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

Ocular fluorophotometry was performed in 24 patients with hypertension due to toxemia of pregnancy and in ten normal subjects. Patients showing features of accelerated hypertension in the fundus (eg, hemorrhage, cotton-wool spots, and disc edema) were excluded from the study. Fluorescein concentrations in the aqueous and posterior vitreous increased significantly in toxemic patients compared with those in normal subjects; the blood-aqueous barrier was disrupted earlier than the blood-retinal barrier. Nevertheless, these barriers were only disrupted when the arterial diameter was altered. Ocular fluorometric abnormalities disappeared after delivery in all but two cases.
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PMID:Ocular fluorophotometric and angiographic findings in toxemia of pregnancy. 377 78

Peripartum heart disease is reviewed in the light of reports in the literature and personal experience from the University College Hospital, Ibadan. It is concluded that it is worldwide in distribution but appears most commonly in multiparous black women with a low socioeconomic background. The clinical features are the same as those of dilated cardiomyopathy, with the exception of cases from Zaria, northern Nigeria, where heart failure may be induced by high salt and fluid intake. The possible causes of peripartum heart disease are reviewed. Glomerulonephritis, toxemia of pregnancy, and malnutrition have not been shown convincingly to be causal, and infection, hypertension, and alcoholism have been suggested. Hypertensive heart failure and toxemia of pregnancy can induce peripartum heart disease. It is concluded that the myocardial disorder in peripartum heart disease is probably the same condition as dilated cardiomyopathy, and that infection may be an important element. However, diverse other factors may also play a part.
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PMID:Peripartum heart disease. 384 85

The 24-hour urinary excretion of kallikrein (K) and prostaglandin E2 (PGE2), which reflects their intrarenal synthesis, was measured in 7 normal women (NW), 10 women with essential hypertension (EH), 26 normal pregnant women (NP), 12 women with hypertension in pregnancy (HP), and 4 women with toxemia. All pregnant women were in the last trimester of their pregnancy (week 24-40). K was raised in NP (99.6 +/- 8.1 KU/24 h) and HP (106.5 +/- 8 KU/24 h) compared to NW (57 +/- 8.23 KU/24 h) (p less than 0.05). PGE2 excretion was decreased in EH (403.25 +/- 90.6 ng/24 h) compared to NW (508.6 +/- 80.26 ng/24 h). During pregnancy PGE2 was increased to 1,088 +/- 93.2 ng/24 h in NP and significantly more in HP, 1,885 +/- 40 ng/24 h (p less than 0.002). In this regard it differed from K. These data may suggest that, in addition to K, other factors (as angiotensin II and/or antidiuretic hormone) possibly activate renal PGE2 production in HP. In toxemia, K (23 +/- 6.1 KU/24 h) and PGE2 (583 +/- 172.83 ng/24 h) were markedly decreased. The above results suggest that the renal kallikrein-kinin and prostaglandin systems may play a role in sodium homeostasis during pregnancy. Their exact influence on the pathogenesis of hypertension in nonpregnant, pregnant, and toxemic subjects awaits further investigation.
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PMID:Urinary kallikrein in normal pregnancy, pregnancy with hypertension, and toxemia. 385

