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

Hypertension in the nonpregnant and pregnant nonhuman primate is not found frequently by research investigators. Its incidence is probably infrequent. No well-defined clinical syndrome analogous to toxemia of human pregnancy has been described. The experimental induction of the disease in pregnant nonhuman primates has been difficult. Although there would be an important role for such an animal model, its discovery does not appear imminent.
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PMID:Nonhuman primate models of toxemia of pregnancy. 100 53

The first reported measurement of plasma renin and aldosterone in toxemia with an abdominal pregnancy is presented. In contrast to toxemia where plasma renin and aldosterone are either normal or low, extraordinarily high levels of both were found in this patient which returned to normal after delivery. The role of extrarenal renin in the hypertension of toxemia is discussed and the possibility raised that the elevated renin in this case was of placental origin.
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PMID:Plasma renin and aldosterone in an abdominal pregnancy with toxemia. 114 20

One hundred fifty-seven pregnancies complicated by different degrees of diabetes, toxemia, and hypertension were studied with serial urinary placental estrogen determinations. A simple and fast method for total placental estrogen determination was used. The level of total estrogen excretion was related to Apgar score in cases of class B diabetes, severe toxemia, and also in moderate toxemia when estrogen excretion was falling. Mean estrogen levels did not differ as a function of severity of diabetes. Levels did differ with severity of toxemia; however, only the difference in mean estrogen excretion between mild and severe toxemia was significant. Estrogen excretion was very low in hypertension but was not related to Apgar score. This study concludes that total urinary estrogens constitute only a single parameter necessary in the management of high-risk pregnancies.
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PMID:Total urinary estrogens in complicated pregnancies. 116 30

Experimental toxemia of pregnancy was induced in 51 of 122 rabbits by constriction of the aorta below the renal arteries. The approach was extraperitoneal and dependent on the accuracy in calibrating this stricture between 0.6 and 1.0 mm. Experimental toxemia in the rabbit was characterized by hypertension, proteinuria, weight gain, and reduced weight of the fetus. Blood pressure and blood flow studies distal to the aortic constriction demonstrated a marked diminution of blood supply below the constriction. The light microscopic changes in the kidneys and in the liver were similar to those of human toxemia. The electron microscopic changes consisted of endothelial swelling and subendothelial deposits. In a separate experiment, 22 pregnant rabbits near term had an aortic constriction varying between 0.6 and 1.0 mm. This constriction lasted 4 to 12 days. Glomerular deposits of fibrinogen were demonstrated by immunofluorescence in 20 of 22 animals. The intensity of the immunofluorescence was related to the severity and duration of the aortic stricture.
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PMID:Production of experimental toxemia in the pregnant rabbit. 125 1

The criteria for pregnancy induced hypertension (PIH: hypertensive type of toxemia) have been determined by the Japanese Obstetrics and Gynecology Society. Mild PIH is classified into two types. One is "Absolute PIH (A-PIH)" diagnosed by (1) systolic blood pressure (SBP) greater than or equal to 140 mmHg and less than 160 mmHg or (2) diastolic blood pressure (DBP) greater than or equal to 90 mmHg and less than 110 mmHg. The other one is "relative-PIH (R-PIH)" diagnosed by (3) an increase in SBP greater than or equal to 30 mmHg compared to the usual SBP or (4) an increase in DBP greater than or equal to 15 mmHg compared to the usual DBP (In this paper, blood pressure prior to the 12th gestational week is considered as "usual" blood pressure). However, there has been no report in which two types of PIH are assessed. Our hypothesis is that the pathophysiology of the two types of PIH is different. We have already reported the clinical background of two types of PIH. The purpose of this study is to clarify the pathophysiological difference by evaluating the blood pressure change during pregnancy. We evaluated 963 nullipara and 747 multipara whose pregnancies were recorded from the 1st trimester (multiple pregnancy and pre-term delivery before the 32nd gestational week were excluded). Among the nullipara, 765 women (79.4%) were diagnosed as having normal blood pressure (N-group), 7.1% as A-PIH, and 13.0% as R-PIH. Among the multipara, the N-group consisted of 632 women (84.6%), the A-PIH: 4.6% and R-PIH: 10.3%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in blood pressure in two types (absolute and relative) of pregnancy induced hypertension (hypertensive type of toxemia)]. 160 50

