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Biomedical subjects

B R Fink

Publications and source records attributed to B R Fink.

At least 37 records · Page 2Linked to original sources
PubMed1986

Mechanism of differential epidural block.

Pain block in obstetric epidural anesthesia is usually accompanied by relatively persistent retention of motor power; however, the reason for this is not entirely clear. The differential effect has been ascribed to a relatively high resistance of large fibers to conduction block. However, recent results from individual axons are incompatible with that explanation and have prompted the suggestion that greater vascularity in ventral than in dorsal roots might account for the phenomenon. To test this hypothesis, transverse sections of five sets of human dorsal and ventral C-8, T-7, and L-5 roots were examined by an immunohistochemical method that is specific for factor VIII and stains the vascular endothelium. A naive tally of the stained vessels failed to reveal any excess vascularity of the ventral roots, and the hypothesis was therefore rejected. However, it was noted at autopsy that the thin dural sleeve surrounding the roots, where epidural anesthetic is most likely to penetrate to the nerve fibers, may measure less than 5 mm from the dural sac to the intervertebral foramen, a distance probably too short to contain three internodes of motor fibers, the minimum length of fiber necessary for block by local anesthetic. This anatomy might help explain the clinical differential.

Adult↗
PubMed1986

2020 glimpses through the anesthesia retroprospectroscope. The 1985 John J. Bonica lecture.

The Department of Anesthesiology at the University of Washington has grown steadily throughout its first 25 years. Personal reminiscences of old-fashioned anesthesia induction lead to philosophizing on the role of the larynx in the evolution of the human mind and the limited future of computerized administration of anesthesia. Machines will never substitute for the alliance between science and the humane that characterizes modern anesthesiology.

Anesthesiology↗
PubMed1985

Laryngeal injury in a dog model of prolonged endotracheal intubation.

Using a dog model of prolonged translaryngeal intubation, the authors studied laryngeal injury. Segments of 10.7 mm diameter endotracheal tube were sutured in place in the larynges of anesthetized animals, and the animals were allowed to awaken and the tubes left in place for periods of 24 h to 84 days in a total of 13 dogs. Each animal's larynx was studied endoscopically at weekly intervals and at the time of death. Both endoscopic and postmortem examination revealed erythematous laryngeal mucosa at 24 h and severe mucosal ulceration by 1 week. Microscopic examination revealed mucosal inflammation at 24 h with loss of mucosal architecture by 1 week. In several animals intubated 1 week or longer, inflammatory infiltrates were present in the arytenoid cartilage. While damage was generally severe by 1 week, it did not tend to become more severe after that time. Between week 1 and week 12, there was no significant correlation of the severity of laryngeal injury with the duration of endotracheal intubation. The results suggest that duration alone may not be a factor in laryngeal injury after the first week of intubation.

Animals↗
PubMed1985

Differential margin of safety of conduction in individual peripheral axons.

The relation between fiber size and safety of conduction was tested in vitro on individual afferent axons of rabbit vagus nerve by lowering the external sodium ion concentration and noting the effect on threshold excitability and conduction velocity. Conduction safety of myelinated axons was found to be independent of fiber size and slightly less than among unmyelinated axons. The results are consistent with previous data from the same model, where blocking concentration and diffusion time of lidocaine to the excitable membrane of individual axons also were independent of myelinated axonal size. The evidence from these single-unit studies implies that the differential blocks of functional modalities observed with spinal and epidural anesthesia probably do not arise from fiber size-related differences in susceptibility to block: possible alternatives are mentioned briefly.

Animals↗
PubMed1985

Differential effect of nerve fiber structure on block by local anesthetic.

The incidence of conduction block by lidocaine 0.3 mmol/l (8.1 mg/dl) in several successive lengths of individual afferent axons of rabbit was compared. The conduction velocity of the axons was either "slow," "intermediate" (1.3-4 m/s), or "fast." The "intermediate" group showed a higher incidence of proximal acceleration of conduction (P less than 0.001) and a greater incidence of block (P less than 0.001) than the "slow" and "fast" fiber groups. The results were interpreted as indicating that the fibers of the "intermediate" group had an unmyelinated peripheral and a myelinated proximal length, with a junctional heminodal region that was the seat of the high sensitivity to block. The potential clinical significance of the observation is discussed in terms of the known distribution of heminodes in the peripheral nervous system.

