Dynamic autoregulation of cerebral blood flow is limited to frequencies below 0.1 Hz in rats

Abstract

Impaired cerebrovascular myogenic function (CVMF) contributes to hemorrhagic stroke in stroke-prone spontaneously hypertensive rats. Furthermore, impaired CVMF may cause specific patterns of blood pressure variability (BPV) that may indicate elevated risk for hemorrhagic stroke. In order to identify these BPV patterns, we tested the hypothesis that dynamic autoregulation of cerebral blood flow is most effective at very low frequencies (<0.1 Hz) in rats. Normotensive Wistar Kyoto rats were instrumented with catheters in the left carotid artery and jugular vein and Transonic flow probes around the right internal carotid artery. During control conditions (n=7) and inhibition of myogenic function (n=6, nifedipine, 0.25 mg/kg BW, i.v.), fluctuations in cerebral perfusion pressure were elicited by periodically clamping the abdominal aorta at 8 different frequencies between 0.008 Hz and 0.5 Hz. Increases in cerebral perfusion pressure elicited initial increases in cerebrovascular conductance that returned to baseline levels within 30 s, indicating myogenic vasoconstriction. Nifedipine blocked this response. At aortic clamping frequencies of 0.1 Hz and above, the normalized gain of the transfer function between cerebral perfusion pressure and cerebral blood flow was close to 2.0 in the control and nifedipine trial, indicating that flow follows pressure passively. At aortic clamping frequencies below 0.1 Hz the normalized gain of the transfer function declined and reached 1.37±0.11 during control conditions and 1.69±0.16 (P<0.05 vs. control) during nifedipine application at an aortic clamping frequency of 0.008 Hz. Dynamic cerebrovascular autoregulation in rats is restricted to very low frequencies (<0.1 Hz). Reduced BPV at very low frequencies may indicate impaired cerebrovascular autoregulation and predict hemorrhagic stroke in hypertensive subjects.