Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA001

Poster Communications

Sodium nitroprusside dilates cerebral vessels in young men

N. D. Olesen1,2, M. Fischer1,3, N. H. Secher1

1. Department of Anaesthesia, Rigshospitalet, Copenhagen Ø, Denmark. 2. Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark. 3. Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark.


  • Fig. 1. A: internal carotid artery blood flow, B: vertebral artery blood flow, C: cerebral blood flow, and D: cerebral blood flow conductance at baseline and during infusion of sodium nitroprusside (SNP). Variables are without ‘correction' for change in PaCO2. P-values represent the overall effect as estimated by a repeated measure mixed model. *P < 0.05 vs. baseline. †P < 0.05 for low vs. high SNP infusion rate.

Introduction Cerebral autoregulation maintains cerebral blood flow (CBF) despite marked changes in mean arterial pressure (MAP) (1). Sodium nitroprusside (SNP) reduces MAP by vasodilatation, but is reported to lower CBF suggesting a critical role for its perfusion pressure when MAP is lowered (2, 3). We evaluated the influence of SNP on CBF and aimed for a 20% and 40% reduction in MAP, while keeping MAP ≥ 50 mmHg, to challenge cerebral autoregulation. Methods In 19 healthy men (age 24 ± 4 years; mean ± SD) right internal carotid (ICA) and vertebral artery (VA) blood flow was evaluated by duplex ultrasound and transcranial Doppler measured middle cerebral artery mean blood velocity (MCA Vmean). Cerebral CO2 reactivity was determined by hyperventilation at rest and CBF ((ICA + VA flow) x 2) also ‘corrected' according to reduction in arterial CO2 tension (PaCO2) with the reservation that CO2 reactivity may be affected by SNP. Brachial artery catheterisation determined MAP and total peripheral resistance was derived by pulse contour analysis (Modelflow). Analysis was by a repeated measure mixed model. Values are presented as mean ± SD. Results Three subjects developed presyncopal symptoms during the large reduction in MAP and data obtained at that time was not included in the analysis. Infusion of SNP (2.0 (1.5-2.5) and 8.6 (6.0-9.4) µg kg-1 min-1) reduced MAP (from 83 ± 8 to 69 ± 8 and 58 ± 4 mmHg; both P < 0.0001), total peripheral resistance, and PaCO2 (41 ± 3 vs. 39 ± 3 and 37 ± 4 mmHg; both P < 0.01). Yet, ICA flow increased at the moderate reduction in MAP (by 27 ml min-1; 95% CI: 6-48; P = 0.013) but returned to the baseline value by the large reduction in MAP while VA flow and CBF were maintained with increased ICA and VA conductance (Fig. 1). In contrast, SNP decreased MCA Vmean from 69 ± 16 to 59 ± 14 and 52 ± 14 cm s-1 (both P < 0.001). With ‘correction' for the reduction in PaCO2 (2.8 ± 1.0% mmHg-1 for CBF) SNP increased ICA flow while VA flow was unaffected and thus CBF increased whereas MCA Vmean remained reduced. Discussion Similar to the present results CBF increases in response to vasodilatation by, e.g. L-arginine (4) and adenosine (5). Yet, evaluation of CBF by 133Xe clearance indicates that CBF is reduced by even a minor SNP-induced reduction in MAP (2, 3). The discrepancy between results using duplex ultrasound and 133Xe clearance may relate to cerebral vasodilatation that may increase transient time for blood whereby clearance of 133Xe would be slowed and interpreted as a decrease in CBF. We took changes in PaCO2 into account but cerebral CO2 reactivity may be affected by SNP. Conclusion Sodium nitroprusside induces systemic and cerebral vasodilation and increased cerebrovascular conductance. The results indicate different regional regulation of CBF as SNP increased ICA but not VA flow.

Where applicable, experiments conform with Society ethical requirements