 189 ms) with the same time course as mechanical restitution (recovery of contraction) and with a similar time course to electrical restitution. 4. Substantial reduction of inward INa-Ca, by buffering intracellular Ca2+ with the acetyl methyl ester form of BAPTA, shortened the action potential and greatly altered the electrical restitution curve. Subsequent addition of nifedipine (to block ICa) or 4-aminopyridine (4-AP) (to block the transient outward current, ITO) further altered the electrical restitution curve. 5. Any time-dependent current that contributes to the action potential is likely to affect the time course of electrical restitution. Although ICa, IK and ITO were previously thought to be the only currents involved in electrical restitution, we conclude that inward INa-Ca also plays an important role.

4-Aminopyridine↗

Dissociation between electrical and mechanical responses to nitrergic stimulation in the canine gastric fundus.

1. We examined the relationships between membrane potential, intracellular [Ca2+] ([Ca2+]i), and tension in muscles of the canine gastric fundus in response to nitrergic stimulation by NO donors and electrical field stimulation (EFS) of intrinsic enteric inhibitory neurons when adrenergic and cholinergic responses were blocked. 2. NO donors reduced [Ca2+]i and tension in a concentration-dependent manner. A close relationship was noted between these parameters. 3. In terms of the [Ca2+] vs. force relationship, relaxation responses to EFS differed from responses to NO donors. EFS resulted in smaller decreases in [Ca2+]i to produce a given relaxation compared with responses to NO donors. Thus, muscles stimulated with EFS were less sensitive to [Ca2+]i than muscles stimulated with exogenous NO. 4. When membrane potential, [Ca2+]i and tension were monitored simultaneously in the same muscles, a temporal dissociation was noted between the electrical responses and changes in [Ca2+]i and tension. Brief electrical responses were associated with more sustained changes in [Ca2+]i and tension. 5. Further dissociation between electrical and mechanical effects was noted. Changes in [Ca2+]i and tension caused by sodium nitroprusside and EFS were blocked by arginine analogues and by oxyhaemoglobin, but electrical responses were unaffected. 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylyl cyclase, also blocked the effects of nitrergic stimulation on [Ca2+]i and tension, without affecting hyperpolarization. Thus, in the presence of continued hyperpolarization, the reductions in [Ca2+]i and tension caused by nitrergic stimulation were blocked. 6. Block of hyperpolarization in response to nitrergic stimulation with tetrapentylammonium chloride (TPEA) had relatively little effect on the [Ca2+]i and tension responses. Thus, hyperpolarization is not required for nitrergic effects on [Ca2+]i and tension. 7. In summary, reduction in [Ca2+]i and tension in response to nitrergic stimulation of the canine gastric fundus does not depend upon electrical hyperpolarization. Non-electrical mechanisms such as enhanced uptake of Ca2+ by the sarcoplasmic reticulum or reduction in the Ca2+ sensitivity of the contractile apparatus may be the primary mechanisms mediating nitrergic responses in these muscles.

Animals↗

Inhibitory responses to nicotine and transmural stimulation in hyoscine-treated guinea-pig isolated trachealis: an electrical and mechanical study.

Guinea-pig isolated trachealis muscle treated with hyoscine (1 microM) exhibited mechanical tone which could be suppressed by transmural stimulation and, in a concentration-dependent manner, by nicotine (10-1000 microM). Hexamethonium (500 microM) did not itself cause tone changes, antagonized effects of nicotine but did not antagonize those of isoprenaline. Tetrodotoxin (0.3 microM) did not itself cause tone changes, did not modify the action of isoprenaline but antagonized the effects of nicotine and very markedly reduced responses to transmural electrical stimulation. Guanethidine (50 microM) did not itself cause tone changes, potentiated the action of isoprenaline, antagonized effects of nicotine and reduced responses to transmural electrical stimulation. Propranolol (1 microM) did not itself cause tone changes, antagonized effects of both isoprenaline and nicotine and reduced responses to transmural electrical stimulation. Propranolol (10 microM) caused greater antagonism of isoprenaline but did not further antagonize nicotine or further reduce responses to electrical stimulation. Intracellular electrophysiological recording from hyoscine-treated trachealis showed that 10 microM nicotine caused little or no mechanical or electrical change. Higher concentrations (100 microM and 1 mM) evoked relaxation which was often though not invariably accompanied by transient hyperpolarization and transient inhibition of electrical slow waves in the impaled cell. Hexamethonium (500 microM), tetrodotoxin (0.3 microM), guanethidine (50 microM) and propranolol (1 microM) each suppressed the electrical or mechanical changes evoked by nicotine (100 microM). However, nicotine (1 mM) tested in the presence of propranolol (1 microM), caused relaxation which could be accompanied by slow wave suppression but not by change in resting membrane potential. Transmural stimulation of hyoscine-treated trachea with single pulses of supramaximal voltage and 0.5 ms duration evoked neither relaxation nor membrane potential changes. Stimulation with similar pulses in trains of 5 s duration evoked relaxation which was dependent on pulse frequency. In many cells this relaxation was not accompanied by membrane potential change. In other cells suppression of slow waves occurred. At high pulse frequencies (greater than 16 Hz) this was generally accompanied by membrane hyperpolarization. In tissue treated with hyoscine and propranolol (both 1 microM), transmural stimulation with pulse trains as described above always evoked relaxation but no membrane potential changes were observed. 10 It is concluded that nicotine and transmural stimulation can excite intramural noradrenergic nerves in guinea-pig trachea and thereby evoke relaxation. The membrane potential changes (slow wave suppression and hyperpolarization) are similar to those evoked by the administration of agonists at beta-adrenoceptors. Nicotine and transmural stimulation also excite non-adrenergic non-cholinergic inhibitory (NANCI) nerves. The relaxation evoked by the NANCI neurotransmitter is accompanied by little, if any, membrane potential change.

