Effect of bilateral carotid occlusion on cerebral hemodynamics and perivascular innervation : An experimental rat model

We aimed to investigate the effect of chronic cerebral hypoperfusion on cerebral hemodynamics and perivascular nerve density in a rat model. Bilateral common carotid artery (CCA) ligation (n = 24) or sham-operation (n = 24) was performed with a 1-week interval. A subgroup (ligated n = 6; sham-operated n = 3) underwent magnetic resonance imaging (MRI) before the procedures and 2 and 4 weeks after the second procedure. After termination, carotids were harvested for assessment of complete ligation and nerve density in cerebral arteries that were stained for the general neural marker PGP 9.5 and sympathetic marker TH by computerized image analysis. Five rats were excluded because of incomplete ligation. MRI-based tortuosity of the posterior communicating artery (Pcom), first part of the posterior cerebral artery (P1) and basilar artery was observed in the ligated group, as well as an increased volume (p = 0.05) and relative signal intensity in the basilar artery (p = 0.04; sham-group unchanged). Immunohistochemical analysis revealed that compared to sham-operated rats, ligated rats had increased diameters of all intracircular segments and the extracircular part of the internal carotid artery (p < 0.05). Ligated rats showed a higher general nerve density compared to controls in P1 (10%, IQR:8.7–10.5 vs. 6.6%, IQR:5.5–7.4, p = 0.003) and Pcom segments (6.4%, IQR:5.8–6.5 vs. 3.2%, IQR:2.4–4.3, p = 0.003) and higher sympathetic nerve density in Pcom segments (3.7%, IQR:2.8–4.8 vs. 1.7%, IQR:1.3–2.2, p = 0.02). Bilateral CCA occlusion resulted in redistribution of blood flow to posteriorly located cerebral arteries with remarkable changes in morphology and perivascular nerve density, suggesting a functional role for perivascular nerves in cerebral autoregulation

Шантарский архипелаг: основные направления природопользования

BACKGROUND: Short-acting vasopressor agents like phenylephrine or ephedrine can be used during carotid endarterectomy (CEA) to achieve adequate blood pressure (BP) to prevent periprocedural stroke by preserving the cerebral perfusion. Previous studies in healthy subjects showed that these vasopressors also affected the frontal lobe cerebral tissue oxygenation (rSO 2) with a decrease after administration of phenylephrine. This decrease is unwarranted in patients with jeopardized cerebral perfusion, like CEA patients. The study aimed to evaluate the impact of both phenylephrine and ephedrine on the rSO 2 during CEA. METHODS: In this double-blinded randomized controlled trial, 29 patients with symptomatic carotid artery stenosis underwent CEA under volatile general anesthesia in a tertiary referral medical center. Patients were preoperative allocated randomly (1:1) for receiving either phenylephrine (50 µg; n = 14) or ephedrine (5 mg; n = 15) in case intraoperative hypotension occurred, defined as a decreased mean arterial pressure (MAP) ≥ 20% compared to (awake) baseline. Intraoperative MAP was measured by an intra-arterial cannula placed in the radial artery. After administration, the MAP, cardiac output (CO), heart rate (HR), stroke volume, and rSO 2 both ipsilateral and contralateral were measured. The timeframe for data analysis was 120 s before, until 600 s after administration. RESULTS: Both phenylephrine (70 ± 9 to 101 ± 22 mmHg; p < 0.001; mean ± SD) and ephedrine (75 ± 11 mmHg to 122 ± 22 mmHg; p < 0.001) adequately restored MAP. After administration, HR did not change significantly over time, and CO increased 19% for both phenylephrine and ephedrine. rSO 2 ipsilateral and contralateral did not change significantly after administration at 300 and 600 s for either phenylephrine or ephedrine (phenylephrine 73%, 73%, 73% and 73%, 73%, 74%; ephedrine 72%, 73%, 73% and 75%, 74%, 74%). CONCLUSIONS: Within this randomized prospective study, MAP correction by either phenylephrine or ephedrine showed to be equally effective in maintaining rSO 2 in patients who underwent CEA. Clinical Trial Registration ClincalTrials.gov, NCT01451294