A study evaluated the effect of Sildenafil ( Viagra ) in hypertensive pregnancy.
Results of this experimental study seem to indicate possible utility of Sildenafil in preeclampsia.

Although Viagra didn’t lower mothers’ blood pressure, it did produce some very significant and beneficial effects on pregnancy-induced vascular adaptation and fetal outcome.

The research was performed by George Osol et coll , Department of Obstetrics and Gynecology, University of Vermont College of Medicine.

The study was presented at the 35th Congress of the International Union of Physiological Sciences in San Diego.

Osol said that when given to pregnant rats with induced hypertension, Sildenafil:

- helped arteries of the uterus grow as they should during pregnancy.
Hypertension decreases the growth and alters contractility of blood vessels in the uterus, but giving Sildenafil reversed these effects, resulting in improved function of the uterine circulation.
Arterial diameters of Sildenafil-treated animals were significantly larger than those with hypertension, suggesting that it may have increased blood flow to the uterus and placenta.

- increased fetal weights to normal values, compared with untreated hypertensive offspring whose weights were reduced by more than 20%.
This observation also supports an effect on uterine blood flow since it well known that restriction of uterine blood flow during pregnancy is associated with reduced fetal weight.

- completely prevented fetal resorption, or fetal mortality.
Whereas 11% of fetuses were lost in the hypertensive group, none were lost in the group that received Sildenafil, even though they were still hypertensive,

The findings suggest that Sildenafil ( or other drugs that inhibit PDE-5, the enzyme that normally inhibits blood vessels’ ability to expand ) may have beneficial effects in hypertensive pregnancy and, possibly, preeclampsia.
It is also intriguing that the benefits of Sildenafil were observed without any reduction in maternal blood pressure, thereby dissociating hypertension per se from the loss of NO ( nitrous oxide ) signaling in the uterine circulation.

Source: American Physiological Society, 2005


XagenaMedicine2005