الفهرس 
Pregnancy Induced HypertensionOnly 14 pages are availabe for public view
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Abstract
Hypertensive disorders complicating pregnancy are common and
form one of the great triad, along with hemorrhage and infection, that
continues to be responsible for large number of maternal death
(Roberts, et al, 1989). It is a multlfacted syndrome with variable
involvement of several organ system. The classic triad of hypertension,
edema and proteinuria is stlll the most common presentation (Entmar,
1983).
Most investigative efforts have focused on the hypertensive
component of this disorder with reduced attention given to other equally
important characteristics. Many studies indicate that pathologic and
pathophysiologic changes in preeclamptic women are not secondary to
increased blood pressure (Chesley 1978; Reberts, et al., 1989).
Theories about pathophysiologic changes as activation of the
coagulation cascade, increased sensitivity to pressors; reduced plasma
volume, and abnormalities of renal proximal tubular function, all
antedate increased blood pressure (Roberts, et al., 1989).
One of such theories explained the physiologic abnormalities of
preeclampsia by dysfunction of vascular endothelial cells (Roberts, et al
1989).
Hubel, et al. (1989) have suggested that lipoperoxide levels in
patients with preeclampsia increase beyond normal pregnancy levels
and there is conflicting evidence regarding the role of the reduced
uteroplacental perfusion which intensifies the release of placental lipid
peroxidation products into the circulation. Upid peroxides are highly reactive and very damaging compounds. They are very toxic to enzymes.
cells, and proteins (Mead, et al., 1986, Hennig et al., 1988). Although
they affect many cellular components, the primary sites involve
membrane associated polyunsaturated fatty acids and protein thiols.
(Freeman and Crapo, 1982).
In view of its potentially destructive character, uncontrolled lipid
peroxidation has been suggested as an etiologic factor in preeclampsia
(Roberts et al., 1989). Impaired function of the vascular endothelium
may, in turn, cause vasospasm, the general increase in sensitivity to
vasopressors, and associated cardiovascular complications occurring in
the disease (Rodegers et al., 1988).
Antioxidant mechanisms normally control lipid peroxidation and
protect against its propagation. Deficiency of physiological free radical
scavengers such as vitamin E, Selenium, glutathione and uric acid,
causes oxidative stress With resultant overwhelming peroxidation
process. (Warso and Lands, 1985).
The placenta is a rich source of polyunsaturated fatty acids .
(Ogburn et al., 1988), so the combination of increased oxygen radicals
generated from thromboxane production With the high placental content
of fatty acids would result in increased placental formation of lipid
peroxides. Placental lipid peroxides apparently contribute to maternal
circulating levels because plasma lipid peroxide levels decrease
precipitately after delivery (Wickens et al., 1981). The placental tissue actively transports a small quantity of lipid by
pinocytosis from the maternal blood to the cord blood and at the
sametlme, it is possible that superoxide and lipoperoxides also reach
the fetal tissue and affect its development (Yamaguchi et al., 1964).
Yoshioka, et al., 1987, reported that maternal , fetal and placental
levels of lipoperoxides and antioxidant change during pregnancy.
Takehara et al ( 1990) confmned that the lipoperoxide concentration
in blood of pregnant women increased as gestation progressed, but it
was kept lower in the cord blood than in the maternal blood.
Diamant et al. (1980) suggested that the placental tissue supresses
lipoperoxide formation and protects the fetus from any kinds of
radicals. Yoshioka et al., (1979) observed that antioxidant activity was
higher in the maternal blood than the cord blood, however the
difference was not statistically significant.