Prostacyclin is a potent vasodilator and inhibitor of platelet aggregation. Because toxemia is characterized by increased vasoconstriction frequently associated with increased platelet aggregation and reduced uteroplacental blood flow, a deficiency in prostacyclin production during pregnancy could contribute to the development of toxemia. Placentally produced prostacyclin could have both local effects on the uteroplacental vasculature and systemic effects because prostacyclin, unlike the other prostaglandins, is not extensively metabolized by the lungs. Fresh human term placentas were obtained immediately after delivery from 12 normal and 12 toxemic (blood pressure greater than or equal to 140/90 mm Hg, urinary protein greater than 0.3 gm/24 hours) pregnancies. Tissues (300 mg) were incubated in a sterile manner in 5 ml of Dulbecco's Modified Eagle's Medium for 48 hours at 37 degrees C with 95% oxygen and 5% carbon dioxide in a metabolic shaker. Samples were collected at 8, 20, 32, and 48 hours and analyzed for prostacyclin by radioimmunoassay of its stable metabolite, 6-keto-prostaglandin F1 alpha. Prostacyclin production was significantly decreased in toxemic placental tissue compared with normal placental tissue (2.72 +/- 0.49 versus 7.22 +/- 0.44 pg/mg/hr, mean +/- SE, p less than 0.01). In both normal and toxemic placentas, prostacyclin production was inhibited by indomethacin (5 or 50 mumol/L) and not affected (p greater than 0.10) by arachidonic acid (5 or 100 mumol/L). Lowering the oxygen concentration from 95% to 20% significantly (p less than 0.01) decreased prostacyclin production in normal but not toxemic placentas. Prostacyclin production rates in the amnion and chorion were not affected (p greater than 0.10) by toxemia. The amniotic and chorionic prostacyclin production rates were not different from each other (p greater than 0.10) and were only one seventh of the normal placental production rate. These data indicate that placental prostacyclin production is decreased in toxemia; therefore, this vasoactive prostaglandin may be involved in the causation and the associated hypertension and coagulation abnormalities of this disorder.
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PMID:Placental prostacyclin production in normal and toxemic pregnancies. 388 Oct 24

Vesicoureteral reflux (VUR) is mainly a primary phenomenon due to incompetence of the ureterovesical junction, mostly affecting a pediatric population. During micturition cystourethrography (MCU) reflux into the kidney--intrarenal reflux (IRR)--is occasionally seen. In areas with IRR the kidney surface may subsequently be depressed and the papillae retracted (reflux nephropathy (RN]. VUR may lead to hypertension and/or end-stage renal failure. Most commonly, VUR is discovered during evaluation for urinary tract infection, but it may also be present in patients with hypertension, toxemia of pregnancy, chronic renal failure and proteinuria, and it may be found in siblings of patients with VUR. For the time being VUR is demonstrated at radiographic MCU, whereas RN is diagnosed by demonstration of focal scars and of abnormal parenchymal thickness at urography. In children with VUR and no abnormalities of calyces or parenchymal defects standardized measurement of the parenchymal thickness at three sites may identify kidneys which are likely to develop focal scars. Quantitation of focal scarring should be performed in connection with a measure of the overall kidney size. The occurrence of IRR is dependent of the papillary morphology, intrapelvic pressure and urine flow. There may be an important relationship between renal ischemia and IRR in producing a 'vicious circle of deleterious effects' which, combined with parenchymal extravasation, may lead to RN. Treatment of VUR includes medical and surgical management. Since renal scarring may occur in infancy, prevention should focus on infants and young children. Infants and young children with severe VUR may have normal urograms. Therefore a MCU should also be performed, preferably with the recommended standardized technique.
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PMID:Vesicoureteral reflux and reflux nephropathy. 388 98

Renal transplantation is compatible with pregnancy in women under permanent dialysis, and leads to no problems for the mother or the transplant. The seven pregnancies observed in the authors' center over the past fifteen years progressed satisfactorily. There were no rejections, no cases of renal failure. In two cases, however, there was an aggravation of hypertension with acute gravidic toxemia and spontaneous abortion. The effects on the fetus of immunosuppressive drugs are difficult to evaluate; the main risk is prematurity.
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PMID:[Pregnancy in renal transplant patients]. 388 36

