计算机数据采集和评估揭示了大鼠肠系膜和股血流的差异调节

A. Heinemann, C. H. Wachter, P. Holzer
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引用次数: 12

摘要

建立了血流动力学数据的计算机采集和评估系统。用超声传递时移技术测定了麻醉大鼠肠系膜上动脉和股动脉血流。动脉血压和心率信号通过模数转换器输入个人计算机。在线计算平均动脉血压、心率和血管导度(CV)。为了对数据进行后续分析,编写了算法来过滤数据,并确定每个参数的平均值和峰值。苯肾上腺素(3 ~ 300 nmol kg−1)、血管紧张素II (0.1 ~ 3.0 nmol kg−1)和精氨酸加压素(0.03 ~ 1.0 nmol kg−1)诱导的全身高血压伴肠系膜动脉收缩。相反,股动脉对苯肾上腺素的反应是收缩,对血管紧张素II的反应是扩张,对精氨酸加压素的反应是扩张后收缩。内皮素-1 (0.03-3.0 nmol kg -1)对血流动力学的影响通常是双相的,初始低血压与扩张有关,迟发性高血压伴随着肠系膜和股动脉床的收缩。特布他林(3-1.0 nmol kg−1)和降钙素基因相关肽(0.03-1 nmol kg−1)引起全身低血压,并伴有肠系膜和股动脉血管扩张。替米沙坦(1mg kg−1),一种血管紧张素AT1受体拮抗剂,扩张肠系膜动脉,但对股VC无影响。相比之下,α1-肾上腺素受体拮抗剂吡唑嗪(0.1 mg kg−1)扩张股动脉,但不改变肠系膜VC。同样,β-肾上腺素能受体拮抗剂心得安(1mg kg−1)对肠系膜VC无影响,但收缩股动脉床。这些数据表明,外源性给药药物对尿素麻醉大鼠肠系膜和股动脉床的血流动力学影响可能存在很大差异。此外,这两种动脉床的血管张力是由不同的血管收缩系统维持的。股动脉主要受肾上腺素能控制,肾素-血管紧张素轴主要位于肠系膜动脉床。此外,本研究还表明,计算机分析可以快速准确地估计血流动力学药物效应,并且优于“手工”评估所研究的血管床功能直径的峰值变化。
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Differential regulation of mesenteric and femoral blood flow in the rat as revealed by computerized data acquisition and evaluation

  • A set-up for computerized acquisition and evaluation of haemodynamic data was constructed. Blood flow (BF) in the superior mesenteric and femoral artery of urethane-anaesthetized rats was measured with the ultrasonic transit time shift technique. The signals for arteial blood pressure and BF were fed into a personal computer via an analogue-digital converter. Mean arterial blood pressure, heart rate and vascular conductance (CV) were calculated on-line. For subsequent analysis of the data, algorithms were programmed to filter the data, and to determine average and peak values for each parameter.

  • Systemic hypertension induced by phenylephrine (3–300 nmol kg−1), angiotensin II (0.1–3.0 nmol kg−1) and arginine vasopressin (0.03–1.0 nmol kg−1) was accompanied by constriction of the mesenteric artery. In contrast, the femoral artery responded to phenylephrine with constriction, to angiotensin II with dilatation and to arginine vasopressin with dilation followed by constriction. The haemodynamic effects of endothelin-1 (0.03–3.0 nmol kg−1) were generally biphasic, the initial hypotension being associated with dilatation, and the delayed hypertension being accompanied by constriction of both the mesenteric and femoral arterial bed.

  • Terbutaline (3–1.0 nmol kg−1) and calcitonin gene-related peptide (0.03–1 nmol kg−1) caused systemic hypotension along with mesenteric and femoral vasodilatation.

  • Telmisartan (1 mg kg−1), an angiotensin AT1 receptor antagonist, dilated the mesenteric artery, but had no effect on femoral VC. In contrast, the α1-adrenoceptor antagonist prazosin (0.1 mg kg−1), dilated the femoral artery without altering mesenteric VC. Similarly, the β-adrenoceptor antagonist propranolol (1 mg kg−1) had no effect on mesenteric VC, but constricted the femoral arterial bed.

  • These data demonstrate that the haemodynamic effects of exogenously administered drugs can widely differ between the mesenteric and femoral arterial beds of urethane-anaesthetized rats. Furthermore, vascular tone of these two arterial beds in maintained by different vasoconstrictor systems. While the femoral artery is mainly under adrenergic control, the renin-angiotensin axis is predominant in the mesenteric arterial bed. In addition, this study also demonstrates that computerized analysis enables quick and accurate estimation of haemodynamic drug effects, and is superior to ‘by hand’ evaluation of peak changes in the functional diameter of the vascular bed under study.

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