TU‐G‐217A‐04: Assessment of Cerebral Autoregulation by Inducing Acute Hypertension in Rats

Abstract

Purpose: We developed a rat model of acute hypertension by occluding the descending aorta and used cerebral blood flow (CBF) MRI to evaluate cerebral autoregulation (CA) under normocapnia and hypercanpia. This method avoids potential pharmaceutical complications and can be repeatedly applied in the scanner. The long term goal is to apply this approach to study CA in rat models of chronic hypertension, stroke and diabetes. Methods: 9 Long‐Evans rats were used for MRI and blood‐gas measurements. They were mechanically ventilated under normocapnia, and then hypercapnia. Blood pressure (BP) was modulated by a balloon catheter placed in the descending aorta near diaphragm. MRI studies were performed on an 11.7 T MRI using continuous arterial spin labeling. Modulation paradigm: OFF‐ ON(1min)‐OFF. The mean CBF and BOLD (extracted from non‐labeled images) signals of the cerebrum was reported. The changes of CBF, BP and BOLD (▵CBF, ▵BP and ▵BOLD) from the baseline to the occlusion period were analyzed. Total 23 trials under normocapnia and 21 trails under hypercapnia were performed. Results: CBF, BOLD, BP, arterial pO2 and pH increased significantly during the occlusion under both hypercapnia and normocapnia. BP elevation was sustainable. After initial instant transient increase, CBF returned toward the baseline at a faster(p=0.047) rate under normocapnia than under hypercapnia(∼3x). Under normocapnia, ACBF was not linearly correlated to ▵BP(p=0.53). The absence of correlation and faster returning rate under normocapnia indicates CA. By contrast, under hypercapnia, ACBF increased linearly with ABP(p=0.002), which indicates autoregulation impairment. %▵CBF vs. %▵BOLD remained linearly correlated under both conditions. Conclusions: We developed a model of acute hypertension in rat for use in the MRI scanner. CBF MRI results indicated that there were apparent CA under normocapnia but was markedly impaired under hypercapnia. This approach sets the stage for study of CA in rat models of chronic hypertension, stroke and diabetes.