Cardiovascular Systems Laboratory, Physiological Rhythms Unit, Department of Surgery and Anesthesia, University of Otago, Wellington, Wellington South, New Zealand.
Hypertension. 2010 Aug;56(2):268-73. doi: 10.1161/HYPERTENSIONAHA.110.152066. Epub 2010 Jun 14.
The cerebrovasculature dilates or constricts in response to acute blood pressure changes to stabilize cerebral blood flow across a range of blood pressures. It is unclear, however, whether such dynamic cerebral autoregulation (dCA) is equally effective in responding to falling versus rising blood pressure. In this study we applied a pharmacological approach to evaluate dCA gain to transient hypotension and hypertension and compared this method with 2 established indices of dCA that do not explicitly differentiate between dCA efficacy and falling versus rising blood pressure. Middle cerebral arterial velocity and blood pressure recordings were made in 26 healthy volunteers randomized to 2 protocols. In 10 subjects, dCA gain to transient hypotension induced with intravenous nitroprusside was compared with dCA gain to transient hypertension induced with intravenous phenylephrine. In 16 subjects, dCA gain to transient hypotension induced with intravenous nitroprusside was compared with the rate of regulation and autoregulatory index derived from transient hypotension induced with the thigh cuff deflation technique. dCA gain to transient hypotension induced with intravenous nitroprusside was unrelated to dCA gain to transient hypertension induced with intravenous phenylephrine (r=0.06; P=0.87) and was consistently greater than dCA gain to transient hypertension induced with intravenous phenylephrine (0.57+/-0.16 versus 0.31+/-0.20 cm/s per millimeter of mercury; P<0.01). However, dCA gain to transient hypotension induced with intravenous nitroprusside was inversely related to the rate of regulation (r=-0.52; P=0.037) and autoregulatory index (r=-0.66; P=0.005). These data indicate that, under our laboratory conditions, dCA appears to be inherently nonlinear with disparate efficacy against rising and falling blood pressure, and dCA gain derived from pharmacologically induced transient hypotension correlates with established nonpharmacological indices of dCA.
脑血管会对急性血压变化做出扩张或收缩的反应，以稳定在一定血压范围内的脑血流。然而，目前尚不清楚这种动态脑自动调节（dCA）在应对血压下降和上升时是否同样有效。在这项研究中，我们应用药理学方法来评估短暂性低血压和高血压时的 dCA 增益，并将这种方法与两种不明确区分 dCA 效能和血压下降与上升的已确立的 dCA 指数进行比较。我们在 26 名随机分为 2 组的健康志愿者中进行了大脑中动脉速度和血压记录。在 10 名受试者中，我们比较了静脉注射硝普钠引起的短暂性低血压时的 dCA 增益与静脉注射苯肾上腺素引起的短暂性高血压时的 dCA 增益。在 16 名受试者中，我们比较了静脉注射硝普钠引起的短暂性低血压时的 dCA 增益与使用大腿袖带放气技术引起的短暂性低血压时的调节率和自动调节指数。静脉注射硝普钠引起的短暂性低血压时的 dCA 增益与静脉注射苯肾上腺素引起的短暂性高血压时的 dCA 增益无关（r=0.06；P=0.87），并且始终大于静脉注射苯肾上腺素引起的短暂性高血压时的 dCA 增益（0.57+/-0.16 对 0.31+/-0.20 cm/s/mmHg；P<0.01）。然而，静脉注射硝普钠引起的短暂性低血压时的 dCA 增益与调节率（r=-0.52；P=0.037）和自动调节指数（r=-0.66；P=0.005）呈反比关系。这些数据表明，在我们的实验室条件下，dCA 似乎具有内在的非线性，对血压上升和下降的效能存在差异，并且来自药理学诱导的短暂性低血压的 dCA 增益与已确立的非药理学 dCA 指数相关。
