一氧化氮合酶抑制后心率和动脉压变异性的频谱分析。

D Mikhov, P Markova, R Girchev
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引用次数: 0

摘要

实验是在有意识的雄性Wistar大鼠身上进行的。在40分钟的控制期内,通过连接到mp100ws BIOPAC工作站的Statham GOULD P23 ID压力传感器进行模拟-数字转换,记录股动脉压力。通过股静脉导管在生理盐水中注射n -omega-硝基- l -精氨酸甲酯(L-NAME) 100微升,10 mg/kg b.w抑制一氧化氮合酶。20分钟后开始动脉压记录并持续40分钟。采用AcqKnowledge 2.0软件的峰值检测器和速率检测器,测量收缩压、舒张压和平均动脉压的逐脉值以及脉间期。使用我们实验室在图形化编程环境Lab VIEW 3.1.1中开发的虚拟仪器对行数据进行处理。L-NAME使收缩压、舒张压和平均动脉压分别升高16.6%、25%和35%。心率谱PMF/PHF比值降低,表明迷走神经对心脏的影响增强。一氧化氮合酶抑制使收缩压变异性的低频成分增加了39.5%。一氧化氮是动脉血压快速波动的生理调节剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Spectral analysis of heart rate and arterial pressure variability after nitric oxide synthase inhibition.

The experiments were performed on male, conscious Wistar rats. Femoral arterial pressure was registered by Statham GOULD P23 ID pressure transducer connected to MP 100WS BIOPAC work station after analog to digital conversion during 40 minutes long control period. Nitric oxide synthase inhibition was performed by injection of 100 microliters, 10 mg/kg b.w. N-omega-nitro-L-arginine methyl ester (L-NAME) in saline through femoral vein catheter. Twenty minutes later arterial pressure registration was started and was continued for 40 minutes. The pulse-by-pulse values of systolic, diastolic and mean arterial pressure as well as the pulse intervals were measured by peak and rate detectors of the AcqKnowledge 2.0 software. Row data were processed using a virtual instrument developed in our laboratory in the graphical programming environment Lab VIEW 3.1.1. L-NAME increased systolic, diastolic and mean arterial pressure by 16.6%, 25% and 35%, respectively. The PMF/PHF ratio in heart rate spectrum decreased, indicating an increased vagal effect on the heart. Nitric oxide synthase inhibition increased the low-frequency component of systolic arterial blood pressure variability by 39.5%. Nitric oxide is a physiological regulator of rapid fluctuations of arterial blood pressure.

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