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Biomedical subjects

B R Fink

Publications and source records attributed to B R Fink.

At least 55 records · Page 3Linked to original sources
PubMed1983

Differential peripheral axon block with lidocaine: unit studies in the cervical vagus nerve.

The differential susceptibility of large and small axons to lidocaine was studied on units in the rabbit vagus nerve. The results classified the units into three groups: 1) myelinated, conduction velocity 37.5-5 m/s, which were blocked by lidocaine 0.4-0.8 mM; 2) slow, unmyelinated axons, conduction velocity 1.2-0.5 m/s, and these axons were not blocked by 0.2, 0.4, or 0.6 mM lidocaine but usually were blocked by 0.8 mM lidocaine; and 3) Axons of intermediate conduction velocity, between 1.2 and 4 m/s. The last group of axons was the most sensitive: some were blocked by as little as 0.2 mM lidocaine. No size-related trend was detected within the groups.

Action Potentials↗
PubMed1982

Paradoxical preservation of neural conduction by lidocaine.

The interaction of glucose lack and local anesthetic on impulse conduction was investigated in rabbit vagus nerve. Glucose lack depressed the compound action potential 50 per cent in 47 +/- 7 min (+/- SD, n = 5) and extinguished it in 69 +/- 7 min. Lidocaine hydrochloride, 0.1 mmol/1 (0.0027 g/dl), delayed the onset of inexcitability caused by glucose lack: 50 per cent depression required 85 +/- 9 min, extinction required 131 +/- 20 min (P less than 0.001). The delay decreased with lower and higher lidocaine concentrations. Lidocaine also significantly decreased the potassium loss and sodium gain occasioned by 2.5 h of glucose deprivation. Thus, delayed extinction of excitability by local anesthetic in very low concentration may be due to decrease in permeability of the axonal plasma membrane not only to sodium but also to potassium ions.

Action Potentials↗
PubMed1982

Functional and structural changes in the rabbit vagus nerve in vivo following exposure to various hypoosmotic solutions.

Hypoosmolar solutions were recently shown to produce a reversible conduction block of rabbit vagus nerve and to potentiate local anesthetic agents. The object of the present study was to determine the ability of neural tissue to recover structurally and functionally following exposure to hypoosmotic solutions. Cervical vagus nerves of rabbits were bathed in situ for 2 hours in a control solution or in 0.4, 0.5, and 0.6 aqueous dilutions of physiologic salt solution. Nerves excised immediately after exposure, or 1 to 4 weeks later, were subjected to light and electron microscopic examination. Following exposure to control and 0.6 dilution, nerves were normal in all respects at 8 days. However, nerves exposed to 0.4 and 0.5 dilutions, although apparently functionally intact as tested by conduction of C fiber action potentials, showed evidence of axonal damage characterized by accumulation of macrophages and proliferation of Schwann cell processes. It may be inferred that the osmotic fragility of axons is similar to that of erythrocytes and that immersion in 0.6 N osmotic solution is probably harmless to the nerve.

Animals↗
PubMed1982

A comparative in vivo study of local neurotoxicity of lidocaine, bupivacaine, 2-chloroprocaine, and a mixture of 2-chloroprocaine and bupivacaine.

This study was undertaken because of several recent reports of adverse neurologic reactions following the use of 2-chloroprocaine. Carotid sheaths containing undisturbed vagus nerve were surgically exposed in rabbits and bathed in situ for up to 1 hour in one of the following-isotonic solutions: physiologic salt solution, lidocaine 2%, bupivacaine 0.75%, 2-chloroprocaine 3%, or a mixture of 2-chloroprocaine 1.5% and bupivacaine 0.375%. Each solution contained epinephrine, 5 micrograms/ml, (1:200,000). In other animals the carotid sheaths were bathed in physiologic salt solution, or 2-chloroprocaine 3% without epinephrine. The nerves were excised 10 to 12 days later. C-fiber impulse conduction was normal in nerves that had been exposed to physiologic salt solution with or without epinephrine, to lidocaine, or to bupivacaine. Conduction was absent or markedly impaired in several nerve specimens following exposure to 2-chloroprocaine. Histologic sections revealed the presence of epineurial cellular infiltration and fibrosis, perineurial fibrosis, and axonal degeneration in nerves that had been exposed to 2-chloroprocaine or the mixture of 2-chloroprocaine and bupivacaine. Histologic abnormalities were minor or absent following exposure to lidocaine, to bupivacaine, or to physiologic salt solution. These findings suggest that, under the conditions of the experiments, 2-chloroprocaine is more neurotoxic than lidocaine or bupivacaine.

