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Review ofLiterature and is considered to be a growth factor' which in turn can generate reactive oxygen species (Meier et al., 1989) and this can eventually lead to imbalance of PGh and TXA2 as stated above . The fourth is lipoxygenase products that have been suggested to suppress PGI2 synthesis and are known to be increased in P.l.H. Both PGh and TxA2 are derived from arachidonic acid through the action of cyclooxygenase. If the serum factor(s) described affect this special enzyme the production of PGh and TxA2 should be equally affected . However, the serum from P.E.T. women with proteinuria show only 'significant increased TxA2 synthesis' and has little effect on PGh formation. Therefore the reaction by this serum factor(s) may be located on the levels of TXA2 and PGh synthetase rather on the level of cyclooxygenase (Satoh et al., 1991). At least two vasoconstrictor mechanisms may be operative III preeclamptic women in whom arachidonic acid is converted by cyclooygenase into thromboxane A2with an accompanying reduction of prostacyclin and prostaglandin E2as evidenced by Cattela et al., (1990); Mitchell and Koenig, (1991) and Tannirandom et al., (1991). This pathway is responsive to low dose aspirin therapy. The second route is via lipoxygenase pathway, which results in an increased placental production of 15-hydroxy-eicosa-tetra-enoic acid. This inhibits prostacyclin production, resulting in further vasoconstriction (Mitchell and Koenig, 1991) In conclusion, it has been shown that there is an imbalance between PGh and TXA2 production in peripheral blood mononuclear cells from patients with P.E.T., and a factor (s) was discovered especially in those with proteinuria and found to contribute at least in part to the abnornral production ofPGs however-the nature ofthis serum factor(s) is not yet fully understood (Gong et al., 1993). 15
(5) Nitric oxide in P.tH. : Review ofLiterature The role of nitric oxide-endothelium derived relaxing factor or its endothelial loss is unclear in P.I.H. , but experimental studies have proved that withdrawal ofnitric oxide from pregnant rats and guinea pigs resulted in the development ofa clinical picture similar to preeclampsia (Weiner et al., 1989). Nitric oxide appears to be important in the maintenance ofa low fetal vascular resistance in the placental circulation (Myatt et al., 1991). Fiona et al., (1996) found that. there were no significant differences in maternal serum nitrites concentrations between P.I.H. women and control group, but significant high serum nitrites concentrations were found in the umbilical venous serum in fetuses of P.I.H. group compared to control group. This increased nitrites concentration in fetoplacental circulation in P.I.H. group may support the hypothesis that, it may be compensatory response to improve blood flow or may playa role in limiting platelets adhesion and aggregation. Decreased nitric oxide release or production has not been shown to develop prior to the onset ofhypertension .. Thus, changes in nitric oxide release and concentrations in women with pregnancy induced hypertension appear to be the consequence ofhypertension and not the inciting event (Morns et al., 1996). (6) Hyperplacentosis : It was found that hyperplacentosis is a major factor influencing the development of pre eclampsia and this may occur in diabetes mellitus, multiple pregnancy, molar pregnancy and erythroblastosis fetalis (Walker and Gant, 1997). 16 .. .'T
- Page 3 and 4: ACKNOWLEDGMENT Above all and first
- Page 5: List of Abbreviations : Apolipoprot
- Page 8 and 9: INTRODUCTION AND AIM OF THE WORK
- Page 10 and 11: Aim of The Work Aim ofthe work Is t
- Page 12 and 13: I . HYPERTENSIVE DISORDERS IN PREGN
- Page 15: -f Etiology of Preeclampsia Review
- Page 18 and 19: Pathogenesis of pre- eclampsia Revi
- Page 20 and 21: -.-- Review ofLiterature Changes in
- Page 22 and 23: --f' -,- Review ofLiterature clinic
- Page 27 and 28: Review ofLiterature next pregnancy
- Page 29 and 30: Review ofLiterature On the other ha
- Page 31 and 32: Review ofLiterature which is define
- Page 34 and 35: 1. Gestational hypertension (withou
- Page 36: Review ofLiterature However, severe
- Page 40 and 41: Review ofLiterature It is an indica
- Page 42: Review ofLiterature above hemodynam
- Page 45: Review ofLiterature patients (Nahee
- Page 49: Proteinuria and microalbuminuria :
- Page 55: Review ofLiterature peptides includ
- Page 58 and 59: .... -,:-" Review ofLiterature a. T
- Page 60 and 61: .... 'I, - 2. Occular complications
- Page 62 and 63: ,- - 6. HELLP syndrome: ReviewofLit
- Page 64 and 65: II. Maternal mortality: Review ofLi
- Page 66: Review ofLiterature Management of p
- Page 70 and 71: i- Review ofLiterature 5. High dens
- Page 73 and 74: unesterified Apoliporobein choleste
(5) Nitric oxide in P.tH. :<br />
Review ofLiterature<br />
The role of nitric oxide-endothelium derived relaxing factor or its<br />
endothelial loss is unclear in P.I.H. , but experimental studies have<br />
proved that withdrawal ofnitric oxide from pregnant rats and guinea pigs<br />
resulted in the development ofa clinical picture similar to preeclampsia<br />
(Weiner et al., 1989). Nitric oxide appears to be important in the<br />
maintenance ofa low fetal vascular resistance in the placental circulation<br />
(Myatt et al., 1991).<br />
Fiona et al., (1996) found that. there were no significant<br />
differences in maternal serum nitrites concentrations between P.I.H.<br />
women and control group, but significant high serum nitrites<br />
concentrations were found in the umbilical venous serum in fetuses of<br />
P.I.H. group compared to control group. This increased nitrites<br />
concentration in fetoplacental circulation in P.I.H. group may support the<br />
hypothesis that, it may be compensatory response to improve blood flow<br />
or may playa role in limiting platelets adhesion and aggregation.<br />
Decreased nitric oxide release or production has not been shown to<br />
develop prior to the onset ofhypertension .. Thus, changes in nitric oxide<br />
release and concentrations in women with pregnancy induced<br />
hypertension appear to be the consequence ofhypertension and not the<br />
inciting event (Morns et al., 1996).<br />
(6) Hyperplacentosis :<br />
It was found that hyperplacentosis is a major factor influencing the<br />
development of pre eclampsia and this may occur in diabetes mellitus,<br />
multiple pregnancy, molar pregnancy and erythroblastosis fetalis<br />
(Walker and Gant, 1997).<br />
16<br />
.. .'T
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