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  • 1
    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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  • 2
    ISSN: 1432-0533
    Keywords: Carbon monoxide encephalopathy ; Selective topography of CNS lesion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experimental studies were performed to elucidate the significance of various physiological factors contributing to the pathogenesis of carbon monoxide (CO) encephalopathy, such as systemic blood pressure (BP), common carotid artery blood flow (CF), local blood flow (LBF) of the brain and blood gas including pH, and to analyse the morphological character of the cerebral white matter lesions in the acute phases with light and electron microscopes; 14 adult cats were exposed to 0.3% CO/air gas under respiratory control for 1 h and 17 min to 2 h and 50 min and killed 1.5 h to 3 weeks later. During the 1st h the CF and LBF increased along with the concentration of CO haemoglobin and the BP showed slight decrease in all the CO-exposed cats. After the 1st h, the BP dropped progressively as well as the CF and LBF. The LBF of the cortex and white matter changed in parallel, but often that of the latter approximated or exceeded that of the former in the cerebrum. During CO exposure, acidosis occurred in all the cats and haemoconcentration resulted in almost all of the cats. In all the cats except one which showed the least BP drop, lesions occurred selectively in the cerebral white matter and in six or seven cats focal coagulation necrosis or ischaemic changes occurred in the nerve cells in the bilateral pallidum, substantia nigra, and hippocampus similar to human patients. The cerebral white matter lesions were suggestive of those caused by circulatory disturbance. The severity of the white matter damage showed a good positive correlation with the intensity of the BP drop, but not with other factors, such as the duration of CO-exposure, CO-haemoglobin level, acidosis, or haemoconcentration. On the basis of such physiological and morphological findings, we have found the following to be essential for the selective damage of the cerebral white matter rather than the cerebral cortex or white matter of other regions of the CNS: (1) the coexistence of the initial phase of increase in and the succeeding decrease in the cerebral blood flow and (2) the anatomical finding that the cerebral white matter is supplied by its own long nourishing arteries with small amounts of capillary beds and a thinner media compared with that of the subarach-noidal artery.
    Type of Medium: Electronic Resource
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