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  • 1
    ISSN: 1432-0533
    Keywords: Cyanide encephalopathy ; Selective white matter lesion ; Cerebral local blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A study was performed to elucidate the significance of various physiological factors contributing to the pathogenesis of experimental cyanide encephalopathy, such as the systemic arterial blood pressure, venous pressure, common carotid blood flow and local blood flow of the cerebral grey and white matters, and blood gas including pH. The histology and topography of the brain damage was also analysed. Twenty-one cats were divided into four groups. The animals in groups 1, 2 and 3 were subjected to continuous infusion of 0.2% sodium cyanide solution and to the ensuing hypotension below 100 mm Hg by administering a ganglion-blocking drug and by respiratory arrest. Severe damage developed in the deep cerebral white matter, corpus callosum, pallidum and substantia nigra, but the damage of the cerebral cortex and hippocampus was not remarkable. The animals in group 4 that were subjected to cyanide infusion without significant hypotension (above 100 mm Hg), but to the same degree of acidosis as that of the the other groups, had similar morphological changes, but to a lesser degree. On the basis of our physiological and morphological findings, we speculated that the pathophysiological factors of tissue hypoxia and subsequent hypotension operated in cyanide leucoencephalopathy. The topographic selectivity seemed to be related to the characteristic cerebral vascular system, and the severity of the white matter lesions was related to the intensity of both hypoxia and hypotension during cyanide infusion, but not to the extent of acidosis, total dose of cyanide or duration of its infusion per se.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0533
    Keywords: Carbon monoxide encephalopathy ; Nitrogen hypoxia ; Selective white matter lesion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Since in a previous study hypoxia and subsequent hypotension were considered to be essential for the pathogenesis of carbon monoxide encephalopathy (CO-encephalopathy), experiments were conducted to see whether a combination of nitrogen hypoxia and subsequent systemic hypotension of similar degree and duration as in the previous experimental CO poisoning could induce the same lesion in the CNS of cats. The partial pressure of blood oxygen was reduced to less than 26 mm Hg by increasing the concentration of nitrogen in N2/O2 gas to be inhaled in 1.5 h and then the aortic blood pressure (BP) was reduced to 60–80 mm Hg by blood depletion and ganglion-blockage for 1 h. In 11 of the 15 cats, lesions were produced in the CNS which were similar by light and electron microscopy to those in CO-encephalopathy. In control groups which were treated by hypoxemia only, hypotension only or a combination of CO2-gas inhalation and hypotension without hypoxemia, such lesions were not found in the cerebral white matter. Considering the pathogenesis of lesions in the cerebral white matter in both nitrogen hypoxia and CO-poisoning, two factors, i.e., hypoxemia and subsequent systemic hypotension, are common and essential. Further, the enormous vasodilation in the cerebral white matter induced by hypoxemia and subsequent drop in BP seem to cause a more severe circulatory disturbance in the cerebral white matter than in the cortex.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Grinker's myelinopathy ; Carbon monoxide intoxication
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The change of Grinker's myelinopathy in carbon monoxide (CO) poisoning occurs not only in patients with the clinically diphasic type of CO-poisoning but is also found around the destructive lesions in patients with the acute form of CO-poisoning. The distribution of this myelinopathy is similar to that of the acute form of CO-poisoning. The cerebral change of experimental acute CO-encephalopathy is a sort of hypoxic-ischemic encephalopathy. Based on these findings an experiment was conducted to analyze the pathogenesis of Grinker's myelinopathy as follows: 43 cats were separated into four groups. Group A was subjected at first to inhalation of 0.3% CO/Air gas lasting for 2 h and then 2 or 3 days later to hypotension ranging from 60 to 90mm Hg for 1 h under the state of slight hypoxia (PaO2: 50–80 mm Hg). Group B was also exposed to CO-gas and hypotension similarly to Group A, but hypoxia was not imposed during hypotension. Groups C and D were subjected only to hypotension and to CO-gas, respectively. Myelin pallor was found selectively in the cerebral white matter of all cats of Group A and 18 of the 23 cats of Group B, and the subcortical U-fibers and perivascular myelin were spared. This was similar to Grinker's myelinopathy. The myelin pallor was investigated by light and electron microscopy and considered to be due to edema and separation of the myelin sheath and axon. In Groups C and D such a change was either absent or only slight. The conditions necessary for the onset of Grinker's myelinopathy were discussed, and it was proposed that the patients recovering from acute CO-poisoning should be kept in hospital for several weeks so that their blood pressure and blood gas could be monitored continuously.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0533
    Keywords: Selective lesion of the globus pallidus ; Acute carbon monoxide poisoning ; Cerebral local blood flow ; Hydrogen clearance method
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty-eight mature cats were exposed to 0.3% carbon monoxide (CO) gas for 90–193 min using artificial ventilation. The systemic blood pressure (BP), venous pressure (VP), blood flow of the left common carotid artery (CF), and blood gas were monitored. The local blood flow (LBF) of the globus pallidus, putamen, or claustrum was measured by the hydrogen clearance method. Pallidal lesions were found histologically in 14 cats. The period of CO inhalation and the time thereafter were divided into the following four stages in the animals with pallidal lesions. Stage 1: Initial phase with rapid increase in the CF and LBF, and rapid decrease in the BP. Stage 2: Middle phase with slow decrease in the BP, CF, and LBF. Stage 3: Terminal phase with rapid decrease in the BP, CF, and LBF. Stage 4: Recovery phase. The changes in stage 3 were not so prominent in the animals without pallidal lesions. The LBF of the globus pallidus of the animals with lesions decreased to 67.3±20.7% of the initial value at the terminal stage of CO inhalation, while it was 188±46.7% in those without lesions. The difference was statistically significant (P〈0.01). The LBF of the putamen or claustrum in the animals with lesions in the globus pallidus was 140±24.6% at this stage, and it was significantly higher than that of the globus pallidus (P〈0.01). Other factors, such as CO inhalation time, degree of acidosis, and terminal CO-Hb concentration, did not correlate with the occurrence of the pallidal lesion.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 434 (1984), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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