是不是省略了一些东西？

In the intact animal, CBF is increased in response to Pco2 by a combination of vasodilatation of cerebral blood vessels and an increase in blood pressure (see later). Changes in Pco2 lead to a complex series of events that bring about vasodilation of cerebral blood vessels.2In adults, the effect is initiated by changes in the extracellular pH in the region of the arterioles, which alters intracellular calcium levels both directly and indirectly via nitric oxide production and the formation of cyclic guanosine monophosphate. With prolonged hypocapnia, and to a lesser extent hypercapnia, changes in CBF return towards baseline after a few hours, an effect thought to result from changes in cerebrospinal fluid pH correcting the extracellular acidosis. Sensitivity of the cerebral circulation to carbon dioxide may be lost in a variety of pathological circumstances such as cerebral tumour, infarction or trauma. There is commonly a fixed vasodilatation in damaged areas of brain, which if widespread may cause dangerous increases in intracranial pressure (ICP).

在完整动物个体中，通过脑血管舒张和血压上升的复合效应，Pco₂ 增加导致CBF上升（见后）。Pco₂改变引发一系列复杂反应从而舒张脑血管。²成人研究中，这种效应源自微动脉区域的细胞外pH 变化，通过一氧化氮的产生和环鸟苷酸（cyclic guanosine monophosphate，cGMP）的合成直接和间接地改变了细胞内钙水平。而长期低碳酸血症及相对较轻的高碳酸血症中，CBF的变化在数小时后恢复至基线水平，此系脑脊液pH改变代偿了细胞外酸中毒效应。在脑部肿瘤、脑梗死或脑外伤等病理情况下，脑循环对二氧化碳的敏感度可能丧失。通常在大脑受伤区域会有固定的血管舒张，若弥散性血管舒张可引起颅内压（intracranial pressure，ICP）增加。

1.CBF is increased in response to Pco2 Pco2 导致CBF上升？明显不对啊，是Pco2 “增加”导致CBF上升吧？是不是要把“增加”补上去啊

2.With prolonged hypocapnia，如果前面确实讲的是Pco2 增加，那这里突然讲长期低碳酸血症，是不是前面要加个“而”