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Not all possible drug interactions are listed here. Your pharmacist can provide more information about sildenafil. Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed. Every effort has been made to ensure that the information provided by Cerner Multum, Inc. ('Multum') is accurate, up-to-date, and complete, but no guarantee is made to that effect.

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The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions about the drugs you are taking, check with your doctor, nurse or pharmacist. Sildenafil Citrate (Viagra) Enhances Vasodilatation in Fetal Growth Restriction.

Baker, Sildenafil Citrate (Viagra) Enhances Vasodilatation in Fetal Growth Restriction, The Journal of Clinical Endocrinology & Metabolism , Volume 90, Issue 5, 1 May 2005, Pages 2550–2555, https://doi.org/10.1210/jc.2004-1831. Background: Fetal growth restriction (FGR) affects up to 8% of all pregnancies and has massive short-term (increased fetal morbidity and mortality) and long-term (increased incidence of cardiovascular disease in adulthood) health

implications

Methods: Small arteries dissected from myometrial biopsies obtained at cesarean section from normal pregnant women (n = 27) or women whose pregnancies were complicated by FGR (n = 12) were mounted on wire

myographs

Results: We demonstrated increased myometrial small artery vasoconstriction and decreased endothelium-dependent vasodilatation in vessels from women whose pregnancies were complicated by FGR. Sildenafil citrate significantly reduced vasoconstriction and significantly improved relaxation of FGR small arteries.

Conclusions: We conclude that sildenafil citrate improves endothelial function of myometrial vessels from women whose pregnancies are complicated by intrauterine growth restriction.

Sildenafil citrate may offer a potential therapeutic cheap viagra with prescription strategy to improve uteroplacental blood flow in FGR pregnancies.

FETAL GROWTH RESTRICTION (FGR), when the fetus fails to attain its growth potential, affects approximately 8% of all pregnancies contributing to infant prematurity ( 1).

FGR is responsible for considerable perinatal mortality and morbidity; infants are at increased risk of perinatal complications such as fetal distress, asphyxia, neonatal encephalopathy, hypothermia, hypoglycemia, and poor feeding as well as risks of long-term neurological and developmental disorders ( 2, 3).

These

show

In the long term, deficient growth in utero is related to an increased incidence of hypertension, diabetes mellitus, and coronary heart disease in adulthood ( 6– 8).

The underlying pathology of FGR is multifactorial and poorly understood. For example, growth restriction has been shown to have a genetic component such as trisomies and cases of placental mosaicism ( 9) or be a result of physiological factors such as maternal undernutrition ( 10, 11) or smoking during pregnancy ( 12). However, the reduced growth of the FGR fetus is typically associated with placental insufficiency, i.e .

abnormalities in placental growth, development, and function. In normal pregnancy (NP), uterine blood flow increases dramatically

from

Magnetic resonance imaging studies of the placental bed in FGR pregnancies have suggested that uteroplacental flow is indeed reduced, leading to a hypoperfused placenta ( 16, 17).

A poorly modified uteroplacental vasculature is also a hallmark of the current pathogenic model of preeclampsia ( 18, 19) where aberrant spiral artery modification leads to a hypoperfused uteroplacental unit later in pregnancy ( 20, 21).

This results in the release of a factor(s) from the placenta that activates the maternal vascular endothelium. These data suggest that the pathophysiology of FGR and preeclampsia may be related. A recent report that markers of endothelial dysfunction are increased in FGR ( 22), a commonly reported phenomenon of preeclampsia, supports such a hypothesis ( 23, 24).

Endothelium-dependent responses in a variety of blood vessels from women with preeclampsia are markedly different, compared with those isolated from NP women ( 25– 27). We have demonstrated, using small-vessel myography, reduced endothelium-dependent responses to bradykinin in myometrial resistance arteries isolated from women with preeclampsia ( 26, 27) and have shown that the small residual response to bradykinin is entirely mediated via nitric oxide ( 28). The viagra buy near me first aim of the current study was to investigate our hypothesis that uterine resistance artery function is aberrant in FGR, by performing the first comparison of myometrial small-artery vasoconstriction and endothelium-dependent relaxation in pregnancies complicated by FGR with that seen in NP. Animal studies suggest that phosphodiesterase-5 (PDE5) inhibitors, such as sildenafil citrate, may improve uterine blood flow via cGMP-mediated endothelial relaxation of uterine vessels ( 29).

Our second aim was thus to assess the effects of PDE5 inhibition in small arteries from women whose pregnancies were complicated by FGR. Mary’s Hospital, Manchester, gave approval for this work, and consent was obtained for all tissue samples used in the study.

The investigation conforms to the principles outlined in the Declaration of Helsinki ( 30). Myometrial biopsies were obtained at delivery by cesarean section from the upper lip of the lower segment incision from healthy women (NP; n = 27) with uncomplicated pregnancies. Women with hypertension, diabetes, or other significant medical disorders were excluded. Biopsies were also obtained from women with intrauterine growth restriction (FGR; n = 12).

