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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Pregnancy-induced hypertension (or pre-eclampsia) is characterized by vasoconstriction, platelet aggregation and altered capillary permeability, implying disordered endothelial function and/or structure. Serum from women with pregnancy-induced hypertension has been reported by others to be cytotoxic to endothelial cells in vitro. We hypothesized that such serum contains a factor that limits the ability of endothelial cells to produce and/or release prostacyclin. 2. Prostacyclin production by intact and damaged cultured human umbilical vein endothelial cells was measured after incubating these cells with serum from non-pregnant and normal pregnant women and women with pregnancy-induced hypertension. Confluent human umbilical vein endothelial cell monolayers (intact and damaged) were incubated with sera for 24 h at 37 degrees C followed by 1 h of incubation with added thrombin (stimulated production) or media (basal production). Supernatants were then collected for measurement of 6-keto-prostaglandin F1 alpha by radioimmunoassay. 3. Basal production of 6-keto-prostaglandin F1 alpha was greater in response to serum from non-pregnant women than to that from pregnant women. Within each group, sub-lethally damaged cells had a similar basal production of 6-keto-prostaglandin F1 alpha to that of intact cells. 4. Basal production of 6-keto-prostaglandin F1 alpha by intact or damaged cells incubated with sera from normal pregnant women and from women with pregnancy-induced hypertension was similar. 5. In all groups the addition of thrombin to intact endothelial cells increased 6-keto-prostaglandin F1 alpha production approximately 15-30-fold over basal levels, but only three- to five-fold in damaged endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelium-derived prostacyclin: effect of serum from women with normal and hypertensive pregnancy. 131 48

A defect of placenta maturation has been described in hypertension of pregnancy. Plasma beta chorionic gonadotropins (beta HCG) of placental origin rise at the onset of pregnancy and reach a peak between 9 and 10 weeks of amenorrhoea. As we were making systematic assays between 14 and 20 weeks in a trisomy detection programme, we looked for differences in plasma beta HCG levels between women with pregnancy-induced arterial hypertension and pregnant women with normal blood pressure. We also studied the predictive value of such assays. Pregnancy-induced hypertension was found in 6 women in a population of 89 nulliparas and in 12 women in a population of 163 multiparas. beta HCG levels were significantly higher in women who later developed hypertension among both nulliparas (52,833 +/- 19,538 IU vs 24,499 +/- 16,485 IU) and multiparas (50,558 +/- 23,597 IU vs 20,911 +/- 11,677 IU). In nulliparas, taking 43,000 IU as threshold of pathology we found that the predictive value of beta HCG was higher than that of other tests which had gone through controlled studies (sensitivity 67 percent, specificity 91.6 percent, positive predictive value 36 percent, negative predictive value 97.4 percent, relative risk 5.4). In multiparas, taking 38,000 as threshold and combining this marker with obstetrical history it was possible to predict the occurrence of hypertension more precisely than with other markers which had gone through controlled studies (sensitivity 66.7 percent, specificity 98 percent, positive predictive value 61.4 percent, negative predictive value 97.3 percent, relative risk 8.4).
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PMID:[Plasma beta chorionic gonadotropin between 14 and 20 weeks of amenorrhea: a sign of pregnancy-related hypertension]. 145 78

Gestational hypertension is the development of hypertension and proteinuria after the 20th week of gestation. The most common causes of increased peripheral resistance are the vasoconstriction and hemoconcentration with plasma volume contraction. Additional rheological parameters are an elevated red blood cell aggregation and impaired erythrocyte deformability. Preeclamptic patients showed a significantly low cardiac output and central venous pressure than normal pregnant women. It has already been shown by the studies by Hytten and Paintin (1963) and also by the subsequent studies by Garn et al. (1981), Murphy et al. (1986) that a strong correlation exists between newborn weight and plasma volume. Other authors (Gallery et al. (1979/1981)) show the possibility that plasma volume contraction plays an even larger role than vasoconstriction in the fetal growth retardation that often accompanies maternal hypertension. This possibility is supported by the finding that hypertension and perinatal complications can be reduced in some pregnant women by the admission of oncotic solutions (i.e. hydroxyethyl-starch) that expand plasma volume. Volume expansion with hydroxyethyl-starch appears to be of therapeutic benefit for hypertensive patients and patients with fetal growth retardation with low cardiac output.
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PMID:[Rheology and gravidic hypertension]. 172 87

Pregnancy-induced hypertension is a disorder of unknown etiology unique to pregnant women. Classic clinical manifestations include hypertension, proteinuria, and edema. Early recognition and proper management of this disease may serve to avoid serious maternal complications. Ultimate maternal treatment depends on delivery of the fetus and placenta. Advanced stages of this disease result in multi-organ system dysfunction that may be life-threatening to the mother and her fetus. Such maternal complications of PIH include severe hypertension, oliguria or anuria, HELLP syndrome, eclamptic seizures, liver rupture, pulmonary edema, cerebral edema, and abruptio placentae. A multidisciplinary approach of the critical care team often will effect a reduction in maternal morbidity and mortality.
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PMID:Management of severe preeclampsia and eclampsia. 174 3

Pregnancy-induced hypertension (PIH) still remains an area in obstetrics of active research and investigation. Despite widespread academic attention, the cause of this disorder still remains unknown. The purpose of this paper is to review the important contributions to the literature during the period of July, 1990 through June, 1991. Elucidation of the pathophysiology of PIH has been enhanced by investigations of altered platelet calcium metabolism, the renin-aldosterone-angiotensin system, and other potent vasopressors. Recent reports of clinical management for eclampsia, liver rupture, HELLP syndrome, severe PIH in the second trimester, severe hypertension, and magnesium toxicity are presented.
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PMID:Recent developments in pregnancy-induced hypertension. 181 15

