scholarly journals Maternal and fetal hemodynamic effects induced by nitric oxide donors and plasma volume expansion in pregnancies with gestational hypertension complicated by intrauterine growth restriction with absent end-diastolic flow in the umbilical artery

2007 ◽  
Vol 31 (1) ◽  
pp. 55-64 ◽  
Author(s):  
H. Valensise ◽  
B. Vasapollo ◽  
G. P. Novelli ◽  
G. Giorgi ◽  
P. Verallo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Plasma Volume ◽  
Intrauterine Growth Restriction ◽  
Volume Expansion ◽  
Umbilical Artery ◽  
Gestational Hypertension ◽  
Nitric Oxide Donors ◽  
Hemodynamic Effects ◽  
Plasma Volume Expansion ◽  
Intrauterine Growth

scholarly journals Placental Underperfusion in a Rat Model of Intrauterine Growth Restriction Induced by a Reduced Plasma Volume Expansion

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0145982 ◽  
Author(s):  
Karine Bibeau ◽  
Benoit Sicotte ◽  
Mélanie Béland ◽  
Menakshi Bhat ◽  
Louis Gaboury ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Rat Model ◽  
Intrauterine Growth Restriction ◽  
Volume Expansion ◽  
Growth Restriction ◽  
Plasma Volume Expansion ◽  
Intrauterine Growth

Effects of Long-term Nitric Oxide Synthesis Inhibition on Plasma Volume Expansion and Fetal Growth in the Pregnant Rat

Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1019-1023 ◽  
Author(s):  
Sofía P. Salas ◽  
Fernando Altermatt ◽  
Mauricio Campos ◽  
Andrea Giacaman ◽  
Pedro Rosso
Keyword(s):  
Nitric Oxide ◽  
Fetal Growth ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Nitric Oxide Synthesis ◽  
Plasma Volume Expansion ◽  
Pregnant Rat ◽  
Synthesis Inhibition

Hemodynamic effects of anemia with and without plasma volume expansion

1956 ◽  
Vol 20 (6) ◽  
pp. 948
Author(s):  
N.O Fowler ◽  
J.A Ward ◽  
R.H Franch ◽  
W.L Bloom
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Hemodynamic Effects ◽  
Plasma Volume Expansion

Effect of acute plasma volume expansion on peripheral arteriolar tone in healthy subjects

1992 ◽  
Vol 83 (5) ◽  
pp. 541-547 ◽  
Author(s):  
Alison Calver ◽  
Joe Collier ◽  
Daniel Green ◽  
Patrick Vallance
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Plasma Volume ◽  
Healthy Subjects ◽  
Volume Expansion ◽  
Forearm Blood Flow ◽  
Plasma Volume Expansion ◽  
Arterial Infusion ◽  
Vasodilator Response ◽  
Flow Response

1. Using venous occlusion plethysmography, we have investigated the forearm blood flow response in healthy subjects to the acute plasma volume expansion caused by a rapid intravenous infusion of saline. The contribution made to this response by nitric oxide has been investigated using local intra-arterial infusions of the nitric oxide synthase inhibitor NG-monomethyl-l-arginine. 2. The infusion of 1000 ml of saline over 25 min caused plasma volume to increase by about 7%, and resulted in a rise in forearm blood flow, with no change in arterial blood pressure. The onset of the blood flow response occurred within 10 min and blood flow remained elevated above baseline 20 mm after the end of the saline infusion. 3. Local intra-arterial infusion of NG-monomethyl-l-arginine alone caused a reduction in forearm blood flow which was maximal at the end of the infusion and gradually recovered to baseline levels over 40 min. 4. When local intra-arterial infusion of NG-monomethyl-l-arginine was followed by plasma volume expansion, the calculated effect of NG-monomethyl-l-arginine was such as to abolish the vasodilator response to saline. 5. The effect of local intra-arterial infusion of NG-monomethyl-l-arginine on forearm blood flow was greater when the drug was given after volume expansion had occurred, than when it was given before the administration of saline. However, in control experiments the vasoconstrictor response to noradrenaline was also enhanced after the administration of the volume load in comparison with the response to noradrenaline given alone. 6. These results are consistent with the possibility that increased local synthesis of nitric oxide contributes to the vasodilator response to volume expansion.

Activated NO pathway in uterine arteries during pregnancy in an IUGR rat model

2018 ◽  
Vol 315 (2) ◽  
pp. H415-H422 ◽  
Author(s):  
Emilie Bigonnesse ◽  
Benoit Sicotte ◽  
Michèle Brochu
Keyword(s):  
Nitric Oxide ◽  
Rat Model ◽  
Intrauterine Growth Restriction ◽  
Volume Expansion ◽  
Uterine Artery ◽  
No Synthase ◽  
Relaxation Response ◽  
Vasoactive Agents ◽  
Intrauterine Growth ◽  
Uterine Arteries

Insufficient development of the uteroplacental circulation may contribute to the development of intrauterine growth restriction (IUGR). We developed a rat model of IUGR by administering a low-Na+ diet. This diet reduces maternal blood volume expansion and uteroplacental perfusion. We hypothesized that an impaired endothelial function in radial arteries decreases vasorelaxation and lowers placental perfusion in this IUGR model. The objective was to assess radial uterine artery responses to vasoactive agents in the IUGR model versus controls. The vasoactive agents included phenylephrine and carbachol, use of a pressurized artery myograph, in the absence or presence of inhibitors of nitric oxide (NO) synthase [ N-nitro-l-arginine methyl ester (l-NAME)], cyclooxygenase (Ibuprofen), and endothelium-dependent hyperpolarization {apamin/1-[(2-chlorophenyl)diphenylmethyl]-1H-pyrazole}, allowing better characterization of the mechanism implicated in endothelium-dependent relaxation. The results show that 1) the diameter of uterine radial arteries was significantly decreased in the IUGR group; 2) sensitivity to phenylephrine was reduced in IUGR arteries, which could be returned to control group values by inhibition of NO production; 3) the relaxation response to carbachol was increased in IUGR rats, principally mediated by endothelium-dependent hyperpolarization in both groups; 4) NO synthase inhibition by l-NAME decreased the maximum relaxation to carbachol only in the IUGR group; and 5) relaxation response to NO donors is increased in IUGR compared with control radial arteries. Contrary to the hypothesis, results in the IUGR model indicate that the NO pathway is activated in radial uterine arteries, most likely in compensation for the reduction in blood uteroplacental perfusion. NEW & NOTEWORTHY In contrast to genetic or surgical models of intrauterine growth restriction, the diet-induced model of reduced maternal volume expansion shows the nitric oxide pathway to be activated in the uterine artery, possibly from increased shear stress and/or placental factors.

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