All women in this group were identified on the basis of serial antenatal ultrasound scans demonstrating deficient fetal growth and delivered by cesarean section for maternal or fetal reasons; the diagnosis of FGR was confirmed by an individualized birthweight ratio (IBR) found to be less than the fifth centile.

IBR is a correction of birthweight for known confounding variables and relates to a predicted birthweight calculated using independent coefficients for gestation at delivery, fetal sex, parity, ethnic origin, maternal height, and booking weight.

The IBR enables a more accurate prediction of pregnancies with a poor outcome than birthweight for gestational age alone ( 31).

General chemicals were obtained from Sigma-Aldrich (Poole, UK) or BDH (Poole, UK). Arginine vasopressin (AVP) and bradykinin (BK) were obtained from Sigma-Aldrich.

The thromboxane mimetic U46619 was obtained from Calbiochem (Nottingham, UK). The PDE5 inhibitors sildenafil citrate (Viagra) and UK-343664 were obtained from Pfizer (Sandwich, UK). Biopsies were placed directly into ice-cold physiological salt solution, a modified Krebs solution (see below for chemical composition).

Myometrial small arteries were identified and dissected under a stereomicroscope.

Myometrial artery diameters were 379 ± 4 ?m for NP biopsies (n = 49 arteries from 27 patients) and 310 ± 2 ?m for FGR biopsies (n = 62 arteries from 12 patients). Myometrial small arteries were carefully cut into small (approximately 2 mm) lengths and mounted onto 40-?m steel wire in a Danish Myo Technology (Aarhus, Denmark) M610 wire myograph as described elsewhere ( 32). Myometrial arteries were normalized to 0.9 of L 13.3kPa using the classical normalization procedure ( 33) as we have described in detail elsewhere ( 32, 34).

Initially, the bath contained 7 ml of physiological salt solution (in mmol/liter: 127.76 NaCl, 25 NaHCO 3 , 4.69 KCl, 2.4 MgSO 4 , 1.6 CaCl 2 , 1.18 KH 2 PO 4 , 6.05 glucose, 0.034 EDTA; pH 7.4), warmed to 37 C and gassed with air/5%CO 2 .

Contraction/relaxation responses of myometrial small arteries. Dose-response constriction curves to AVP (0.1–10 nmol/liter; 2-min intervals) or the thromboxane-mimetic U46619 (0.1–1000 nmol/liter; 2-min intervals) were constructed followed by relaxation to BK (0.1–1000 nmol/liter; 2-min intervals). Vessels were washed to baseline buy generic viagra online no prescription tension and then incubated for 1 h in the presence of 0, 10, or 100 nmol/liter of the PDE5 inhibitor sildenafil citrate or UK-343664. The protocol of constriction to AVP or U46619/relaxation to BK was repeated as outlined above in the maintained presence of the PDE5 inhibitor.

Data were first tested whether they fitted to a Gaussian (normal) distribution using the Kolmogorov-Smirnov test. Data that passed the normality test were compared

using

BK-induced relaxation of myometrial small arteries was compared using repeated-measures ANOVA.

Data for the number of patients are indicated by (N). Women whose pregnancies were complicated by FGR delivered significantly earlier in gestation than the NP group ( P TABLE 1.

NP 27 30 (19–40) 2 (1–5) 1 (0–4) 123 (110–150) 75 (60–85) 38.9 (37.4–41.5) 3300 (2690–4110) 46 (7–88) FGR 12 28.5 (22–37) 3.5 (1–5) 1 (0–4) 120 (115–140) 81 (70–90) 37.9 (29.8–39.0) a 2460 (745–2860) b 3 (0–5) b.

NP 27 30 (19–40) 2 (1–5) 1 (0–4) 123 (110–150) 75 (60–85) 38.9 (37.4–41.5) 3300 (2690–4110) 46 (7–88) FGR 12 28.5 (22–37) 3.5 (1–5) 1 (0–4) 120 (115–140) 81 (70–90) 37.9 (29.8–39.0) a 2460 (745–2860) b 3 (0–5) b. Demographic and clinical details are given for NP women and women whose pregnancies were complicated by FGR. All data are median with range in parentheses for maternal age at delivery, gravidity, parity, maximum attained blood pressure (BP), gestation at delivery, birthweight, and IBR. Groups were compared statistically using the Mann-Whitney U test.

NP 27 30 (19–40) 2 (1–5) 1 (0–4) 123 (110–150) 75 (60–85) 38.9 (37.4–41.5) 3300 (2690–4110) 46 (7–88) FGR 12 28.5 (22–37) 3.5 (1–5) 1 (0–4) 120 (115–140) 81 (70–90) 37.9 (29.8–39.0) a 2460 (745–2860) b 3 (0–5) b.

NP 27 30 (19–40) 2 (1–5) 1 (0–4) 123 (110–150) 75 (60–85) 38.9 (37.4–41.5) 3300 (2690–4110) 46 (7–88) FGR 12 28.5 (22–37) 3.5 (1–5) 1 (0–4) 120 (115–140) 81 (70–90) 37.9 (29.8–39.0) a 2460 (745–2860) b 3 (0–5) b.