A 29 year-old pregnant woman with occlusive disease of the internal carotid arteries and formation of collateral networks (moyamoya disease) is reported. Because of moyamoya disease and toxemia of pregnancy, cesarean section was performed at the 38th week of pregnancy. The patient had a second intracranial hemorrhage 7 months after cesarean section. Encephalo-duro-arterio synangiosis (EDAS) was performed for the prevention of further intracranial hemorrhage and at present she is well. Since intracranial hemorrhage is sometimes associated with bearing down and since hyperventilation-induced cerebral ischemia and hypertension are provoked by active labor, elective cesarean section may be recommended for pregnant women with moyamoya disease.
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PMID:Occlusive disease of the internal carotid arteries with vascular collaterals (moyamoya disease) in pregnancy. 395 53

Forty-three patients hospitalised for chronic hypertension or superimposed toxemia in late pregnancy were treated with Dopegyt-orally in constant dosage. Blood pressure dropped at the beginning of therapy. In the further course of treatment blood pressure re-increased in 14 patients, that other antihypertensive drugs had to be administered additionally. alpha-methyldopa alone is sufficient only in a part of the hypertensive patients.
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PMID:[Effect of alpha-methyldopa (Dopegyt) on blood pressure in hypertensive pregnant patients]. 400 21

A representative sample (N = 120, 96%) of all pre-term (gestational age less than or equal to 36 weeks) infants born alive to mothers resident in the province of Kuopio, Finland, during a two year period, were studied at birth to evaluate the signs of intrauterine growth retardation (IUGR). Norms for somatic growth were based on measurements of birth weight, length and Ponderal Index (100 X birth weight (g) X birth length (cm)-3) of 51 pre-term singletons, born to healthy mothers after uncomplicated pregnancies, in relation to whom there were no discrepancies between menstrual dates and pediatric assessment of gestational age. The lower limits for normal ranges were defined as values two standard deviations below the expected means for the gestational age. Pre-term IUGR was diagnosed if birth weight and/or birth length and/or PI were more than 2 SD below the expected mean for gestational age. Different types of IUGR were found in 49 pre-term infants (41% of the pre-term population). A low PI was the most common descriptor of IUGR, being present in 42 out of 49 infants. A third of infants had more than one indicator of IUGR. In this population, pre-term IUGR was strongly associated with perinatal maternal pathology (especially hypertension, toxemia and prolonged leakage of amniotic fluid). The neonatal morbidity and mortality among pre-term IUGR infants was markedly higher than that among appropriately grown pre-term infants with corresponding gestational age. There were significantly more cases with fatal intraventricular hemorrhage in pre-term IUGR than in pre-term normally-grown infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intrauterine growth retardation (IUGR) in pre-term infants. 405 33

Alterations in the thyroid metabolism of hypoxic, fasted, and chronically ill adults and older children have been described. We evaluated the effects of asphyxia on thyroidal indices of term newborns and compared them to those of a control population. Blood was drawn from the cord and then serially at 5 min and 3, 24, and 48 h after delivery in all patients. Seven term healthy newborns (group 1)increased their free thyroxine (FT4) concentrations significantly after delivery from a mean +/- SD baseline of 0.94 +/- 0.13 ng/dl in cord blood to a mean +/- SD peak of 2.6 +/- 0.6 ng/dl 48 h after delivery (p less than 0.001 at 3, 24, and 48 h), while their free triiodothyronine (FT3) levels increased from a mean +/- SD baseline level of 2.3 +/- 0.5 pg/ml in cord blood to a mean +/- SD peak of 3.7 baseline level of 2.3 +/- 0.5 pg/ml 48 h after delivery (p less than 0.001 at 24 and 48 h). Seven term newborns with transient low Apgar scores at birth (group 2) and seven term neonates born to mothers with toxemia or hypertension (group 3) failed to increase their FT4 and FT3 concentrations above baseline during the first 48 h of life. FT4 and FT3 values at 3, 24, and 48 h were significantly higher in the control group than in groups 2 and 3. Cord blood thyroid-stimulating hormone, FT4, and FT3 levels were not statistically different in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of asphyxia on free thyroid hormone levels in full term newborns. 408 Apr 49


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