30-32006-1982

CONCENTRATION-RELATED EFFECTS OF HEXANE ON EVOKED RESPONESES FROM BRAIN AND PERIPHERAL NERVE

30-32006-1982 发布历史

Introduction n-Hexane produces@ by way of its metabolite 2@S-hexanedione@ peripheral and central axonopathies with secondary myelinopathies [ 1 ]. Extensive ncuromorphologic investigations have described the anatomic changes associated with hexane exposures [2. 3]@ but there have been few studies of the functional@ electrophysiologic@ consequences of hexacarbon neuropathy. Of these studies@ most have focused on the peripheral nervous system@ even though the central nervous system (CNS) is known to undergo morphologic changes |4]. Ciancetti el al. |5J@ for example@ observed electromyographic and nerve conduction velocity changes in a large number of exposed shoe-industry workers@ and several investigators have described similar changes in animals with experimentally induced hexacarbon polyneuropathy [6@ 7]. In an earlier study (^ we showed@ by measuring the brainstem auditory-evoked response (BAER) and action potential (AP) of the ventral caudal nerve of the rat's tail@ that hexane causes a nerve conduction delay in auditory brainstem tracts as well as in peripheral nerve. This finding@ and a report that n-hexane causes pathology in the hypothalamus and optic tracts of cats [4]@ suggest that manifestations of hexane poisoning would be evident in evoked responses obtained from several sensory systems. Indeed@ Seppatainen et al. [9] found@ that n-hexane Induced changes in the visual-evoked response (VER) of exposed workers. In order to characterize further the electrophysiologic concomitants of hexacarbon neuropathy@ biopotentials?voked in peripheral nerve and brain by somatosensory@ auditory@ and visual stimulation were studied in rats exposed by inhalation to three concentrations of hexane.

30-32006-1982由API - American Petroleum Institute 发布于 1982-01-01，并于 2010-08-05 实施。

30-32006-1982的历代版本如下：

• 1982年01月01日 30-32006-1982

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标准号

30-32006-1982

发布日期

1982年01月01日

实施日期

2010年08月05日

废止日期

无

中国标准分类号

/

国际标准分类号

/

发布单位

API - American Petroleum Institute

引用标准

14

适用范围

Introduction n-Hexane produces@ by way of its metabolite 2@S-hexanedione@ peripheral and central axonopathies with secondary myelinopathies [ 1 ]. Extensive ncuromorphologic investigations have described the anatomic changes associated with hexane exposures [2. 3]@ but there have been few studies of the functional@ electrophysiologic@ consequences of hexacarbon neuropathy. Of these studies@ most have focused on the peripheral nervous system@ even though the central nervous system (CNS) is known to undergo morphologic changes |4]. Ciancetti el al. |5J@ for example@ observed electromyographic and nerve conduction velocity changes in a large number of exposed shoe-industry workers@ and several investigators have described similar changes in animals with experimentally induced hexacarbon polyneuropathy [6@ 7]. In an earlier study (^ we showed@ by measuring the brainstem auditory-evoked response (BAER) and action potential (AP) of the ventral caudal nerve of the rat's tail@ that hexane causes a nerve conduction delay in auditory brainstem tracts as well as in peripheral nerve. This finding@ and a report that n-hexane causes pathology in the hypothalamus and optic tracts of cats [4]@ suggest that manifestations of hexane poisoning would be evident in evoked responses obtained from several sensory systems. Indeed@ Seppatainen et al. [9] found@ that n-hexane Induced changes in the visual-evoked response (VER) of exposed workers. In order to characterize further the electrophysiologic concomitants of hexacarbon neuropathy@ biopotentials?voked in peripheral nerve and brain by somatosensory@ auditory@ and visual stimulation were studied in rats exposed by inhalation to three concentrations of hexane.

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