Abstract:
Postural hypotension abruptly lowers cerebral perfusion, producing unsteadiness which worsens with aging. This study addressed the hypothesis that maintenance of cerebral perfusion weakens in the elderly due to less effective cerebrovascular autoregulation and systemic cardiovascular responses to hypotension. In healthy elderly (n = 13, 68 ± 1 years) and young (n = 13, 26 ± 1 years) adults, systemic hypotension was induced by rapid deflation of bilateral thigh cuffs after 3-min suprasystolic occlusion, while heart rate (HR), mean arterial pressure (MAP), and blood flow velocity of the middle cerebral artery (VMCA) were recorded. VMCA/MAP indexed cerebrovascular conductance (CVC). Durations and rates of recovery of MAP and VMCA from their respective postdeflation nadirs were compared between the groups. Thigh-cuff deflation elicited similar hypotension and cerebral hypoperfusion in the elderly and young adults. However, the time elapsed (TΔ) from cuff deflation to the nadirs of MAP and VMCA, and the time for full recovery (TR) from nadirs to baselines were significantly prolonged in the elderly subjects. The response rates of HR (ΔHR, i.e. cardiac factor), MAP (ΔMAP, i.e. vasomotor factor), and CVC following cuff deflation were significantly slower in the elderly. Collectively, the response rates of the cardiac, vasomotor, and CVC factors largely explained TRVMCA. However, the TRVMCA/ΔMAP slope (-3.0 ± 0.9) was steeper (P = 0.046) than the TRVMCA/ΔHR slope (-1.1 ± 0.4). The TRVMCA/ΔCVC slope (-2.4 ± 0.6) was greater (P = 0.072) than the TRVMCA/ΔHR slope, but did not differ from the TRVMCA/ΔMAP slope (P = 0.52). Both cerebrovascular autoregulatory and systemic mechanisms contributed to cerebral perfusion recovery during systemic hypotension, and the vasomotor factor was predominant over the cardiac factor. Recovery from cerebral hypoperfusion was slower in the elderly adults because of the age-diminished rates of the CVC response and cardiovascular reflex regulation. Systemic vasoconstriction predominated over increased HR for restoring cerebral perfusion after abrupt onset of systemic hypotension.
摘要:
体位性低血压突然降低脑灌注,产生随着年龄增长而恶化的不稳定性。这项研究解决了以下假设:由于脑血管自动调节效果较差以及对低血压的全身性心血管反应,老年人的脑灌注维持减弱。在健康的老年人(n=13,68±1岁)和年轻的成年人(n=13,26±1岁),系统性低血压是由双侧大腿袖带快速放气引起的,而心率(HR),平均动脉压(MAP),记录大脑中动脉血流速度。VMCA/MAP指数脑血管电导(CVC)。两组之间比较了MAP和VMCA从各自的通货紧缩后最低点的持续时间和恢复率。大腿袖套放气在老年人和年轻人中引起类似的低血压和脑灌注不足。然而,从袖带放气到MAP和VMCA最低点所经过的时间(TΔ),老年受试者从最低点到基线的完全恢复(TR)时间显着延长。HR的反应率(ΔHR,即心脏因素),MAP(ΔMAP,即血管舒缩因子),老年人袖带放气后的CVC明显减慢。总的来说,心脏的反应率,血管舒缩,和CVC因素在很大程度上解释了TRVMCA。然而,TRVMCA/ΔMAP斜率(-3.0±0.9)比TRVMCA/ΔHR斜率(-1.1±0.4)更陡(P=0.046)。TRVMCA/ΔCVC斜率(-2.4±0.6)大于(P=0.072)TRVMCA/ΔHR斜率,但与TRVMCA/ΔMAP斜率无差异(P=0.52)。脑血管自动调节和全身机制都有助于全身低血压期间的脑灌注恢复,血管舒缩因子比心脏因子占优势。由于CVC反应和心血管反射调节的年龄降低,老年人从脑灌注不足中恢复的速度较慢。系统性低血压突然发作后,全身血管收缩主导于HR增加,以恢复脑灌注。