Action Potentials↗
PubMed1981

Role of glucose or potassium lack in nerve block.

Potassium and glucose are usually lacking in solutions employed for nerve conduction block. The significance of this for impulse conduction was studied in rabbit vagus nerve in vitro, incubated for 2 h Ringer's bicarbonate solution containing or lacking 5 mM glucose and 4 mM potassium chloride (n = 5 for each conditions). The c-fiber actin potential was recorded by periodic stimulation and the Na and K content of the desheathed nerve core was determined at the end of the incubation. In the presence of glucose, apparently normal conduction persisted for at least 2 h, even though the nerves incubated in potassium-free medium lost 20 per cent of their potassium. In the absence of glucose, reversible extinction of conduction was complete in 78 +/- 9 min when external potassium was present, and in 110 +/- 10 min when external potassium was absent. The data suggest that lack of glucose may reinforce C-fiber inexcitability during conduction block and that inclusion of a physiologic amount of potassium chloride in the solution may also be desirable.

Animals↗
PubMed1981

Duration of action of nerve blocks produced by mixtures of local anesthetics and low molecular weight dextran: studies in rat infraorbital nerve blocks.

The duration of rat infraorbital nerve block by 1% lidocaine or 0.25% bupivacaine, and its modification by low molecular weight dextran, was investigated in a randomized, observer-blind study. The addition of low molecular weight dextran did not prolong the duration of the blocks. No evidence of slow releasing or local anesthetic binding properties attributed to low molecular weight dextran was found.

Anesthetics, Local↗
PubMed1981

[Pain research].

Explore the source record for details and available documents.

Humans↗
PubMed1980

Laryngeal mucous gland excess in victims of sudden infant death.

Larynges from 13 victims of sudden infant death syndrome (SIDS) and from ten controls of comparable age were subjected to serial histological transverse section and examined for structural differences that bear on functional performance. The cross-sectional area of mucous glands in the vestibular fold, expressed as a percent of the total cross-sectional area of the fold was 19.52 +/- 8.56 (mean +/- SD in the SIDS specimens), and 12.56 +/- 6.25 in the controls. The difference is statistically significant and suggests that excess mucous laryngeal secretion may be present in at least some cases of the syndrome.

Humans↗
PubMed1980

Experimental evaluation of local anaesthetic solutions using rat infraorbital nerve block.

The analgesic effectiveness of various local anaesthetic solutions was measured in the distribution of the infraorbital nerve of the rat. Using Sprague-Dawley rats sedated with phenobarbitone 25 mg/kg intraperitoneally and a simple stereotactic technique, 0.2 ml of solution was deposited at the infraorbital notch. The onset and duration of analgesia were ascertained by timing the unilateral absence of aversive response to pinching the upper lip, tested at intervals of five minutes. The experiments were performed with coded solutions, the entire code being preserved intact until completion of the study. Solutions were tested on sets of eight animals weighing 500--600 g. The average duration (minutes +/- S.D.) of analgesia produced by the respective injectates was as follows: Lidocaine 0.5% -42+/-12 Lidocaine 1.0% -47+/-10 Mepivacaine 0.5% -58+/-13 Mepivacaine 1.0% -78+/-23 Procaine 0.5% -0+/-0 Procaine 1.0% -34+/-10 Procaine 1.5% -46+/-13 2-Chloroprocaine 1.5% -38+/-9 Bupivacaine 0.5% -100+/-40 Etidocaine 1.0% -59+/-25 Tetracaine 0.2% -0+/-0 Tetracaine 0.3% -0+/-0 Comparison with other animal models used to evaluate conduction block indicates that this technique affords an improved, standardized and reliable experimental guide to the clinical analgesic properties of local anaesthetic agents.

