This Article Full Text Full Text (PDF) CME: Take the course for this article: Hypertension: August 2008,Volume 52, Number 2 All Versions of this Article: 52/2/236    most recent HYPERTENSIONAHA.108.110395v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Immink, R. V. Articles by van Lieshout, J. J. PubMed PubMed Citation Articles by Immink, R. V. Articles by van Lieshout, J. J. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB LABETALOL Related Collections Cardiovascular Pharmacology Cerebrovascular disease/stroke Other hypertension Doppler ultrasound, Transcranial Doppler etc.

(Hypertension. 2008;52:236.)
© 2008 American Heart Association, Inc.

Original Articles

Cerebral Hemodynamics During Treatment With Sodium Nitroprusside Versus Labetalol in Malignant Hypertension

Rogier V. Immink; Bert-Jan H. van den Born; Gert A. van Montfrans; Yu-Sok Kim; Markus W. Hollmann; Johannes J. van Lieshout

From the Departments of Anesthesiology (R.V.I., M.W.H.) and Internal and Vascular Medicine (B-J.H.v.d.B., G.A.v.M., Y-S.K., J.J.v.L.), Laboratory for Clinical Cardiovascular Physiology, AMC Heart Failure Research Center (R.V.I., Y-S.K., J.J.v.L.), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

Correspondence to Johannes J. van Lieshout, Medium Care Unit, Department of Internal Medicine, Academic Medical Center F7-205, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, The Netherlands. E-mail j.j.vanlieshout{at}amc.uva.nl

In patients with malignant hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler–determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for malignant hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (n=8) or labetalol (n=7). The reduction in mean arterial blood pressure with sodium nitroprusside (–28±3%; mean±SEM) and labetalol (–28±4%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (–13±10% and –17±5%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (–53±4% and –7±4%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.45±0.05% versus 0.78±0.04% cm · s^–1 · %mm Hg^–1; P<0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flow to the low resistance systemic vascular bed rather than the cerebral vascular bed.

Key Words: cardiovascular disease/stroke • other hypertension • Doppler ultrasound • transcranial Doppler • cardiovascular pharmacology