The criteria for pregnancy induced hypertension ("PIH" which is a hypertensive type of toxemia) have been determined by the Japanese Obstetrics and Gynecology Society. Mild PIH is classified into two types. One is "Absolute PIH (A-PIH)" diagnosed by (1) systolic blood pressure (SBP) greater than or equal to 140 mmHg and less than 160 mmHg or (2) diastolic blood pressure (DBP) greater than or equal to 90 mmHg and less than 110 mmHg. The other one is "relative-PIH (R-PIH)" diagnosed by (3) an increase in SBP greater than or equal to 30 mmHg compared to usual SBP or (4) an increase in DBP greater than or equal to 15 mmHg compared to usual DBP (In this paper, blood pressure prior to the 12th gestational week is considered as "usual" blood pressure). We have already investigated the pathophysiological difference through the background and the change in blood pressure throughout pregnancy and puerperium in these two types of PIH. The purpose of this study is to clarify the pathophysiological difference by evaluating the influence of hypertension on fetal growth. We evaluated 963 nullipara and 747 multipara whose pregnancies were recorded from the 1st trimester (multiple pregnancy and pre-term delivery before the 32nd gestational week were excluded). Among nullipara, 765 women (79.4%) were diagnosed as having normal blood pressure (N-group), 7.1% as A-PIH, and 13.0% as R-PIH. Among multipara, the N-group consisted of 632 women (84.6%), A-PIH: 4.6% and R-PIH: 10.3%. There is no difference among the three groups in gestational days but the body weight, the chest circumference, and the abdominal girth at birth of A-PIH show a significant difference from those of the R-PIH and N-groups in both nullipara and multipara.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fetal growth in two types (absolute and relative) of pregnancy induced hypertension (hypertensive type of toxemia)]. 160 51

A retrospective study in two university hospitals investigating retinal changes in pregnancies complicated by hypertension, seldom revealed retinal vascular changes in pre-eclamptic toxemia. Fluorescein angiography was performed on 16 severe pre-eclamptic toxemias and 14 chronic hypertension pregnancies. Normal caliber retinal vessels and normal filling time, with no subretinal or subepithelium leakage, was found in all pre-eclamptic toxemic patients. Four out of the 14 chronic hypertensive patients showed signs of mild hypertensive retinopathy. A review of the literature on fluorescein angiography in pregnancy showed that vascular changes in pre-eclamptic toxemia are choroidal rather than retinal.
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PMID:Fluorescein angiography in hypertensive pregnancies. 167 66

A total of ten patients with lesions of neurofibromatosis during pregnancy were followed up for pregnancy complications. Seven cases (70%) had hypertensive disorders of pregnancy; four had severe PET (pre-eclamptic toxemia) including one case of eclampsia, one had mild PET and the other two had only mild gestational hypertension. A total of 60% had preterm labor and in none of these did the baby survive; thus perinatal mortality was 600/1000. Mean gestation was 33.0 weeks and mean birthweight was only 1.924 kg. Thus, neurofibromatosis during pregnancy is associated with poor obstetrical outcome and requires greater care.
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PMID:Maternal and perinatal complications in neurofibromatosis during pregnancy. 167 38

A better understanding of the hemodynamic abnormalities in gestational hypertension together with the use of effective antihypertensive agents have resulted in more rational therapeutic approaches and a substantial improvement in maternal and fetal welfare. In normal pregnancy, there is reduced vascular reactivity with peripheral pooling and decreased circulatory responses to pressor agents. These are prostacyclin-dependent processes. In gestational hypertension, the normal increase in plasma volume and cardiac output with pregnancy is attenuated and prostacyclin-dependent processes are impaired, resulting in persistent vasoconstriction, enhanced responses to pressor agonists, and failure to develop adequate uteroplacental interchange. Among the modern antihypertensive agents, alpha- and beta-adrenergic antagonists and calcium ion entry blockers have permitted safe and effective long-term blood pressure control with sustained fetal growth. The development of proteinuria that can occur in chronic hypertension or in previously normotensive women (toxemia of pregnancy) can be prevented by the use of beta-adrenergic blocking agents and possibly by low-dose aspirin (75 mg/day). Maternal prostacyclin-thromboxane imbalance, important in the pathogenesis of gestational hypertension, is corrected by low-dose aspirin treatment. With the prevention of pre-eclampsia, the adverse maternal and fetal prognosis in gestational hypertension has been improved.
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PMID:Treatment of hypertension in pregnancy. 170 7

The aim of this study was to assess any changes in cause-specific fetal death rates in the nonreferred population of a tertiary care unit. The fetal death rate (per 1000 births) among 88,651 births diminished from 11.5 in the 1960s to 5.1 in the 1980s. Fetal death due to intrapartum asphyxia and Rh isoimmunization has almost disappeared. Toxemia and diabetes continue to make similar and small contributions to fetal death rates. There has been a significant decline in unexplained antepartum fetal deaths and in those caused by fetal growth retardation, but no significant change in the death rate due to intrauterine infection or abruptio placentae. During the 1960s, the risk of fetal death was increased in women with hypertension, diabetes, or a history of stillbirth; during the 1980s, only women with a history of insulin-dependent diabetes were at risk. Improved application of current knowledge may help decrease the fetal death rate caused by fetal growth retardation. Reduction in deaths due to abruptio placentae, intrauterine infections, or lethal malformations, as well as unexplained antepartum deaths, appears to depend on better understanding of the etiology of these disorders.
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PMID:The changing pattern of fetal death, 1961-1988. 172 82


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