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

A cohort of 86 low birth weight (LBW infants (< 1751 g) including 23 subjects with bronchopulmonary dysplasia (BPD) and 23 matched controls without BPD were checked up at corrected ages of 1, 2, 4, 6, 8 and 12 months. Thirty-six of the subjects were re-hospitalized, mostly because of infections, there being no significant difference in the number of hospitalizations between BPD cases and their controls. Delayed growth was frequent, but a catch-up growth was seen. Eighteen of the subjects (5 with BPD and 7 of controls) were of height below 2 SD at a corrected age of 12 months. Twenty-four (14 with BPD and 3 controls) had persistent respiratory symptoms during the follow-up period and 4 of the BPD subjects still had such symptoms at the age of 1 year. Hoarseness was more frequent in BPD cases than in the controls (8/1 cases). One subject with BPD had transient symptoms of cor pulmonale and 1 without BPD developed transient systemic hypertension. Nine subjects (4 with BPD and 2 controls) had a diagnosis of cerebral palsy at the age of 1 year.
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PMID:A 1-year follow-up of low birth weight infants with and without bronchopulmonary dysplasia: health, growth, clinical lung disease, cardiovascular and neurological sequelae. 149 64

To determine the incidence and risk factors for neonatal hypertension we studied the entire population of 3179 infants admitted to our neonatal intensive care unit over a 6-year period. We report a 0.81% (26/3179) incidence of hypertension in this population. In 13 patients (50%) the hypertension was renal in origin. In four patients (15.4%), the etiology of hypertension could not be determined. Significant risk factors for neonatal hypertension included: bronchopulmonary dysplasia (5.9% in affected infants v 0.5% in unaffected infants, P less than .001); patent ductus arteriosus (3.07% in affected v 0.5% in unaffected infants, P less than .001); intraventricular hemorrhage (2.89% in affected infants v 0.56% in unaffected infants, P less than .001); and umbilical arterial catheterization (8.8% v 0.2% in infants with and without catheterization, respectively, P less than .001).
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PMID:Neonatal hypertension. Incidence and risk factors. 155 Jun 65

The pharmacokinetics and associated pharmacodynamics of nifedipine were studied in nine children aged 5 to 68 mo with bronchopulmonary dysplasia and pulmonary artery hypertension after a single oral dose of 1.44 mumol/kg (0.5 mg/kg). In the cardiac catheterization laboratory, hemodynamic measurements were made in duplicate just before the nifedipine dose and at 5 min and 0.5 and 1.0 h after the dose. The plasma nifedipine concentration was measured by HPLC at each of the above times and at 2.5, 4.0, 6.0, and 8.0 h after the dose. The mean (+/- SD) maximum plasma concentration and the time to maximum plasma concentration were 243.4 +/- 194.5 nmol/L and 1.0 +/- 0.8 h, respectively. The mean area under the plasma concentration-time curve was 761 +/- 509 nmol.h/L. The mean elimination rate constant and t1/2 were 0.456 +/- 0.194 h-1 and 1.8 +/- 0.8 h, respectively. Nifedipine caused a significant (p less than or equal to 0.05) reduction in the mean pulmonary artery pressure by 5 min and in the mean pulmonary vascular resistance index and mean aortic pressure by 30 min, and these reductions remained significant through the 1-h measurement interval. The magnitude of acute hemodynamic response correlated closely with the plasma nifedipine concentrations. No significant change occurred in the mean arterial oxygen saturation or cardiac index during the study period. The percentage changes from baseline in the mean pulmonary artery pressure and mean pulmonary vascular resistance index were approximately double the percentage change in the mean aortic pressure, suggesting that nifedipine had some degree of selective impact on the pulmonary vascular bed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacokinetics and pharmacodynamics of nifedipine in children with bronchopulmonary dysplasia and pulmonary hypertension. 189 55

In order to study the effect of dexamethasone on the ventilatory function of 13 neonates with bronchopulmonary dysplasia, a retrospective investigation was carried out in the University Hospital Rotterdam, Sophia Children's Hospital, Neonatal Intensive Care Unit. Thirteen preterm neonates, 7 boys and 6 girls, born after 26 4/7-32 weeks' gestation with birth weights between 680 and 1800 g were studied. At the age of 21 days they all showed clinical and radiological evidence of BPD and despite maximal therapy they deteriorated during the last week before entering into the study. The potentially successful dexamethasone schedule of Avery was started. After four days' therapy only 3 patients out of 13 were still on the ventilator. Ventilatory support could be stopped in all neonates after 4.7 (SD 2.0) days. No hypertension or hyperglycaemia was seen. Only 1 child had a positive blood culture; this was successfully treated. In the end two children died. The use of corticosteroids in bronchopulmonary dysplasia in this study showed a positive short-term effect. Long-term sequelae and the risk of infection are still controversial.
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PMID:[The use of corticosteroids in bronchopulmonary dysplasia]. 205 11

