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犬正常碳酸血症和低碳酸血症期间脑血流量的自动调节

Autoregulation of cerebral blood flow during normocapnia and hypocapnia in dogs.

作者信息

Artru A A, Katz R A, Colley P S

机构信息

Department of Anesthesiology, University of Washington School of Medicine, Seattle 98195.

出版信息

Anesthesiology. 1989 Feb;70(2):288-92. doi: 10.1097/00000542-198902000-00018.

DOI:10.1097/00000542-198902000-00018
PMID:2492410
Abstract

The effect of hypocapnia on autoregulation of cerebral blood flow (CBF) and the lower limit of autoregulation (LLA) was determined in dogs anesthetized with nitrous oxide (66%) and halothane (0.2%, end-expired concentration). CBF and cerebral vascular resistance (CVR) were determined during both normocapnia and hypocapnia (PaCO2 21-22 mmHg) at control cerebral perfusion pressure (CPP) and after reducing CPP (by hemorrhage) to 80%, 60%, 50%, and 40% of control. At control CPP hypocapnia decreased CBF from 75 +/- 5 to 48 +/- 3 ml.100 g-1.min-1 (mean +/- SEM, P less than 0.05). During both normocapnia and hypocapnia CVR decreased and CBF did not change as CPP was reduced to 60% of control. When CPP was reduced to 50% or 40% of control, CVR remained decreased and CBF fell sharply. The LLA during hypocapnia, 61 +/- 2% of control CPP, was not different than that during normocapnia, 59 +/- 3% of control CPP. Below the LLA the CBF-CPP slopes differed from zero but did not differ between hypocapnia and normocapnia. Hypocapnia does not produce a substantial shift of the LLA, and over the range of CPP values studied here, autoregulatory cerebral vasodilation only partially abolishes hypocapnia-induced cerebral vasoconstriction. The results suggest that when cerebral autoregulation is intact and in the absence of cerebrovascular disease, hypocapnia does not reduce global CBF to a level that is likely to produce ischemia and remains a useful therapeutic treatment so long as CPP remains above the LLA.

摘要

在使用氧化亚氮(66%)和氟烷(0.2%,呼气末浓度)麻醉的犬中,测定了低碳酸血症对脑血流量(CBF)自动调节及自动调节下限(LLA)的影响。在正常碳酸血症和低碳酸血症(动脉血二氧化碳分压[PaCO₂]为21 - 22 mmHg)时,于对照脑灌注压(CPP)下以及将CPP(通过放血)降低至对照值的80%、60%、50%和40%后,测定CBF和脑血管阻力(CVR)。在对照CPP时,低碳酸血症使CBF从75±5降至48±3 ml·100 g⁻¹·min⁻¹(均值±标准误,P<0.05)。在正常碳酸血症和低碳酸血症期间,当CPP降至对照值的60%时,CVR降低而CBF未改变。当CPP降至对照值的50%或40%时,CVR持续降低且CBF急剧下降。低碳酸血症时的LLA为对照CPP的61±2%,与正常碳酸血症时对照CPP的59±3%无差异。低于LLA时,CBF-CPP斜率不同于零,但低碳酸血症和正常碳酸血症之间无差异。低碳酸血症不会使LLA发生实质性偏移,并且在此处研究的CPP值范围内,自动调节性脑血管舒张仅部分消除低碳酸血症诱导的脑血管收缩。结果表明,当脑自动调节功能完好且无脑血管疾病时,低碳酸血症不会将整体CBF降低至可能导致缺血的水平,并且只要CPP保持在LLA之上,低碳酸血症仍是一种有用的治疗方法。

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