Browsing by Author "Salas, SP"

Now showing 1 - 4 of 4
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    Maternal factors modulate the increase in vasoactive substances during rat pregnancy
    (MARCEL DEKKER INC, 1999) Giacaman, A; Salas, SP; Rosso, P
    Objective: To explore if the changes in vasoactive substances observed during early pregnancy in the rat are modulated by maternal or fetoplacental factors.
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    Plasma volume, renal function, and hormonal levels in pregnant women with idiopathic fetal growth restriction or preeclampsia
    (1998) Salas, SP; Rosso, P
    Objective: To compare changes in maternal plasma volume, renal function, and several hormones related to volume regulation in pregnant women with idiopathic fetal growth restriction (FGR), mild preeclampsia (PE), and matched controls.
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    Role of nitric oxide in maternal hemodynamics and hormonal changes in pregnant rats
    (SOCIEDAD BIOLGIA CHILE, 1998) Salas, SP
    Normal pregnancy is characterized by a significant reduction in total peripheral vascular resistance and decreased presser responsiveness to vasodilator agents. This review will consider whether nitric oxide (NO) contributes to these changes, and whether a deficiency of NO produces a pre-eclampsia bike syndrome. The biosynthesis of NO increases in pregnant animals, as assessed by the raised plasma concentration, urinary excretion and metabolic production rate of guanosine 3',5'-cyclic monophosphate (cGMP), the second messenger of NO. In addition urinary excretion of nitrate, the stable metabolites of NO, increases during pregnancy, paralleling the rise in cGMP. Several studies provide convincing evidence indicating that expression and activity of different NO synthases (NOS) are increased in gravid animals. Acute blockade of NOS causes a dose response increase in blood pressure and reverses the blunted vasopressor response to vasoconstrictor agents. Long-term NOS inhibition produces a pre-eclampsia like syndrome, characterized by maternal hypertension, proteinuria, thrombocytopenia, and renal damage, and lower Litter size and fetal weight. Both acute and chronic responses are reduced when L-arginine, the substrate for NOS, is administered in high doses, indicating that these changes are specific to NO inhibition. In conclusion, present data suggest that a disturbance in NO release may contribute to the pathogenesis of preeclampsia.
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    What causes pre-eclampsia?
    (BAILLIERE TINDALL, 1999) Salas, SP
    Pre-eclampsia remains a leading cause of maternal and fetal morbidity and mortality. Despite extensive research, the mechanisms that cause pre-eclampsia are unknown and it has been considered to be. the 'disease of theories'. Hippocrates wrote in one of his Aphorisms that 'convulsions take place from either repletion or depletion'. Since then, obstetricians have been divided on the question of which factor accounted for the convulsions observed during childbirth. Some considered that a sudden reduction in intraabdominal pressure at delivery led to a pooling of blood diverted from the brain, causing collapse of the cerebral blood vessels and convulsions. Others postulated that cerebral congestion, secondary to compression of the abdominal organs by the large uterus, diverted blood to the brain, causing eclamptic convulsions. it is the purpose of this review to examine those theories about the cause of pre-eclampsia for which modern evidence is available. At present, it is believed that the pathological chain of events leading to preeclampsia is scheduled in two steps: an absolute or relative placental ischaemia is followed by a diffuse endothelial cell activation, which causes the clinical features of the disease.