Cerebral blood flow autoregulation during intracranial hypertension in hypoxic lambs.
Cerebral blood flow autoregulation during intracranial hypertension in hypoxic lambs.
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缺氧羔羊颅内高压期间脑血流的自动调节。
DOI：
10.1152/ajpheart.1987.253.6.h1342
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Traystman,RJ
中科院分区：
文献类型：
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作者：
Borel,CO;Backofen,JE;Koehler,RC;JonesJr,MD;Traystman,RJ
我们测试了这样的假设：当戊巴比妥麻醉的羔羊（3至9天大）颅内压（ICP）升高时，缺氧会干扰脑血流（CBF）自动调节。通过脑室输注人工脑脊液，8只常氧羔羊的脑灌注压（CPP）从73毫米汞柱逐步降低至23毫米汞柱，将其他8只缺氧羔羊的脑灌注压从65毫米汞柱逐步降低至31毫米汞柱。在含氧量正常的羔羊中，通过微球测量的 CBF 在此 CPP 范围内没有显着变化。动物缺氧[动脉氧分压 (PaO2) 为 28 托； 47% 动脉氧饱和度]，基线 CBF 是常氧羔羊的两倍。 CBF 不变，CPP 降至 31 mmHg。由于随着 ICP 进一步升高而发生升压反应，因此未达到较低的 CPP 水平。 ICP 升高时，未检测到流向皮质动脉分水岭区域或更多尾部区域（如小脑、脑干或丘脑）的血流出现区域性减少。两组的脑氧摄取量相似，并且当 CPP 降低时，脑氧摄取量并未减少。这些结果表明，当 ICP 升高时，含氧量正常的羔羊具有相当大的有效自动调节 CBF 的能力。此外，当 ICP 在产后第一周升高时，对接近产前正常情况的缺氧水平做出的脑血管舒张不会消除 CBF 的自动调节。
We tested the hypothesis that hypoxic hypoxia interferes with cerebral blood flow (CBF) autoregulation when intracranial pressure (ICP) is elevated in pentobarbital-anesthetized lambs (3 to 9 days old). Cerebral perfusion pressure (CPP) was lowered stepwise from 73 to 23 mmHg in eight normoxic lambs and from 65 to 31 mmHg in eight other hypoxic lambs by ventricular infusion of artificial cerebrospinal fluid. In normoxic lambs, CBF measured by microspheres was not significantly changed over this range of CPP. In animals made hypoxic [arterial O2 tension (PaO2) of 28 Torr; 47% arterial O2 saturation], base-line CBF was twice that of normoxic lambs. CBF was unchanged as CPP was reduced to 31 mmHg. Lower levels of CPP were not attained because a pressor response occurred with further elevations of ICP. No regional decrements in blood flow to cortical arterial watershed areas or to more caudal regions, such as cerebellum, brain stem, or thalamus, were detected with elevated ICP. Cerebral O2 uptake was similar in both groups and did not decrease when CPP was reduced. These results demonstrate that normoxic lambs have a considerable capacity for effective autoregulation of CBF when ICP is elevated. Moreover, cerebral vasodilation in response to a level of hypoxia approximating that normally seen prenatally does not abolish CBF autoregulation when ICP is elevated during the first postnatal week.