Animals↗

Effect of the tachykinin NK1 receptor antagonists, RP 67580 and SR 140333, on electrically-evoked substance P release from rat spinal cord.

1. The effects of the non-peptide tachykinin NK1 receptor antagonists, RP 67580, SR 140333, CP-96,345 and CP-99,994 have been investigated on electrically-evoked release of substance P-like immunoreactivity (SP-LI) from rat spinal cord slices. 2. RP 67580 (10 nM) and SR 140333 (1 nM), perfused 5 min prior to and during 8 min stimulation of the dorsal roots (20 V, 0.5 ms, 1 Hz), significantly enhanced SP-LI release by 213 +/- 43 (n = 8) and 203 +/- 31 (n = 5) % of control evoked release (187 +/- 16% of basal outflow, n = 22) respectively. Neither compound modified basal outflow of SP-LI (15.3 +/- 2.5 fmol/8 ml, n = 10). 3. RP 67580 (10 nM) did not modify electrically-evoked release of calcitonin gene-related peptide-LI from rat spinal cord slices. 4. CP-96,345 (10 nM) and CP-99,994 (1 and 10 nM) did not alter electrically-evoked SP-LI release; however, they both inhibited release at 1 microM. Inhibition was also induced by 1 microM RP 67580 but not 1 microM SR 140333. 5. The effect of the NK1 receptor agonists, [Sar9 Met (O2)11]SP and [Sar9]SP, could not be tested on SP-LI release due to interference with the substance P radioimmunoassay (RIA). The other NK1 receptor agonists used, GR 73632, [Pro9]SP and septide, which did not interfere with the RIA, increased SP-LI basal outflow by 1807 +/- 713% (n = 3), 1259 +/- 160% (n = 3) and 620 +/- 69% (n = 3) at 10 nM, 1 nM and 1 microM, respectively. At the same concentrations, the three agonists also enhanced electrically evoked SP-LI release by 204 +/- 38% (n = 6), 753 +/- 40% (n = 3) and 504 +/- 97% (n = 3), respectively. The GR 73632 (10 nM)-induced increase in electrically-evoked SP-LI release, was not prevented by SR140333 (100 nM). None of the agonists inhibited SP-LI release at lower concentrations (0.1 nM GR73632; 0.01 and 0.1 nM [Pro9]SP and 1-100 nM septide).6 NKA and NKB, at concentrations up to 10 nM which did not interfere with the RIA, did not modify electrically-evoked release of SP-LI.7 The ability of NKI receptor antagonists to enhance electrically-evoked SP-LI release supports the concept of an NK1 autoreceptor control mechanism at substance P nerve terminals within the dorsal horn of the rat spinal cord.

Amino Acid Sequence↗

The "electrical way" to cure gastroparesis.

The treatment of gastroparesis recently received a heavy blow from the restrictions on the use of the prokinetic drug cisapride, but, fortunately, at the same time, a nonpharmacological approach, such as gastric electrical stimulation, came up again with new techniques. After an ultra-decennial experimentation with a large variety of electrical stimuli delivered to the gastric wall of animals and patients with gastroparesis, three principal methods are available at the moment: gastric electrical pacing, high-frequency gastric electrical stimulation, and sequential neural electrical stimulation. The first method aims to reset a regular slow-wave rhythm, but is unable to re-establish efficient contractions and a normal gastric emptying. High-frequency gastric electrical stimulation, although inadequate to restore a normal gastric emptying, nevertheless strikingly improves the dyspeptic symptoms, such as nausea and vomiting, giving the patients a better quality of life and a more satisfactory nutritional status. The last method, neural electrical gastric stimulation, consists of a microprocessor-controlled sequential activation of a series of annular electrodes which encircle the distal two thirds of the stomach and induce propagated contractions causing a forceful emptying of the gastric content. The latter method is the most promising, but it has so far only been tested in animals and would need to be tested in patients with gastroparesis before it can be used as a solution for this disease. All the aforementioned clinical studies, however, are not controlled and nearly all were published in abstract form. Therefore, further controlled trials are needed to establish which of these techniques is more useful for the treatment of gastroparesis.

