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一氧化氮在介导新生仔猪脑血管控制中的作用有限。

Limited role for nitric oxide in mediating cerebrovascular control of newborn piglets.

作者信息

Patel J, Pryds O, Roberts I, Harris D, Edwards A D

机构信息

Royal Postgraduate Medical School, Hammersmith Hospital, London.

出版信息

Arch Dis Child Fetal Neonatal Ed. 1996 Sep;75(2):F82-6. doi: 10.1136/fn.75.2.f82.

Abstract

AIMS

To investigate the effects of the nitric oxide (NO) synthase inhibitor L-nitro-arginine methyl ester (L-NAME) on cerebral blood flow, and its response to alterations in arterial carbon dioxide tension (CBF-CO2 reactivity).

METHODS

Cerebral blood flow was measured six times at varying arterial carbon dioxide tension (PaCO2) using the intravenous 133Xenon clearance technique in eight mechanically ventilated piglets of less than 24 hours postnatal age. After the third measurement L-NAME was administered as a bolus (20 mg/kg) and subsequently infused (10 mg/kg/hour).

RESULTS

PaCO2 ranged between 2.7-8.9 kPa. Cerebral blood flow decreased by 14.0% (95% confidence interval 1.9-27.4) after L-NAME. CBF-CO2 reactivity was 18.4% per kPa (95% CI 14.1-22.2) before L-NAME and 15.2%/kPa (95% CI 11.1-19.3) afterwards; the difference between the CBF-CO2 reactivities was 3.2%/kPa (95% CI -0.4-6.8): these were not significantly different.

CONCLUSIONS

Inhibition of nitric oxide synthesis reduces cerebral blood flow no more than a 0.5-1.0 kPa fall in PaCO2. Nitric oxide is not an important mediator of CBF-CO2 reactivity.

摘要

目的

研究一氧化氮(NO)合酶抑制剂L-硝基-精氨酸甲酯(L-NAME)对脑血流量的影响及其对动脉二氧化碳分压变化的反应(脑血流量-二氧化碳反应性)。

方法

采用静脉注射133氙清除技术,在8只出生后不到24小时的机械通气仔猪中,于不同的动脉二氧化碳分压(PaCO2)下测量6次脑血流量。在第三次测量后,静脉推注L-NAME(20mg/kg),随后持续输注(10mg/kg/小时)。

结果

PaCO2范围为2.7 - 8.9kPa。注射L-NAME后脑血流量下降了14.0%(95%置信区间1.9 - 27.4)。L-NAME给药前脑血流量-二氧化碳反应性为每kPa 18.4%(95%CI 14.1 - 22.2),给药后为15.2%/kPa(95%CI 11.1 - 19.3);脑血流量-二氧化碳反应性之间的差异为3.2%/kPa(95%CI -0.4 - 6.8):这些差异无统计学意义。

结论

抑制一氧化氮合成使脑血流量减少的幅度不超过PaCO2下降0.5 - 1.0kPa。一氧化氮不是脑血流量-二氧化碳反应性的重要调节因子。

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Role of NO in goat basal cerebral circulation and after vasodilatation to hypercapnia or brief ischemias.
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