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

The effects of a dihydropyridine calcium channel antagonist, nitrendipine 20 mg orally, have been investigated in 24 women in the first trimester human pregnancy in a double-blind, placebo controlled study. The effects on systemic arterial pressure, pulse rate (PR), blood loss at termination of pregnancy (TOP), plasma renin, renin substrate and aldosterone concentrations and platelet aggregation to adenosine diphosphate 0.5 microM, adrenaline bitartrate 0.1-1.0 microM, thrombin 0.05 u ml-1 and sodium arachidonate 0.1-0.2 mM were studied. Administration of nitrendipine was associated with a statistically-significant fall in diastolic pressure (BPD) the magnitude of which was directly related to the individual peak concentrations of the drug (P less than 0.02). No significant effects were observed on systolic pressure (BPS);PR rose slightly. Baseline variability of all three parameters fell in the nitrendipine-treated group over the first 2 h but then increased significantly (BPS, P less than 0.05; BPD, P less than 0.025; PR, P less than 0.005). There was a positive association in both placebo and treated groups between the rates of change of BPD and PR (P less than 0.005 for both); nitrendipine exerted a highly significant (P less than 0.001) effect on this association compatible with its effect as a vasodilator. Blood loss consequent on TOP did not differ in the two groups (nitrendipine 104 +/- 16 ml; placebo 114 +/- 20 ml). There were no significant differences in basal or stimulated hormone concentrations in the two groups. The ex vivo platelet aggregatory response in whole blood to 0.1 mM sodium arachidonate was inhibited by nitrendipine (P less than 0.05); responsiveness to the other aggregatory agents studied was not changed. There was a wide individual variation in both time to peak concentration of nitrendipine and the size of the peak, making classical pharmacokinetic analysis impossible. The median time after ingestion to peak concentration was 105 min; the median concentration was 7.8 ng ml-1. These data suggest that, in the context of the severe vasoconstriction and platelet aggregability of pregnancy-induced hypertension, further studies of this drug in pregnancy are warranted.
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PMID:Some observations on the effects of a calcium channel blocker, nitrendipine, in early human pregnancy. 330 Jul 58

This article reviews the current data available on the most frequently used drugs in bronchopulmonary dysplasia. Oxygen, diuretics, bronchodilators, steroids, ribavirin, and antioxidants, as well as medication available for pulmonary hypertension, systemic hypertension, and gastroesophageal reflux are discussed, with emphasis on known advantages, side effects, and current dosage.
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PMID:Pharmacotherapy in bronchopulmonary dysplasia. 332 29

Ischemic myocardial and papillary muscle dysfunction has considerable implication in newborn infants and children with normal or malformed hearts. Papillary muscle dysfunction in adults primarily involves coronary artery occlusion and ischemic necrosis in the left ventricle and papillary muscles. Infants and children rarely develop coronary artery occlusion. Their myocardial dysfunction and injury occurs with nearly equal frequency in both ventricles as a result of underperfusion from a wide range of causes, including severe birth asphyxia, congenital heart disease, and complications of premature delivery. A history of cardiogenic shock, acute congestive heart failure with cyanosis and atrioventricular murmur, or persistent fetal circulation in a newborn without congenital heart disease should alert the pathologist to the possibility of ischemic myocardial necrosis (IMN). Older infants with ventricular hypertrophy, persistent pulmonary hypertension (PPHN), bronchopulmonary dysplasia (BPD), and those with malformed hearts involving severe ventricular hypertension due to outflow obstruction or pulmonary hypertension may have IMN, fibrosis, or dystrophic calcification alone or in combination. Animal models of adult ischemic cardiac injury may not be suitable for study of the newborn.
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PMID:Ischemic myocardial necrosis and papillary muscle dysfunction in infants and children. 333 39