Animals↗

Epidermal changes in heat and electrically injured pig skin: a light microscopic study of the sequences in morphology.

Biopsies were obtained from heat and electrically exposed pig skin at different at different times after exposure, in order to describe the morphological sequences in heat and electrically injured skin. The work is part of a series of studies in which it is investigated whether morphological methods can be used in disclosing electrical torture. Epidermal changes in heat lesions differed from those of electrical lesions in all experiments. Heat lesions typically showed a detached epidermis with fibrillar or granular cytoplasm. In older lesions the epidermis appeared concrete. Electrical lesions showed an attached epidermis with small defects, a white, homogeneous cytoplasm, vesicular nuclei and curled, clumped keratin. The electrical lesions were rejected at day 4 or 5. The number of characteristic morphological changes in epidermis decreased with the age of the lesions. It is concluded that epidermal electrical lesions differ in morphology from heat lesions and that it is possible to evaluate the age of the lesions.

Animals↗

Network construction of first aid for electrical injury in the east China area of China Power.

Electrical injury is an area of burn medicine that requires specialized treatment. Injury rates have reached 6.56% in 1990, compared to only 1% prior to 1980. In recent years, the morbidity has steadily increased due to the rapid development of the electrical power industry and the popularization of electrical installations. Electrical accidents cause severe damage to muscle and tissue, which makes treatment of these accident patients quite challenging. Therefore, it is very important to promote the widespread use of a first aid network within the electrical power system while strengthening safety measures within the industry to reduce morbidity and mortality among the electrically injured. To date, similar networks have been established in East China, Central China, North China, and Shandong within the six major electrical power industries. We hope to minimize the injury of workers through appropriate supervision, improved safety measures, and improved safeguarding of equipment.

Accidents, Occupational↗

Electrical injuries in Canadian burn care. Identification of unsolved problems.

Over the past decade, the Firefighters' Burn Treatment Unit of the University of Alberta Hospital in Edmonton, Alberta, Canada, has treated 1399 inpatients suffering from thermal injury. Regional burn care is provided in a 10-bed intensive care unit with 18 plastic surgery reconstructive beds for a large referral region of central and northern Alberta, portions of the Northwest Territories, and neighboring provinces of British Columbia and Saskatchewan. Of the total burn inpatients during this period, 74 electrical injuries were treated (5.3% of all admissions): 71 were males (95.9%) and 3 females (4.1%). The mean age of all patients was 33.9 +/- 12.6 years (range 1-67). Compared to our general population of thermally injured patients, those with electrical injuries had smaller injuries [9.9 +/- 12.9% TBSA (range 1-65) versus 15.1 +/- 10.1], shorter length of hospitalization [18.6 +/- 7.3 days (range 1-80) versus 26.2 +/- 0.8], and substantially lower mortality once reaching the hospital (0% versus 4%). Electrical injuries were classified as flash in 30 cases, contact in 42 cases, and lightning in 2 cases; 74.3% of injuries occurred during work-related activities. A total of 118 operative procedures were performed during the acute admission (1.6 procedures per patient), including 19 amputations: 12 in the upper and 7 in the lower extremity. The mean time of amputation was 9.3 +/- 5.3 days after admission. In contact injuries of the upper extremity, 14 patients suffered amputations or neurologic injury that required reconstruction with free tissue transfers and nerve grafts. Long-term functional outcome of these patients using sensory testing, the Jebsen-Taylor hand function test, and wound coverage has revealed that these patients have substantial persistent sensory impairment of their upper extremities postinjury despite reconstruction, although many remain active and functional with acceptable wound coverage. Based on our analysis of electrical injury as it presents to one typical Canadian burn unit, our patients suffer limb loss on a delayed basis, which leads to substantial morbidity. Reconstruction of the upper extremity with microsurgical techniques after profound electrical injury has provided acceptable coverage, but in many instances is associated with poor or marginal sensory recovery limiting reemployment options for patients with upper extremity electrical burns. Further understanding of the cellular biology of delayed tissue loss after electric injury would offer the potential for reduction in amputation rate and improvement in functional outcome and overall morbidity.

Accidents, Occupational↗

Pancreatic acinar cells: acetylcholine-evoked electrical uncoupling and its ionic dependency.

