Maternal hypertension

Hoder et al. (1984) studied clonidine in seven newborn infants with neonatal narcotic abstinence syndrome and found no significant changes in blood pressure, pulse, or electrocardiograms (EKG) in any of the seven infants. One infant had a transient abnormal eye exam and two infants developed a transient mild metabolic acidosis. On follow up 4-9 months later, four infants were found to be developmentally age appropriate. However, Huisjes et al. (1986) reported that 22 children exposed in utero to clonidine as result of treatment for maternal hypertension had increased sleep disturbances and hyperactivity, compared to a control group at a mean age of 6 years. It is unclear whether these differences were a direct effect of clonidine on prenatal development. More sophisticated preclinical studies need to be done in this area. At best the level of short-term and long-term safety regarding clonidine is level C. 

The rate of pregnancy induction ranges from 9.5% to 33.5%. The most common reason for induction is postdatism (>42 weeks), which occurs in 10% of all pregnancies. Other reasons for induction include suspected fetal growth retardation, maternal hypertension, premature rupture of membranes with no active onset of labor, or social factors. Contraindications for induction include placenta previa, oblique or transverse lie, pelvic structure abnormality, prolapsed umbilical cord, and active herpes. The concerns associated with induction of labor are that the labor may be ineffective or that side effects such as uterine hyperstimulation may adversely affect the infant, increasing the likelihood of cesarean section. 

There have been few studies on the fetal toxicity of Cd transported across the placenta, which acts as a barrier to Cd. Nevertheless, a small amount may reach the fetus. Cd is also transferred to neonates through lactation. Maternal hypertension and decrease in birth weight have been associated with elevated levels of Cd in the neonate [155]. A depletion of zinc with increasing number of births and a progressive increase in Cd in smokers negatively affect infant birth weight [156]. Moreover, Marlowe et al. [157] found an association between mental retardation and raised concentrations of Cd in hair in school age children. But overall, there is no substantial evidence that Cd has caused teratogenic effects in humans. 

Maternal grandparents, living, ages 73 and 84 hypertension, osteoarthritis... 

Blood pressure effect. Fruit juice, administered intravenously hy infusion to dogs at a dose of 3 mL/minute for 100 minutes, was active. Initial effect was a decrease in hlood pressure . Oil, administered to male weanling rats at a dose of 10% of diet for 5 weeks, produced significantly higher hlood pressure than other groups. Systolic hlood pressure was found related to the dietary intakes of saturated and unsaturated fatty acids. Prenatal exposure of the rats to a maternal low-protein diet abolished the hypertensive effect of the coconut oil dieH . Butyryl cholinesterase activity. Oil was administered to rats at different doses with or without clofibrate for 15 days. The hypolipidemic action of clofibrate was not... 

The human reproductive process does not fit perfectly into the animal model of reproductive and developmental toxicity. Conditions of the fetal-maternal unit that affect both mother and child have not been adequately addressed in this monograph, although there is some evidence that some of these adverse outcomes, such as pregnancy-induced hypertension, may be related to environmental exposure (Tabacova et al., 1998 Dawson et al., 1999). This is a promising frontier for new research. We have also not dealt with genetic susceptibility to developmental toxicants. Advances in this field may illuminate many of the mysteries of how toxicants act, and on whom. Limited data are available on mechanisms of action (see section 5.2.4). The work on oxidative stress in pregnancy (Tabacova et al., 1998 Hubei,... 

Subsequently, the addition of protirelin to glucocorticoid therapy was the subject of a meta-analysis (7). In 1134 premature infants the serum TSH concentration was increased for the first 6 hours after the last maternal dose of protirelin, then suppressed for 36 hours before returning to control values (8). The largest controlled trial (in 1368 infants) reported a small delay in development at 12 months (5). However, developmental assessment was by questionnaire, with incomplete ascertainment, and these findings have been questioned (6). In the mothers, there was a three-fold increase in nausea, vomiting, or flushing and a two-fold increase in hypertension compared with glucocorticoid therapy alone. 

When oxytocin is used properly, serious toxicity is rare. Among the reported adverse reactions are maternal deaths due to hypertensive episodes, uterine rupture, water intoxication, and fetal deaths. Afibrinogenemia has also been reported. 

Manchester D, Margolis HS, Sheldon RE. Possible association between maternal indomethacin therapy and primary pulmonary hypertension of the newborn. Am J Obstet Gynecol 1976 126(4) 467-9. 

Wilkinson AR, Aynsley-Green A, Mitchell MD. Persistent pulmonary hypertension and abnormal prostaglandin E levels in preterm infants after maternal treatment with naproxen. Arch Dis Child 1979 54(12) 942-5. 

When ritodrine is used to alleviate fetal distress and surgical intervention (cesarean section), atropine premedication must be avoided. The vagolytic action of atropine is synergistic with the action of ritodrine, resulting in severe maternal tachycardia and systohc hypertension (6). 

Serum urate is of value in the monitoring of maternal well-being in pregnancy associated hypertension (pre-cclamp-sia), alongside other markers such as blood pressure, urine protein excretion and creatinine clearance (p. 143). 

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