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Biomedical subjects

L D Fechter

Publications and source records attributed to L D Fechter.

60 records · Page 4Linked to original sources
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Effects of chronic carbon disulfide inhalation on sensory and motor function in the rat.

Chronic carbon disulfide (CS2) exposure produces debilitating motor, sensory and neuropsychiatric consequences in humans. Sensory, especially auditory, tests have been considered for indexing early intoxication. This study examines effects of chronic CS2 exposure in rat upon auditory and neuromuscular function using reflex modulation audiometry to test the feasibility of using pure tone detection thresholds as such an index. This method is sensitive to the differential effects of toxicants upon acoustic and neuromuscular functioning. Rats were tested before, during and after five or 12 weeks of 500 ppm CS2 inhalation, six h/day, five days/week. Neuromuscular integrity, reflected by baseline startle amplitude, decreased 50% after five weeks and 67% following 12 weeks of CS2 exposure; recovery to 70% of preexposure values occurred on the fourth postexposure week. Twelve weeks of CS2 inhalation had no significant effect upon acoustic thresholds. Pure tone detection thresholds, therefore, do not appear adequate to index early CS2 exposure levels in the rat, as severe neuromuscular compromise occurred at a time when acoustic thresholds remained stable.

Acoustic Stimulation↗
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Effects of acute styrene and simultaneous noise exposure on auditory function in the guinea pig.

Although styrene has been demonstrated to disrupt vestibular function acutely, parallel studies have not been conducted in the auditory system. This article presents data on the effects of acute styrene administration by injection and inhalation on cochlear function. No deleterious effect of the maximally tolerated styrene dose on hearing was identified when cochlear function was assessed using a within-subjects design. When guinea pigs were administered styrene by inhalation during a single 7-h period, normal auditory function was observed both 1 and 7 days later as compared to chamber controls which did not receive styrene. In some instances, the interactive effects of noise and simultaneous styrene inhalation were studied to determine whether chemical exposure might enhance the disruptive effects of noise on hearing. While a persistent noise-induced hearing loss was observed 1 day following exposure, subjects administered styrene simultaneously did not show a greater hearing loss than those receiving noise alone. Finally, when a 7-day recovery period for noise-induced hearing loss was interposed before audiometric testing, the combined exposure to styrene and noise was not more potent than noise alone in elevating auditory thresholds. Although auditory dysfunction has been reported following subchronic styrene administration, the current results do not support an ototoxic effect of styrene at the level of the cochlea with short-term exposure.

Action Potentials↗
PubMedDate not supplied

Trimethyltin disrupts loudness recruitment and auditory threshold sensitivity in guinea pigs.

Trimethyltin (TMT) impairs auditory thresholds within minutes of systemic administration. However, there are no data which relate to the output of the auditory nerve at sound levels above threshold. In this experiment, we evaluated the functional effects of TMT on the auditory threshold by identifying the sound level which just produced a detectable compound action potential (CAP). We also assessed outer hair cell function by measuring the cochlear microphonic (CM), a nonpropagated ac potential which is phase-locked to the stimulus. Finally, we measured the growth of the N1 amplitude as a function of stimulus intensity at levels above threshold and of the summating potential (SP), a dc potential which has multiple generators. To isolate cochlear from systemic effects of TMT, the agent was applied directly to the round window, a structure separating the middle and inner ear, of anaesthetized guinea pigs. We show that TMT applied to the round window membrane can disrupt the function of the cochlea. Measurements of auditory function at supra-threshold levels showed clearly that TMT reduced the amplitude of N1 while having no measurable effect on the SP. These findings indicate that TMT blocks the recruitment of neuronal elements by loud sound. This pattern of impairment differs from that observed with aminoglycoside antibiotics, hypothermia, and presbycusis in which loudness recruitment has been reported.

Action Potentials↗
PubMedDate not supplied

Disruption of cochlear potentials by chemical asphyxiants. Cyanide and carbon monoxide.

While ischemia, hypoxic hypoxia, and carbon monoxide (CO) have received extensive study designed to characterize mechanisms by which they disrupt cochlear function, little data are available concerning cyanide's potential to disrupt auditory function. In this study, disruption of the compound action potential (CAP) and endocochlear potential (EP) by cyanide and CO was compared in rats treated with potassium cyanide (KCN) (7 mg/kg ip), saline, CO (35 ml/kg ip), and air. Acute KCN administration significantly suppressed CAP and EP transiently. The effect was seen initially on EP with CAP impairment occurring a few minutes later. Acute CO injection also suppressed the CAP significantly, but the effect was far smaller, occurred later in time, and lasted longer than the effect of KCN. The effect of CO on EP was equivocal. There was a good correspondence between blood cyanide levels and impairment of cochlear function; carboxyhemoglobin (HbCO) levels were elevated during the period when cochlear function was impaired, but recovery of cochlear function preceded the return of normal oxyhemoglobin. Both KCN and CO had somewhat preferential effects on high-frequency tones. Repeated cyanide administration caused a persistent CAP threshold elevation despite the rapid recovery of EP and CAP observed following acute KCN administration. The data suggest that acute KCN administration has a prominent disruptive effect at the stria vascularis presumably by disrupting the electron transport chain in this metabolically active structure. The principal target for acute CO ototoxicity in the cochlea is probably not the stria vascularis.

Action Potentials↗
PubMedDate not supplied

Distribution of manganese in development.

Elimination of manganese is closely related to uptake in the normal adult and is believed to play a critical role in maintaining manganese homeostasis in the face of changing manganese intake. Data from immature rats, mice and cats have suggested that elimination of manganese undergoes a period of maturation with adult patterns of excretion developing at about the time of weaning. In addition, the uptake of manganese from the intestine appears to be more efficient in young animals than in adults. These two sets of findings raise the possibility that exposure to elevated manganese levels during the perinatal period might yield excessive concentrations of this metal in the developing organism. Such an outcome might lead to manganese accumulations in organ systems where subsequent mobilization might be difficult and might produce permanent toxic injury. This review evaluates the patterns of manganese uptake and distribution following prenatal and pre-weaning exposure using a variety of model systems. The data demonstrate that manganese does cross the placenta and enter fetal tissue although the extent of material crossing the placenta appears to be limited. The issue of neonatal manganese elimination following tracer and toxic exposure levels to manganese is addressed. The data show that that the neonatal rodent is significantly more effective in eliminating manganese than previously believed based upon tracer studies. Finally, data are presented on regional brain manganese distribution. These data highlight the lack of agreement on whether manganese is concentrated in specific brain areas.

Age Factors↗