Continuous negative pressure ventilation utilizes subatmospheric pressure around the thorax to improve oxygenation. It has not been routinely used since the mid-1970s. We treated 37 infants with the combination of continuous negative pressure (CNP) and intermittent mandatory ventilation (IMV), after failing to attain a PaO2 of greater than or equal to 50 torr on IMV alone. Lung diseases included pulmonary interstitial emphysema (PIE), respiratory distress syndrome (RDS), and pulmonary artery hypertension (PAH) due either to meconium aspiration syndrome (MAS) or other causes (non-MAS). All infants had evidence of severe parenchymal pulmonary disease, or pulmonary artery hypertension resulting in persistent hypoxemia and hypotension. In the PIE group, CNP was started later in the course of the disease, and both positive pressure and oxygen were maintained for a longer period. The group of infants with non-MAS PAH required CNP and positive pressure ventilation for the shortest period of time. The infants with PIE also had a greater incidence of bronchopulmonary dysplasia (BPD) and intraventricular hemorrhage (IVH). In addition, three patients with PIE died. In the non-MAS patients with PAH, no complications and no deaths occurred. The response to CNP was a rapid improvement in oxygenation in all groups with the greatest increase of PaO2 in the non-MAS PAH infants: from 30 torr prior to the initiation of CNP to 140 torr within 30 minutes. No significant changes in pH or PaCO2 occurred in any group. Significant decreases in ventilator rate, mean airway pressure (Paw) and FIO2 in peak inspiratory pressure were possible by 12 hours of CNP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reintroduction of continuous negative pressure ventilation in neonates: two-year experience. 219 12

In patients with pulmonary disease, pulmonary artery hypertension often occurs as a result of pulmonary artery vasoconstriction, primarily from hypoxia and alveolar hypotension. In this report we describe the hemodynamic effects of breathing supplemental oxygen in a child with bronchopulmonary dysplasia and pulmonary artery hypertension. These hemodynamic effects include an improvement in oxygenation, an increase in systemic vascular resistance, and a decrease in the pulmonary vascular resistance. As a direct result of these changes in vascular resistances, alterations of heart rate, cardiac index, stroke volume, aortic pressure, oxygen consumption, and pulmonary artery pressure have been shown to occur. Oxygen is widely used to treat many physiologic conditions. However, during the administration of supplemental oxygen, rarely do we recognize the hemodynamic changes associated with its use. These hemodynamic effects must be clearly understood and appreciated before oxygen administration in any clinical situation.
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PMID:Effects of supplemental oxygen administration in an infant with pulmonary artery hypertension. 222 53

Seventy-seven very low birthweight (VLBW) infants (mean birthweight 891 +/- 209 g) with a diagnosis of bronchopulmonary dysplasia (BPD) were treated with a steroid (dexamethasone) in an attempt to wean them from mechanical ventilation. Seventeen of 77 (22%) treated infants died. Death from respiratory failure occurred in 13 infants; sepsis occurred in six infants (7.8%) and contributed to death in one. During steroid therapy systemic hypertension occurred in 18 surviving infants (30%), glucose intolerance occurred in 29 infants (38%), and marked irritability occurred in three infants (3.8%). Elevated blood pressure returned to normal and glucose intolerance resolved in all infants following discontinuation of therapy. Fifty infants were available for follow-up at a mean corrected age of 14.9 +/- 9.8 months. Twenty-two percent required rehospitalization in the first year of life for respiratory illnesses. Results of testing by Bayley Scales of Infant Development were normal in 60% of infants. Fifty percent were considered normal based on both developmental testing and physical examination. Twenty-eight percent had mild to moderate abnormalities, and 22% were severely handicapped. These follow-up results are statistically similar to those recorded in LBW infants with BPD not treated with steroids who were hospitalized during the same period. We conclude that the side effects of steroid therapy for BPD consist primarily of blood pressure elevation, glucose intolerance, and irritability. Causes of death are unchanged by steroids. The incidence of severe infection and the long-term neurologic outcome of high-risk infants with BPD are not appreciably compromised by this therapy. These data suggest that concern for steroid side effects should not prevent additional prospective investigation to determine the role of steroid therapy in the overall management of BPD.
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PMID:Side effects and long-term follow-up of corticosteroid therapy in very low birthweight infants with bronchopulmonary dysplasia. 235 96

