This Article Full Text Full Text (PDF) All Versions of this Article: 49/2/334    most recent 01.HYP.0000255791.54655.29v1 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Euser, A. G. Articles by Cipolla, M. J. Search for Related Content PubMed PubMed Citation Articles by Euser, A. G. Articles by Cipolla, M. J. Related Collections Cerebrovascular disease/stroke Other hypertension Endothelium/vascular type/nitric oxide Other Vascular biology Animal models of human disease

(Hypertension. 2007;49:334.)
© 2007 American Heart Association, Inc.

Original Articles

Cerebral Blood Flow Autoregulation and Edema Formation During Pregnancy in Anesthetized Rats

From the Departments of Neurology, Obstetrics/Gynecology, and Pharmacology, University of Vermont, Burlington.

Correspondence to Marilyn J. Cipolla, Department of Neurology, University of Vermont, 89 Beaumont Ave, Given C454, Burlington, VT 05405. E-mail Marilyn.Cipolla{at}uvm.edu

Eclampsia is considered a form of hypertensive encephalopathy in which an acute elevation in blood pressure causes autoregulatory breakthrough, blood–brain barrier disruption, and edema formation. We hypothesized that pregnancy predisposes the brain to eclampsia by lowering the pressure of autoregulatory breakthrough and enhancing cerebral edema formation. Because NO production is increased in pregnancy, we also investigated the role of NO in modulating autoregulation. Cerebral blood flow autoregulation was determined by phenylephrine infusion and laser Doppler flowmetry. Four groups were studied: untreated nonpregnant (n=7) and late-pregnant (days 19 to 21; n=8) Sprague–Dawley rats and nonpregnant (n=8) and late-pregnant (n=8) animals treated with an NO synthase inhibitor (N^G-nitro-L-arginine methyl ester; 0.5 to 0.7 g/L). Brain water content and blood–brain barrier permeability to sodium fluorescein were determined after breakthrough. Pregnancy caused no change in autoregulation or the pressure of breakthrough. However, treatment with the NO synthase inhibitor significantly increased the pressure of autoregulatory breakthrough (nonpregnant: 183.6±3.0 mm Hg versus 212.0±2.8 mm Hg, P<0.05; late-pregnant: 180.8±3.2 mm Hg versus 209.3±4.7 mm Hg, P<0.05). After autoregulatory breakthrough, only late-pregnant animals showed a significant increase in cerebral edema formation, which was attenuated by NO synthase inhibition. There was no difference in blood–brain barrier permeability between nonpregnant and late-pregnant animals in response to acute hypertension, suggesting that pregnancy may predispose the brain to eclampsia by increasing cerebral edema through increased hydraulic conductivity.

Key Words: autoregulation • eclampsia • L-NAME • laser Doppler flowmetry • NO synthase • pregnancy

This article has been cited by other articles:

				B. D. LaMarca, J. Gilbert, and J. P. Granger Recent Progress Toward the Understanding of the Pathophysiology of Hypertension During Preeclampsia Hypertension, April 1, 2008; 51(4): 982 - 988. [Full Text] [PDF]

				M. J. Cipolla, J. Smith, N. Bishop, L. V. Bullinger, and J. A. Godfrey Pregnancy Reverses Hypertensive Remodeling of Cerebral Arteries Hypertension, April 1, 2008; 51(4): 1052 - 1057. [Abstract] [Full Text] [PDF]

				J. A. Hinchey Reversible Posterior Leukoencephalopathy Syndrome: What Have We Learned in the Last 10 Years? Arch Neurol, February 1, 2008; 65(2): 175 - 176. [Full Text] [PDF]

				A. G. Euser, L. Bullinger, and M. J. Cipolla Magnesium sulphate treatment decreases blood-brain barrier permeability during acute hypertension in pregnant rats Exp Physiol, February 1, 2008; 93(2): 254 - 261. [Abstract] [Full Text] [PDF]

				M. J. Cipolla Cerebrovascular Function in Pregnancy and Eclampsia Hypertension, July 1, 2007; 50(1): 14 - 24. [Full Text] [PDF]