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Acute and chronic alterations in blood pressure variability following experimental subarachnoid haemorrhage.

机译:实验性蛛网膜下腔出血后血压变异性的急性和慢性变化。

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This study examined the role of the renin-angiotensin and vasopressin systems on systolic blood pressure (SBP) variability following subarachnoid haemorrhage (SAH) in conscious rats. Animals received no treatment, the angiotensin II AT1 receptor antagonist, losartan, or the vascular vasopressin receptor antagonist, AVPX. SAH resulted in a transient sympathetic activation as estimated from the increase in the mid-frequency oscillations of SBP (3.2 +/- 0.8 mm Hg2, 3 hours after the injury vs. 1.3 +/- 0.3 mm Hg2 in control conditions, p < 0.01). On the second and fourth day following SAH, a marked elevation in the low-frequency component of SBP was observed (7.1 +/- 1.0 mm Hg2 on day 2 vs. 2.6 +/- 0.3 mm Hg2 in control conditions, p < 0.001 and 6.3 +/- 1.1 mm Hg2 on day 4 vs. 2.6 +/- 0.3 mm Hg2 in control conditions, p < 0.01). Pre-treatment with losartan prevented the acute rise in the mid-frequency oscillations in SBP and partially reduced the low-frequency component observed at 2 and 4 days. Administration of AVPX on the second and fourth day following SAH normalised the elevated low-frequency oscillations in SBP. This study indicates that the modifications in SBP variability observed in the early and delayed stage after subarachnoid haemorrhage involve angiotensin II. Vasopressin seems to be implicated in the delayed development of low-frequency fluctuations of SBP.
机译:这项研究检查了清醒大鼠蛛网膜下腔出血(SAH)后肾素-血管紧张素和加压素系统对收缩压(SBP)变异性的作用。动物未接受血管紧张素II AT1受体拮抗剂氯沙坦或血管加压素受体拮抗剂AVPX的治疗。根据损伤后3小时SBP的中频振荡增加(3.2 +/- 0.8 mm Hg2,与对照条件下的1.3 +/- 0.3 mm Hg2相比),SAH导致短暂的交感神经激活,p <0.01 )。在SAH后的第二天和第四天,观察到SBP的低频成分明显升高(第2天为7.1 +/- 1.0 mm Hg2,而在对照条件下为2.6 +/- 0.3 mm Hg2,p <0.001和第4天为6.3 +/- 1.1毫米汞柱,而对照条件下为2.6 +/- 0.3毫米汞柱,p <0.01)。氯沙坦预处理可防止SBP中频振荡急剧上升,并部分减少2天和4天观察到的低频分量。 SAH后第二天和第四天给予AVPX可使SBP中升高的低频振荡正常化。这项研究表明,在蛛网膜下腔出血后早期和延迟阶段观察到的SBP变异性改变涉及血管紧张素II。加压素似乎与SBP低频波动的延迟发展有关。

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