Dexamethasone has recently been introduced for the treatment of bronchopulmonary dysplasia (BPD). Whereas the short-term effect of dexamethasone has been documented in previous publications, studies on the long-term effect do not appear to exist in the literature. The aim of this retrospective study was to investigate the influence of dexamethasone on respiratory parameters, the long-term efficacy, and the side-effects. Dexamethasone was given to premature babies with BPD who could not be weaned from the respirator. Twelve infants were included in this study. The gestational ages ranged from 26 to 30 weeks and the birth weights ranged from 640 to 1410 g. Dexamethasone treatment was initiated at the age of 14 to 44 days. After 6 days of dexamethasone therapy, ventilation rates and FiO2 values improved significantly. All infants were successfully weaned from mechanical ventilation and extubated at 2 to 40 days after the start of dexamethasone therapy. The follow-up for the estimation of the long-term efficacy ranged from 3 to 18 months. Ten out of twelve patients had been weaned permanently from the ventilator; one 12-months-old infant is still respirator-dependent. One patient died at 8 months from BPD. In 5 out of 12 infants we observed a leukocytosis with neither clinical signs nor microbiological signs of an infection. Septicaemia developed in one case and one patient suffered from pneumonia. Arterial hypertension was observed in one infant during dexamethasone therapy. The results suggest that dexamethasone facilitates the weaning of preterm infants with BPD from the ventilator. This treatment may prevent some infants from long-term ventilation.
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PMID:[Dexamethasone therapy in bronchopulmonary dysplasia]. 249 83

A retrospective analysis of infants with bronchopulmonary dysplasia requiring prolonged hospitalization (greater than 100 days) was carried out to determine those factors associated with fatal outcome. Twenty-three infants made up the study population. Eleven infants died and 12 survived (survivors). No differences were noted between the groups regarding ventilator requirement, radiographic changes, and medication use (digoxin, aldactazide), except for furosemide which was used twice as frequently in the group of infants who died v the group of infants who survived (P less than .001). Differences noted between the groups included moderate hypochloremia (chloride less than 80 mEq/L) in all 11 infants who died v six of 12 survivors, severe hypochloremia (chloride less than 70 mEq/L) in the nine of 11 infants who died v two of 12 survivors, metabolic alkalosis (pH greater than 7.45) in nine of 11 infants who died v three of 12 survivors, hypertension (systolic BP greater than 113 mm Hg) in eight of 11 infants who died v one of 12 survivors, decrease in head growth in ten of the 11 infants who died v one of the 12 survivors; these differences were all significant (P less than .001). The metabolic alkalosis and head growth changes appear to be related to the hypochloremia. The data suggest that chloride deficiency may be an important contributing factor in the genesis of poor outcome in infants with bronchopulmonary dysplasia and that close attention to chloride supplementation might influence outcome.
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PMID:Is chloride depletion an important contributing cause of death in infants with bronchopulmonary dysplasia? 293 79

The acute hemodynamic effects of nifedipine were evaluated and compared to the effects of 95% oxygen in six children with bronchopulmonary dysplasia and pulmonary artery hypertension. The children ranged in age from 7-26 months and all were oxygen dependent. In the cardiac catheterization laboratory, hemodynamic data were collected in 95% oxygen, room air, and 15 and 30 min after nifedipine administration (0.5-0.6 mg/kg per nasogastric tube). Compared to values in room air, nifedipine resulted in a 34% decrease in pulmonary artery mean pressure (from 69.3 +/- 2.4 to 45.8 +/- 1.2 mm Hg, p = 0.03) and a 49% decrease in pulmonary vascular resistance (from 14.8 +/- 1.4 to 7.5 +/- 0.9 U/m2, p = 0.03). A linear relationship was found between the arterial pO2 and the change in the ratio of pulmonary to systemic resistance after nifedipine (% decrease in Rp/Rs ratio = 86.3 - 1.3 x pO2, r = -0.95, p = 0.004) suggesting that nifedipine may act to oppose the vascular effects of arterial hypoxemia. There was no significant change in heart rate, arterial pO2, or pCO2 with nifedipine, but cardiac output increased significantly. Compared to 95% oxygen, nifedipine achieved a lower pulmonary vascular resistance (7.5 +/- 0.9 versus 10.9 +/- 1.2 U/m2, p = 0.03) and a greater cardiac output (5.25 +/- 0.71 versus 3.54 +/- 0.35 liter/min/m2, p = 0.03) with comparable systemic oxygen delivery (699 +/- 85 ml versus 698 +/- 91 ml O2/min/m2, p = 1.0). Thus, nifedipine is an acute pulmonary vasodilator in some children with bronchopulmonary dysplasia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute hemodynamic effects of nifedipine in infants with bronchopulmonary dysplasia and pulmonary hypertension. 318 30


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