1. Isolated segments of mouse or rat pancreas were placed in a Perspex bath through which physiological saline solutions were circulated. Intracellular recordings from surface acini were made by inserting up to three separate micro-electrodes into neighbouring cells within the same acinus. Through one of these electrodes current pulses could be injected. Electrical coupling between the cells could be continuously assessed. The acinus under investigation was stimulated by iontophoresis of ACh from an extracellular micropipette.2. During resting conditions all cells within an acinus were fully electrically coupled. A 5-10 sec pulse of a relatively large iontophoretic ACh ejecting current, causing initially the well characterized surface cell membrane depolarization and resistance reduction, was followed by a marked electrical uncoupling of neighbouring cells. In some cases one cell was clearly being isolated equally from the two other cells impaled, in other cases the cell into which current pulses were injected was becoming more isolated from one of the neighbouring cells than from the other one.3. The ACh-evoked electrical uncoupling was completely reversible and could be repeatedly observed in the same cell.4. The electrical uncoupling in response to short pulses of ACh (5-10 sec) was not affected by even prolonged (up to 50 min) exposure to Ca-free solution containing EGTA.5. ACh-evoked uncoupling (short pulses) was not reduced about 5 min after introduction of Mn (2 mM), Ni or Co (5 mM). Mn thereafter gradually reduced and finally (after about half an hour) abolished the ACh-evoked uncoupling. Ni and Co gradually enhanced the uncoupling response. The blocking effect of Mn on the ACh-evoked uncoupling occurred much faster in the absence of superfusion fluid Ca.6. During a period of sustained ACh stimulation sustained electrical uncoupling was observed. If Ni or Co (5 mM) was introduced during such a stimulatory period the cells recoupled. This effect of Ni and Co was immediate and fully reversible.7. The uncoupling responses to short pulses of ACh was not reduced immediately after replacing superfusion fluid Na by Tris at a time when the surface cell membrane depolarization and resistance reduction was already severely reduced. Thereafter a gradual slow reduction of the ACh-evoked uncoupling was observed. This did not occur if Na was replaced by Li.8. It is concluded that the Ca needed to raise [Ca(2+)](i) sufficiently to cause electrical uncoupling comes from the cells in cases of uncoupling evoked by short pulses of ACh, but from the external solution in cases of sustained uncoupling evoked by sustained stimulation of ACh.

Acetylcholine↗

The direction of growth of differentiating neurones and myoblasts from frog embryos in an applied electric field.

1. Disaggregated single neurones and myoblasts obtained from the neural tube and somites of Xenopus laevis embryos (stages 17-21) were cultured in the presence of steady small electric fields. 2. Neurites grew preferentially towards the negative pole, or cathode, in field strengths of 7-190 mV/mm. Many turned through considerable angles to do so. This effect disappeared below a threshold level of about 7 mV/mm. 3. Greater numbers of neurones sprouted neurites in cultures exposed to an electric field compared to control cultures. The difference could be as much as tenfold. The threshold level of this phenomenon was about 6-8 mV/mm. Other cell types such as pigment cells and fibroblasts were also stimulated to differentiate in culture by an electric field, although to a lesser extent than neurones. 4. Applied electric fields had no effect on the location of the origin of neurites on the cell body. 5. Spherical myoblasts cultured in applied electric fields (36-170 mV/mm) elongated with a bipolar axis of growth which was perpendicular to the electric field. The response was graded and disappeared at field strengths below 36 mV/mm. 6. It is suggested that in vivo, the direction of neural outgrowth from the neural tube and the strict spatial organization of somites might be under the control, in part, of endogenous electric fields. Possible sources of these are discussed.

Animals↗

Electrically evoked basilar membrane motion.

Electrically induced outer hair cell (OHC) motility, demonstrated by a number of investigators in isolated OHC preparations, has been considered to be a key mechanism in the active process which brings about the excellent sensitivity and frequency selectivity of the mammalian cochlea. In this study, electrical-to-mechanical transduction in the gerbil cochlea was demonstrated in vivo by direct measurement of basilar membrane motion evoked by sinusoidal electrical current injected into the scala media. The characteristic frequency (CF) of the measurement place was approximately 40 kHz as determined by the basilar membrane (BM) responses to acoustic stimulation. The results showed that basilar membrane motion could be evoked by electrical current of frequencies from below 10 Hz to exceeding 40 kHz. The magnitude and phase of the BM velocity response to constant current stimulation, from 100 Hz to 10,000 Hz, were similar to the acoustically driven BM velocity for constant umbo velocity. For frequencies in this range, the BM motion evoked by a current of 50 microA was comparable to the BM motion evoked by a 60 dB SPL acoustic stimulus. The phase of the electrically evoked BM motion indicates that positive current injected into the scala media caused the BM to move toward scala vestibuli for frequencies between 100 and 10 kHz. This result is consistent with the hypothesis that the electrically evoked BM motion is due to electrically evoked OHC length changes.

Animals↗