Anesthetics, Local↗
PubMed1985

Acid and alkaline solutions of local anesthetics: duration of nerve block and tissue pH.

The effect of solution pH on the duration of rat infraorbital nerve blocks produced by 1% lidocaine or 0.25% bupivacaine at pH 5.0 and 7.4, with and without epinephrine was investigated in a double-blind study. The time course of tissue pH changes subsequent to infections into the infraorbital area or abdominal musculature of rats was measured with a tissue pH microelectrode. Injectable pH had little or no effect upon the duration of block. Tissue pH was minimally changed by the injection of solutions at pH 7.4, but decreased appreciably with injections of solutions at pH 5.0, or if the injectate contained epinephrine.

Abdominal Muscles↗
PubMed1984

Differential slowing and block of conduction by lidocaine in individual afferent myelinated and unmyelinated axons.

The study of compound action potentials has not succeeded in determining exact limits to differential block of nerve fibers by local anesthetics. Further observations on individual neurons therefore were undertaken. Rabbit vagus nerve and ganglion were superfused in vitro at 37 degrees C, pH 7.4. Activity evoked by stimulating the distal end of the nerve was monitored extracellularly from individual somata by a microelectrode in the ganglion. Lidocaine HCl in steps of 0.2-0.1 mmol/l (0.0005-0.0025 g/dl) was applied to the intervening nerve to identify two concentrations, respectively, just sparing and extinguishing conduction in the axon belonging to the soma, the average being regarded as the blocking concentration. The mean blocking concentrations (mM, +/- SD) for axons conducting at control velocities between 3 and 26 m/s (myelinated axons) was 0.43 +/- 0.15, N = 18, for axons slower than 1.4 m/s (unmyelinated axons) 0.63 +/- 0.14, N = 11, for intermediate velocity axons 0.19 +/- 0.18, N = 7. The differences were significant by Scheffé's multiple comparisons test (P less than 0.01). Although the myelinated axons were blocked by a lower average concentration of lidocaine than unmyelinated axons, they manifested significantly more slowing of conduction before block (P less than 0.001). No relation between blocking concentration or latency increase and conduction velocity (fiber size) was evident within any fiber group.

Animals↗
PubMed1984

Differential effects of hypoosmotic hyponatric swelling on A and C fibers.

The differential effects of exposure to a moderately hypoosmotic hyponatric solution (0.35 isoosmotic, Na+ 36 mmol/l) on conduction in myelinated (A) and unmyelinated (C) axons were studied in vitro on compound action potentials of rabbit vagus nerves in which the perineurial sheath had remained undisturbed. Controls were incubated at 37 degrees C in isoosmotic isonatric solution for 5 h (Group 1a, n = 7) or 7 h (Group 3, n = 3). Other controls were incubated in isoosmotic isonatric solution for 2 h followed by 3 h in isoosmotic hyponatric (Na+ 36 mmol/1) solution (Group 1b, n = 6); experimental nerves were incubated in isoosmotic isonatric solution for 2 h followed by 3 h in hypoosmotic hyponatric solution (Group 2, n = 7) and, to study recovery, a further 2 h in isoosmotic isonatric solution (Group 4, n = 8). In Group 1b, isoosmotic hyponatric exposure approximately doubled the latency of the A-component (A-CAP) and decreased the A-CAP amplitude to 44 +/- 8% of control; the amplitude of the C-component decreased to 65 +/- 15% of control. Hypoosmotic hyponatric exposure increased the latency of the A-CAP by 82 +/- 10% (mean +/- SE, P less than 0.001) and extinguished A-CAP within 20 min, whereas the latency increase of the C-component (C-CAP) was more than twice as great and extinction slower and often incomplete; neural wet weight increased 34 +/- 4% and neural sodium and potassium contents decreased 55 and 42%, respectively. Recovery in isoosmotic isonatric solution (Group 4) was absent or very small in the case of A-CAP, as regards latency and amplitude but was complete for C-CAP amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1984

Diffusional delay in local anesthetic block in vitro.

