The Acute Effect of Captopril on Cerebral Blood Flow, Its CO2 Reactivity, and Cerebral Oxygen Metabolism in Human Volunteers

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Abstract
The present study was undertaken to examine the effect of captopril on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and CO2 reactivity in eight young healthy volunteers. The mean arterial blood pressure (MABP) was measured intraarterially, and CBF was measured by inhaled xenon-1233. The CO2 reactivity was defined as the relative change in CBF per 0.1 kPa change in arterial CO2. During the CO2 reactivity tests, the CBF changes were estimated by the arterio-venous-oxygen-difference method (CBFsat). Median CBF was 52 ml/100 g/min (50–56) and without any significant regional side-to-side asymmetries. No significant change was observed after captopril. The median resting MABP was 90 mm Hg (89–93), and was slightly reduced by 5 mm Hg (4–6) 1 h after an oral dose of captopril (50 mg). CMRO2 was 3.7 ml/100 g/min (3.5–3.8) and was unchanged after captopril. For the entire range of PaCO2 the median slope of the ln(CBFsat) versus PaCO2 regression line was 1.4 (1.3–1.6) at baseline compared to 1.4 (1.3–1.7) after captopril (p = 0.23). Considering the PaCO2 values between 4.0 and 6.5, the CO2 reactivity was 2.4%/0.1 kPa (2.1–2.4) at baseline and increased significantly to 2.9%/0.1 kPa (2.1–3.2) after captopril (p <0.05). No side effects were observed. The present study shows an overall unchanged CO2 reactivity; however, with an increased CO2 reactivity of the cerebral vessels for small changes in PaCO2 around the resting value of PaCO2 and a maintained coupling of CBF and CMRO2 after peroral captopril.