Lassen N A
Department of Clinical Physiology and Nuclear Medicine, Bispebjerg Hospital, Copenhagen, Denmark.
Int J Sports Med. 1992 Oct;13 Suppl 1:S47-8. doi: 10.1055/s-2007-1024591.
CBF increases with acute hypoxia despite the opposing vasoconstrictor effects of the drop in pCO2 caused by hyperventilation. Maintaining normocapnia by adding CO2 the hypoxic CBF responsiveness about doubles. As we have shown recently by this test, the hypoxic CBF response is not blunted but rather somewhat sharpened over five days at almost 4000 meters of altitude. This, along with other evidence, shows that CBF does not in itself adapt to chronic hypoxia. Nevertheless, a decrease in CBF is seen over days at constant altitude primarily due to increase in the hematocrit. The cerebral vasodilatation cannot explain the usual (mild) form of AMS. But it may well be involved in the pathogenesis of the rare but severe cerebral form of AMS, as prolonged increased capillary pressure in vasodilated areas could lead to vasogenic cerebral edema.
尽管过度通气导致的二氧化碳分压下降具有相反的血管收缩作用,但急性缺氧时脑血流量(CBF)仍会增加。通过补充二氧化碳维持正常碳酸血症,缺氧时的CBF反应性会增加约一倍。正如我们最近通过该测试所表明的,在近4000米的海拔高度下,缺氧CBF反应在五天内并未减弱,反而有所增强。这与其他证据一起表明,CBF本身并不会适应慢性缺氧。然而,在恒定海拔高度下,数天内CBF会下降,主要是由于红细胞压积增加。脑血管扩张无法解释常见的(轻度)急性高山病(AMS)形式。但它很可能参与了罕见但严重的脑部AMS的发病机制,因为血管扩张区域毛细血管压力的长期升高可能导致血管源性脑水肿。