The diffusion of lidocaine to myelinated and unmyelinated axons was compared on individual afferent fibers of rabbit vagus nerve. The criterion consisted of the time required for more than 95% completion of the asymptotic increase in impulse conduction time produced by a weak, nonblocking concentration of lidocaine. Measurements on sheathed and desheathed nerves for both myelinated and unmyelinated axons detected an apparent but statistically not significant diffusional lag at the perineurial sheath, averaging four minutes in this model; there was no significant difference in the mean time for attainment of criterion in myelinated and unmyelinated axons, which averaged an additional 13 min in both types of fiber. From these observations the authors conclude that lidocaine diffused as readily through the nodal gap to the excitable membrane of the myelinated fiber as through the Schwann cell mesaxon to the unmyelinated fiber. Thus differential diffusion within a nerve seems unlikely to be a contributing factor to clinical differential block.

Anesthetics, Local↗
PubMed1984

Differential effects of glucose and potassium lack in conduction block of myelinated and unmyelinated axons.

The effect of potassium on conduction in myelinated and unmyelinated axons lacking glucose was investigated in vitro. In the presence of ambient potassium neural excitability was lost after the same period of time in both myelinated and unmyelinated fibers. In the absence of potassium in the incubation solution however, the extinction times of the unmyelinated axons only (p less than 0.01), but not those of the myelinated ones were delayed. It is suggested that unmyelinated C fibers are more energy efficient than myelinated A axons.

Action Potentials↗
PubMed1984

Differential vulnerability of large and small mammalian myelinated fibers to glucose lack.

The excitability of A fibers of peripheral nerves in vitro is more susceptible to depression by energy lack than is excitability of C fibers. Whether there is also a differential vulnerability between small myelinated A delta fibers that conduct fast pain and large myelinated A beta fibers is unclear. We evaluated the relative abilities of A beta and A delta fibers to withstand energy lack in rabbit vagus nerve by measuring the amplitudes and latencies of the compound action potentials during incubation in glucose-free Ringer's-bicarbonate solution. We also evaluated the reversibility of the effects after returning the nerves to glucose containing solution. We found that A delta fibers are more susceptible to such energy lack and recover from it less completely than A beta fibers.

Action Potentials↗
PubMed1983

Potentiation of nerve block in vivo by physiological adjuvants in the solution.

One hundred and seventy-four rats received a standardized 0.4-ml injection into the left infraorbital nerve and all solutions contained lignocaine 0.25 g dl-1. In groups 1-4, the solutions were isoosmotic and contained, besides sodium chloride, potassium chloride 0 or 4 mmol litre-1 and glucose 0 or 20 mmol litre-1 (0 or 360 g dl-1). For groups 5-8, the solutions were hypoosmotic, containing sodium chloride to 0.6 of normal tonicity but were otherwise identical to solutions 1-4. Presence and duration of sensory block were determined from the reflex sublingual electromyographic response to periodic homolateral and contralateral electrical stimulation of the upper lip. In groups 1-4, the presence of potassium chloride 4 mmol litre-1 approximately doubled the duration of blockade (P less than 0.001). Groups 5-8 showed that hypoosmolarity also doubled the duration of block (P less than 0.001), but hypoosmolarity and potassium chloride did not have additive effects. It is concluded that addition of potassium- chloride 4 mmol litre-1 to isotonic solutions of lignocaine is likely to enhance their clinical effectiveness.

Adjuvants, Anesthesia↗
PubMed1983

A new approach to differential peripheral nerve fiber block: Na+,K+-ATPase inhibition.

Differential block of peripheral nerve fibers was attempted in vitro by a new approach based on inhibiting the membrane pump with ouabain. Sequential concentration dependent extinction of the components of the compound action potential was obtained: C extinguished first, A delta next, A beta last. The sequence conforms to expectations based on axonal size. Because pain is mediated by C and A delta fibers, and block of these groups by ouabain was not reversed readily, further investigation of the practicability of the new approach seems warranted.

Action Potentials↗