Anesthetics, Local↗
PubMed1979

Lidocaine (without epinephrine) does not affect the fine structure or microtubules of the trigeminal nerve in vivo.

The authors examined the fine structure and microtubules of unmyelinated axons and Schwann cells in the infraorbital branch of rat trigeminal nerve 1, 3.5 and 24 hours after intraneural injection of lidocaine HC1, 1--4 per cent, 0.2 ml, or saline solution, 0.2 ml; untreated control nerves were also examined. These concentrations of lidocaine are more than sufficient to block impulse conduction and rapid axonal transport in rat infraorbital nerve, but contrary to previous reports, significant structural change was not found as compared with control nerves.

Anesthesia, Conduction↗
PubMed1979

Osmotic swelling effects on neural conduction.

Local anesthetics administered intrathecally seen more effective when in hypobaric solution than when in hyperbaric solution. To test whether an unrecognized osmotic effect might be playing a part in this, sheathed vagus nerves of rabbit were incubated in electrolyte-deficient or electrolyte-free media of various degrees of hypo-osmolarity. The nerves gained weight over a period of 15 min. They lost nearly half their sodium, but very little potassium, within 5 min. Electrolyte depletion by incubation in sucrose solutions depressed the amplitude of the C-fiber component of the compound action potential more rapidly in hypo-osmotic than in iso-osmotic solutions. In iso-osmotic sucrose, 50 per cent depression developed in 61 +/- 12 min (mean +/- SD, n = 5), but in 0.6 iso-osmotic sucrose, 50 per cent depression was reached in 17 +/- 3 min (n = 5). Lidocaine, 100 microM (approximately 0.003 g/100 ml) in iso-osmotic sucrose was without observed effect; lidocaine, 100 microM in 0.6 iso-osmotic sucrose produced 50 per cent depression in 7 +/- 2 min (n = 4). Thus, osmotic swelling plus electrolyte depletion, but not electrolyte depletion alone, markedly intensified inhibition of conduction by lidocaine. All effects were reversible by returning the nerves to isotonic physiologic incubation medium. The results suggest that intrathecal osmotic swelling of neural tissue may contribute to the conduction block in hypobaric spinal anesthesia.

Anesthesia, Spinal↗
PubMed1978

Neural pharmacokinetics of epinephrine.

The effects of 3H-epinephrine on the duration of block and on the time course of uptake and efflux of local anesthetic (14C-lidocaine hydrochloride) were determined in the infraorbital nerve of the pentobarbital-obtunded rat. Epinephrine, 1:50,000, doubled the duration of behavioral block produced by 37 mM (1 per cent) lidocaine; 1:100,000, 1:200,000 and 1:400,000 prolonged the block correspondingly less, the relation being inversely proportional to the log of the epinephrine concentration. The nerural level of 3H-epinephrine reached a peak within 10 minutes and then declined linearly with time, as did the associated neural level of 14C-lidocaine. Linearity apparently results from the summation of the time-linked decreasing diffusion gradient of drug and the consequently increasing rate of perfusion with blood. Phentolamine antagonizes the epinephrine-caused prolongation of behavioral block. The results suggest that in spinal anesthesia the extent of dilution of an epinephrine additive by cerebrospinal fluid will significantly affect the duration of the block.

Anesthesia, Local↗
PubMed1976

Reversible inhibition of rapid axonal transport in vivo by lidocaine hydrochloride.

Rats were given standardized injections of 3H-L-proline into the trigeminal ganglion and 14C-lidocaine hydrochloride at the infraorbital foramen. The 3H-L-proline was always injected 2.5 h before removal of the nerve. Lidocaine, 1, 2, and 4%, produced a concentration-related inhibition of entry of 3H-labeled rapid axonal transport into the distal portions of the nerve. Addition of epinephrine, 1:200,000, doubled the intensity of the effect. The time delay of recovery was also concentration-related, and with 4% lidocaine recovery still seemed incomplete after 4.5. h. It is concluded that inhibition of rapid axonal transport is probably a usual byproduct of nerve block with local anesthetics such as lidocaine. The inhibition seems attributable in part to a disturbance of the energy metabolism of the nerve.

Animals↗