An epidemiological investigation of Pregnancy Induced Hypertension (PIH) in a population of 3.7 millions in China is reported in this paper. The incidence of PIH was 9.4%; that of mild moderate-PIH, pre-eclampsia, eclampsia and chronic hypertension with PIH were 4.7, 2.6, 1.7, 0.2 and 0.2% respectively. The maternal and perinatal mortality of PIH groups were higher than the group without PIH (P less than 0.01). Our results revealed that pathogenesis of PIH was positively related to age. Primiparity, multiple pregnancy, labour posture during pregnancy, physical labor intensity, maternal education level, body status, heredity and various complications during pregnancy.
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PMID:[National epidemiological investigation of pregnancy induced-hypertension]. 186 Mar 67

Pregnancy-induced hypertension is associated with a reduction in prostacyclin synthesis that is relative to normotensive pregnancy, whereas thromboxane A2 synthesis is unchanged or increased. The net effect is a decreased prostacyclin/thromboxane ratio that may result in the reduced fetal-placental blood flow seen in pregnancy-induced hypertension because thromboxane is known to constrict this circulation. Low-dose aspirin (acetylsalicylic acid), which is used to treat pregnancy-induced hypertension, selectively inhibits thromboxane synthesis and therefore may alter fetal-placental blood flow. We have investigated the transfer of acetylsalicylic acid in the perfused human placental cotyledon and its effects on fetal-placental perfusion pressure. Human placental cotyledons were perfused with tissue culture medium 199 plus 5% polyvinylpyrrolidone that was gassed with 95% oxygen/5% carbon dioxide at flow rates of 10 ml/min (maternal) and 4 ml/min (fetal). Acetylsalicylic acid (10(-5) mol/L) was added to the maternal circuit, and cotyledons were perfused for 1 hour with aliquots taken from a closed fetal circuit every 5 minutes. Acetylsalicylic acid was assayed by spectrofluorometry at 306/412 nm. Our data indicate an initial rapid transfer of acetylsalicylic acid during the first 5 minutes into the fetal-placental circulation, the concentration then decreased to a steady state at 0.4 x 10(-5) mol/L. Resting perfusion pressure of both maternal and fetal circulation did not change after the addition of acetylsalicylic acid to maternal perfusate and transfer to the fetal circulation.
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PMID:Transfer of aspirin across the perfused human placental cotyledon. 195 59

Insulin-dependent diabetic patients are at increased risk for hypertensive disorders of pregnancy. This study was designed to study prospectively the rate of pregnancy-induced hypertension (PIH) in 175 insulin-dependent diabetic pregnancies (88 White classes B-C, 87 classes D-RT). Pregnancy-induced hypertension was defined as two or more occurrences after 20 weeks' gestation of a mean arterial pressure (MAP) of 105 mmHg or greater or an increase of 20 mmHg or greater from the baseline MAP. The rate of PIH in the diabetic population was 15.4% and was significantly associated with nulliparity, poor glycemic control in the first and second trimesters, and advanced White class. Neonatal outcome was not significantly altered in the presence of PIH. We speculate that improved glycemic control throughout pregnancy might reduce the rate of this complication in diabetic patients.
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PMID:Hypertension during pregnancy in insulin-dependent diabetic women. 200 72

Forty-three pregnancies that were complicated by pregnancy-induced hypertension and either absence of umbilical artery end-diastolic frequencies (n = 32) or reversal of umbilical artery end-diastolic frequencies (n = 11) were reviewed. The incidence of perinatal mortality and morbidity was similar for the two Doppler patterns. Perinatal survival was highly dependent on the gestational age when hypertension first appeared. Presentation at greater than or equal to 30 weeks' gestation was associated with a perinatal survival rate of 86%. Presentation at less than 30 weeks' gestation was associated with a perinatal survival rate of 38% (p less than 0.005). Pregnancy-induced hypertension that presented before 30 weeks was more often associated with a 5-minute Apgar score less than 7 (p less than 0.005) and a nonreactive nonstress test (p less than 0.05) compared with pregnancy-induced hypertension that presented at or beyond 30 weeks. For pregnancies that presented before 30 weeks, the only difference between perinatal survivors (n = 11) and perinatal deaths (n = 18) was a higher incidence of birth weight at or below the 10th percentile among deaths (p = 0.02).
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PMID:Determinants of perinatal outcome in pregnancy-induced hypertension with absence of umbilical artery end-diastolic frequencies. 201 30

Plasma lipoprotein, cholesterol and triglycerides were determined in 34 hypertensive pregnant patients and in 17 healthy full term pregnant women. Pregnancy induced hypertension was diagnosed in 21 patients and chronic hypertension in the remaining 13 women. Serum triglyceride levels were significantly elevated in the hypertensive patients. This elevation was not influenced by either the severity or the etiology of the hypertension. The total cholesterol/HDL and the LDL/HDL ratios were significantly elevated in the severely hypertensive patients, and furthermore the LDL/HDL ratio was elevated in patients receiving anti-hypertensive treatment. The lipid profiles found in hypertensive pregnant patients could be associated with enhancement of pathological lipid deposition in predisposed vessels such as the uterine spiral arteries. Furthermore, the hypertriglyceridemia found in the hypertensive patients may be associated with the hypercoagulability reported in pregnancy induced hypertension.
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PMID:Maternal serum lipid profile in pregnancies complicated by hypertensive disorders. 209 40


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