Stauss Harald M, Petitto Carlo E, Rotella Diane L, Wong Brett J, Sheriff Don D
Department of Integrative Physiology, The University of Iowa, Iowa City, Iowa, USA.
J Hypertens. 2008 Jun;26(6):1127-37. doi: 10.1097/HJH.0b013e3282fb81c8.
Cerebrovascular myogenic function, which protects the brain from hemorrhagic stroke, is impaired in stroke-prone spontaneously hypertensive rats. Furthermore, myogenic function contributes to very low frequency blood pressure variability and dynamic autoregulation of cerebral blood flow is most effective at very low frequency in rats. Therefore, we hypothesized that very low frequency blood pressure variability is reduced in stroke-prone spontaneously hypertensive rats compared with stroke-resistant spontaneously hypertensive rats. In addition, we investigated if myogenic function also contributes to very low frequency blood pressure variability in conscious dogs.
In 8-week-old normotensive Wistar-Kyoto rats, 8-week-old and 15-week-old stroke-prone spontaneously hypertensive rats and stroke-resistant spontaneously hypertensive rats, and dogs, blood pressure variability was studied during control conditions, inhibition of myogenic function (nifedipine) and hypotension induced by sodium nitroprusside. In dogs, transfer function analysis between blood pressure and total peripheral resistance was performed to study the contribution of myogenic function to blood pressure variability.
Inhibition of myogenic function, but not hypotension induced by sodium nitroprusside, significantly reduced very low frequency variability of systolic blood pressure (rats: 0.02-0.2 Hz; dogs: 0.02-0.075 Hz) in conscious rats and dogs. In dogs, the gain of the transfer function was high (0.28 +/- 0.04 min/l) in the very low frequency band and was decreased to 0.11 +/- 0.01 min/l (P < 0.05) by nifedipine but not by sodium nitroprusside (0.26 +/- 0.02 min/l). Very low frequency blood pressure variability was significantly smaller in stroke-prone spontaneously hypertensive rats than in stroke-resistant spontaneously hypertensive rats (8 weeks of age: 7.8 +/- 1.1 vs. 13.1 +/- 2.2 mmHg; P < 0.05; 15 weeks of age: 7.1 +/- 1.2 vs. 16.5 +/- 3.6 mmHg; P < 0.05).
Myogenic function affects very low frequency blood pressure variability in conscious rats and dogs. The smaller very low frequency blood pressure variability in stroke-prone spontaneously hypertensive rats compared with stroke-resistant spontaneously hypertensive rats suggests that impaired cerebrovascular myogenic function is reflected in reduced very low frequency blood pressure variability.
脑血管肌源性功能可保护大脑免受出血性中风影响,而在易中风自发性高血压大鼠中该功能受损。此外,肌源性功能有助于产生极低频血压变异性,并且在大鼠中,脑血流量的动态自动调节在极低频时最为有效。因此,我们推测,与抗中风自发性高血压大鼠相比,易中风自发性高血压大鼠的极低频血压变异性降低。此外,我们研究了肌源性功能是否也有助于清醒犬的极低频血压变异性。
在8周龄的正常血压Wistar-Kyoto大鼠、8周龄和15周龄的易中风自发性高血压大鼠和抗中风自发性高血压大鼠以及犬中,研究了在对照条件下、肌源性功能抑制(硝苯地平)以及硝普钠诱导的低血压期间的血压变异性。在犬中,进行了血压与总外周阻力之间的传递函数分析,以研究肌源性功能对血压变异性的贡献。
抑制肌源性功能而非硝普钠诱导的低血压,显著降低了清醒大鼠和犬的收缩压极低频变异性(大鼠:0.02 - 0.2赫兹;犬:0.02 - 0.075赫兹)。在犬中,传递函数在极低频带的增益较高(0.28±0.04分钟/升),硝苯地平可使其降至0.11±0.01分钟/升(P<0.05),而硝普钠则无此作用(0.26±0.02分钟/升)。易中风自发性高血压大鼠的极低频血压变异性显著小于抗中风自发性高血压大鼠(8周龄:7.8±1.1对13.1±2.2毫米汞柱;P<0.05;15周龄:7.1±1.2对16.5±3.6毫米汞柱;P<0.05)。
肌源性功能影响清醒大鼠和犬的极低频血压变异性。与抗中风自发性高血压大鼠相比,易中风自发性高血压大鼠的极低频血压变异性较小,这表明脑血管肌源性功能受损反映在极低频血压变异性降低上。