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酮色林对健康志愿者脑血流量和脑血管二氧化碳反应性的影响。

The effect of ketanserin on cerebral blood flow and cerebrovascular CO2 reactivity in healthy volunteers.

作者信息

Olsen K S, Videbaek C, Schmidt J F, Paulson O B

机构信息

Department of Anaesthesia, Glostrup Hospital, Denmark.

出版信息

Acta Neurochir (Wien). 1992;119(1-4):7-11. doi: 10.1007/BF01541774.

DOI:10.1007/BF01541774
PMID:1481756
Abstract

The effect of the anti-hypertensive agent ketanserin on the cerebral blood flow (CBF) and the cerebrovascular CO2 reactivity was examined in 10 healthy volunteers. Ketanserin was administered as an intravenous bolus of 10 mg followed by an infusion of 6 mg/h. Before administration CBF was measured by single photon emission computerized tomography (SPECT) of inhaled 133Xenon. Then arterial CO2 tension was subsequently decreased by voluntary hyperventilation and increased by breathing an air/CO2 mixture. The relative changes in CBF induced by the changes in arterial CO2 tension were estimated by the cerebral arterio-venous oxygen content difference method. One hour following the start of ketanserin infusion the SPECT measurement and CO2 manipulations were repeated. The CO2 reactivity (expressed as the slope of the regression line of the linear relation between CBF and PaCO2), was unchanged, i.e. 3.2%/0.1 kPa before ketanserin and 4.1%/0.1 kPa during ketanserin, respectively. Using regression lines from a semi-logarithmic plot the CO2 reactivity was also unchanged 3.4%/0.1 kPa and 3.5%/0.1 kPa, respectively. Ketanserin did not change CBF. The cerebral oxygen metabolism (CMRO2) was decreased 19% one hour after the start of infusion of ketanserin. In conclusion administration of ketanserin in a clinically relevant dose to healthy volunteers does not change the regional CBF not the cerebrovascular CO2 reactivity, but a decrease in CMRO2 was observed. However further studies are needed to clarify whether ketanserin in fact has a depressing effect on CMRO2 or whether the different results are caused by methodological errors or stochastic variation.

摘要

在10名健康志愿者中研究了抗高血压药物酮色林对脑血流量(CBF)和脑血管二氧化碳反应性的影响。酮色林以10mg静脉推注给药,随后以6mg/h的速度输注。给药前,通过吸入133氙的单光子发射计算机断层扫描(SPECT)测量CBF。然后通过自主过度通气使动脉二氧化碳张力降低,通过呼吸空气/二氧化碳混合物使其升高。通过脑动静脉氧含量差法估计动脉二氧化碳张力变化引起的CBF相对变化。酮色林输注开始1小时后,重复SPECT测量和二氧化碳操作。二氧化碳反应性(表示为CBF与动脉血二氧化碳分压(PaCO2)线性关系的回归线斜率)不变,即酮色林给药前为3.2%/0.1kPa,给药期间为4.1%/0.1kPa。使用半对数图的回归线,二氧化碳反应性也分别不变,为3.4%/0.1kPa和3.5%/0.1kPa。酮色林未改变CBF。酮色林输注开始1小时后,脑氧代谢(CMRO2)降低了19%。总之,向健康志愿者给予临床相关剂量的酮色林不会改变局部CBF和脑血管二氧化碳反应性,但观察到CMRO2降低。然而,需要进一步研究以阐明酮色林实际上是否对CMRO2有抑制作用,或者不同结果是否由方法学错误或随机变异引起。

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