Eight ventilator-dependent infants with bronchopulmonary dysplasia (BPD) were treated with dexamethasone (0.5 mg/kg/day). Therapy was initiated at 19.3 +/- 3.9 days of age, continued at the initial dose for 7 days, then tapered over 2 weeks. The clinical course of these infants with BPD was compared to that of 8 similar ventilator-dependent infants with uncomplicated hyaline membrane disease (HMD). At study entry, the BPD patients had significantly higher ventilator rates, peak inspiratory pressures, mean airway pressures, alveolar-arterial oxygen gradients and fraction of inspired oxygen (FiO2) values. After 7 days of dexamethasone therapy, ventilator rates, peak inspiratory pressures, mean airway pressures, FiO2 values and alveolar-arterial oxygen gradients improved significantly. At this time, ventilator rates, peak inspiratory pressures and FiO2 values were similar to those of patients with uncomplicated HMD. BPD patients were extubated after 6.5 +/- 2.4 days of therapy. The incidences of septicemia, rickets and retinopathy of prematurity were similar in the BPD and uncomplicated HMD patients. Most dexamethasone-treated patients developed arterial hypertension during the first 48 h of therapy. Blood pressures returned to normal within 7 days of stopping therapy. All BPD patients had cosyntropin responses tested 5.5 +/- 2.6 weeks after stopping therapy. Six were normal. Two had inadequate responses. At 1 year adjusted age, the dexamethasone-treated BPD infants and HMD infants had similar radiographic bone ages, similar growth patterns and similar scores on the Bayley infant development scale. Dexamethasone was useful in the treatment of early BPD. Used as short-term therapy, the drug had minimal complications and no long-term sequelae.
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PMID:Short-term dexamethasone therapy for bronchopulmonary dysplasia: acute effects and 1-year follow-up. 358 71

Although the pulmonary circulation in infants with advanced bronchopulmonary dysplasia (BPD) is characterized by abnormal structure and vasoreactivity, metabolic lung functions have not been studied in these infants. To test the hypothesis that patients with severe BPD may have abnormal metabolic lung function, we assessed the pulmonary vascular extraction of circulating norepinephrine in six children with BPD during cardiac catheterization. Plasma norepinephrine levels were measured from simultaneously drawn mixed venous (main pulmonary artery) and left atrium or femoral artery samples. In comparison with four infants with mild heart disease without pulmonary hypertension, we found that infants with BPD extract proportionately less norepinephrine than non-BPD infants [-7 +/- 50% (BPD) versus +27 +/- 6% (non-BPD); P less than 0.001, t test]. Three infants with BPD had higher arterial than mixed venous concentrations of plasma norepinephrine, suggesting net production across the lung. Plasma catecholamine levels and percent extraction correlated poorly with cardiac index and systemic and pulmonary vascular resistance indices. However, this study group was characterized by a high incidence of pulmonary (6/6) and systemic (4/6) hypertension, left ventricular hypertrophy (4/6), and subsequent death (3/6). We conclude that infants with severe BPD and pulmonary hypertension have decreased pulmonary vascular clearance or net production of circulating norepinephrine, but links between altered pulmonary catecholamine metabolism and pulmonary hypertension, or other cardiovascular abnormalities associated with BPD, remain speculative.
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PMID:Pulmonary vascular extraction of circulating norepinephrine in infants with bronchopulmonary dysplasia. 369 7

We investigated the antidiuretic hormone (ADH) response in 12 infants with bronchopulmonary dysplasia during acute respiratory distress. All of the infants had hypoxemia with air-trapping in the chest at the time of admission to the hospital. None had documented infection. There was a dramatic increase in the plasma levels of ADH during acute respiratory distress, with a subsequent reduction of levels toward normal when the respiratory distress decreased to the preadmission well state. Three of 12 infants manifested hyponatremia at 24 hours after admission, with two of them exhibiting persistent hypertension for up to three days. The mechanism for elevated ADH levels is air-trapping in the chest, causing pulmonary hypovolemia and decreased left atrial filling and/or decreased transmural pressure of the left atrium.
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PMID:Antidiuretic hormone response in children with bronchopulmonary dysplasia during episodes of acute respiratory distress. 375 83

