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  • Title: Forearm blood flow in pre-eclampsia.
    Author: Bowyer L, Brown MA, Jones M.
    Journal: BJOG; 2003 Apr; 110(4):383-91. PubMed ID: 12699800.
    Abstract:
    UNLABELLED: OBJECTIVE 1. To characterise the forearm vascular reactivity of women with pre-eclampsia in the third trimester of pregnancy and compare it with that in normal or gestational hypertensive pregnancies. 2. To document female sex steroid (oestradiol, progesterone, oestriol and betahCG) levels in the three groups of women. DESIGN: Forearm blood flow was measured by venous occlusion plethysmography during intra-arterial infusion of saline and vasoactive substances: angiotensin II, sodium nitroprusside, acetylcholine and N(G)-monomethyl-L-arginine (L-NMMA). SETTING: Research laboratory at St George Hospital, Kogarah, Sydney, Australia. SAMPLE: Fifteen non-pregnant women in the follicular phase of the menstrual cycle, 15 third trimester normal pregnant women, 13 women in the third trimester with gestational hypertension and 15 women with pre-eclampsia. MAIN OUTCOME MEASURES: Changes in forearm blood flow in response to vasoactive substances. RESULTS: Normal pregnant women had higher baseline forearm blood flow than non-pregnant women, decreased vasodilator responses to sodium nitroprusside and reduced vasoconstrictor responses to angiotensin II. No difference in response to angiotensin II, sodium nitroprusside or L-NMMA was found among normal pregnant, pre-eclampsia or gestational hypertension women, but vasodilatory responses of pre-eclamptic women to acetylcholine were reduced compared with normal pregnant women. Higher serum progesterone levels were found in women with pre-eclampsia and gestational hypertension than in normal pregnancy. CONCLUSION: The hyperdynamic circulation of normal pregnancy is characterised by refractoriness to angiotensin II but this is not altered in pre-eclampsia. Pre-eclamptic women demonstrate a reduced vasodilator response to acetylcholine which, in the absence of any alteration in response to L-NMMA, implies that factors other than nitric oxide deficiency mediate the vasoconstriction of pre-eclampsia.
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