A randomized trial was conducted of dexamethasone therapy in infants with bronchopulmonary dysplasia who were dependent on respirators and were not progressing clinically despite conventional treatment. Babies were admitted to the study if they had a roentgenogram and clinical diagnosis of bronchopulmonary dysplasia, were 2 to 6 weeks in age, weighed less than 1,500 g, had made no progress in weaning for the preceding five days, and were free of sepsis, patent ductus arteriosus, and congenital heart disease, and had had no intravenous fat for at least 24 hours. After parental consent was obtained, infants were randomly assigned to control or treatment groups. The study hypothesis was that with steroid treatment, babies could be weaned from the respirator within 72 hours and would show a significant improvement in lung compliance within that time. Sequential analysis exceeded criterion (P less than .05) when seven consecutive untied pairs showed weaning with dexamethasone and failure to wean in control infants. Pulmonary compliance improved by 64% in the treated group and 5% in the control group (P less than .01). No significant intergroup differences were noted in mortality, length of hospital stay, sepsis, hypertension, hyperglycemia, or electrolyte abnormalities. Study design permits the conclusion that dexamethasone can produce substantial short-term improvement in lung function, often permitting rapid weaning from the respirator, but long-term efficacy and safety must be demonstrated by further investigations.
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PMID:Controlled trial of dexamethasone in respirator-dependent infants with bronchopulmonary dysplasia. 388 Aug 79

Thirteen of 30 infants with bronchopulmonary dysplasia demonstrated systolic blood pressure readings above 113 mm Hg on at least three separate occasions. In contrast, only one of 22 infants without BPD developed hypertension. The onset of hypertension often followed discharge from the nursery, was transient, and responded well to antihypertensive medication. Its significance is exemplified by the presence of left ventricular hypertrophy in three infants and a cerebrovascular accident in one child. We conclude that systemic hypertension is a significant problem in infants with BPD, and recommend close monitoring of blood pressure during their follow-up care.
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PMID:Systemic hypertension in infants with bronchopulmonary dysplasia. 654 71

Gestosis index score at delivery was compared with factors reflecting the fetal development in a series of 95 patients with EPH-gestosis collected in Okayama University Medical School in 1975-1979. The prediction of small for date (SFD) was performed by means of multivariate analysis of 10 variables, i.e. gestosis index, maternal body weight, height, uterine fundal length, abdominal circumference, maternal age at delivery and urinary estriol within one week prior to delivery. The result was that gestosis index was as useful as uterine fundal length in predicting SFD. The more gestosis index score increased, the more markedly the fetal development ws disturbed. Especially in the cases with scoring above 4 and in those with hypertension and proteinuria, the incidence of SFD increased obviously. No correlation between gestosis index and neonatal asphyxia was noticed. From the growth pattern of uterine fundal length and BPD, intrauterine growth retardation (IUGR) in pregnancy with EPH-gestosis occurred mainly within the third trimester of pregnancy. The functional development of the fetus with EPH-gestosis was evaluated with the use of urinary estriol level and fetal heart rate (FHR) monitoring. In the cases with EPH-gestosis scoring above 4, extreme disturbance of functional development of the fetus was observed.
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PMID:Estimation of gestosis of pregnancy (EPH-gestosis), relationship between fetal development and gestosis index. 719 59

There is insufficient data on the value of absent or retrograde end-diastolic flow (AREDF) in the fetal umbilical artery, descending aorta and aortic arch to predict perinatal outcome. In this prospective investigation, 65 pregnant women between 24 and 34 weeks' gestation with pregnancy-induced hypertension were studied by color Doppler echocardiography. Pregnancies leading to birth at or before 34.0 gestational weeks (23 with and 19 without AREDF) were included in the outcome analysis. Fetuses with AREDF were delivered at earlier gestational ages (p = 0.006). They had a higher incidence of gastrointestinal complications (p = 0.01), bronchopulmonary dysplasia (p = 0.03), intraventricular hemorrhage (p = 0.03) and vascular hypotension (p = 0.03) than those without AREDF. The presence of AREDF was associated with a mortality rate of 30%, whereas in fetuses without AREDF there was no mortality (p = 0.01). Using logistic regression and taking into consideration various perinatal factors, the presence of AREDF (p = 0.03) and early gestational age (p = 0.0001) were associated with serious neonatal diseases or death. A reverse diastolic flow in the aortic isthmus was registered in five fetuses; three died during the perinatal period and one was severely damaged. According to our results, AREDF, particularly with the appearance of reverse diastolic flow in the isthmus of the aortic arch, is a predictor of poor neonatal outcome.
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PMID:Value of absent or retrograde end-diastolic flow in fetal aorta and umbilical artery as a predictor of perinatal outcome in pregnancy-induced hypertension. 811 Nov 71


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