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

Chronic pulmonary arterial hypertension was produced in six fetal lambs. In four (126 to 139 days' gestation) unilateral fetal renal artery constriction caused systemic arterial mean blood pressure elevations. In another fetus, constriction of the umbilical artery caused a systemic mean blood pressure elevation; in the sixth, partial occlusion of the ductus arteriosus caused isolated pulmonary arterial hypertension. The right lung of each fetus was perfused with fixative at the in vivo mean arterial pressure and the amount of smooth muscle in the fifth generation (resistance) vessels analyzed using the medial width/external diameter ratio. There was a significant increase in the medial width/external diameter ratio in the six experimental animals as compared to that in six normal fetuses. In separate fetuses the increased ratios were due to a decreased external diameter, increased smooth muscle, or both these factors. The total number of resistance vessels was counted in the right lung of each fetus and no significant difference from normal was observed. We postulate that either fetal systemic hypertension or constriction of the ductus arteriosus causes fetal pulmonary hypertension in utero and that this produces increased smooth muscle development in pulmonary arterial resistance vessels; this may be a pathogenic mechanism for the syndrome of persistent pulmonary hypertension of the newborn infant.
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PMID:Fetal hypertension and the development of increased pulmonary vascular smooth muscle: a possible mechanism for persistent pulmonary hypertension of the newborn infant. 2 21

The mortality of children with posterolateral diaphragmatic hernia (PDH) is mainly dependent upon the degree of lung hypoplasia. Other less significant factors are dysmaturity, associated anomalies, infection and haemorrhages. Children with grave cyanosis from PDH immediately after birth have a poor prognosis due to persistent foetal circulation with pulmonary vascular hypertension and right-left shunting. A better understanding and treatment of this persistent foetal circulation may considerably improve the surgical mortality, though in some cases the lung hypoplasia may be too far advanced.
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PMID:Postoperative causes of death in pediatric surgery: analysis and conclusions for the therapy. 52 54

We report the case of a six-day-old male infant exposed in utero to a prostaglandin synthetase inhibitor, who presented pulmonary arterial hypertension, tricuspid insufficiency, and electrocardiographic signs of diffuse myocardial ischemia. The necropsy showed organizing infarction of the anterior and posterior right papillary muscles (probably occurred in utero) with complete rupture of the former, besides abnormal muscularization of the intraacinar pulmonary arterioles (persistent fetal circulation of the newborn). The authors suggest a possible relation between the myocardial ischemic and pulmonary hypertensive lesions since the prostaglandin synthetase inhibitor can induce precocious pulmonary arteriolar muscularization and constriction of the arterial duct, leading to right ventricular overload, thus facilitating the occurrence of papillary and subendocardial ischemia.
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PMID:Post-ischemic rupture of the anterior papillary muscle of the right ventricle associated with persistent pulmonary hypertension of the newborn: a case report. 162 31

Three children who presented with heart failure in infancy caused by severe hypertension as a result of unilateral renal arterial disease are described. One presented at 3 days of age with persistent fetal circulation and heart failure. He had abnormal great vessels that indicated that the hypertension was of long standing and therefore fetal; this has not been described previously. The other two children failed to thrive because of unrecognised hypertension and subsequently presented with heart failure. All three underwent unilateral nephrectomy which cured their hypertension, and all were thriving at the time of writing. The benefits of nephrectomy outweighed the operative risks and loss of renal function. Blood pressure should be measured in children who are failing to thrive as part of routine clinical practice.
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PMID:Fetal and infantile hypertension caused by unilateral renal arterial disease. 240 Feb 27

Pulmonary arterial hypertension has many causes, only some of which are well understood. The radiographic findings in pulmonary arterial hypertension are very similar regardless of the cause. Some radiographic features such as cardiac chamber enlargement, occur secondary to elevation of pulmonary pressures. In addition, sequential radiographs may demonstrate dramatic changes as the hypertension develops. This article presents examples of the various forms of pulmonary arterial hypertension, with pathologic correlation. Included are chronic pulmonary thromboembolism, plexogenic pulmonary arteriopathy, pulmonary venooclusive disease and persistent fetal circulation. Examples of lesions causing secondary pulmonary arterial hypertension: parenchymal lung disease, pulmonary venous hypertension, and congenital heart disease, are also illustrated.
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PMID:Pulmonary arterial hypertension: a contemporary review. 267 97

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

Fetal circulation was studied by means of combined real-time and pulsed Doppler ultrasound in 14 women with pregnancy-associated hypertension before and during the first and third days of treatment with the beta 1-selective blocker, atenolol; in seven of the women the maternal uterine arcuate blood velocity waveform was also studied. Blood flow characteristics were normal both in the fetus and in the maternal arcuate artery, compared with those in uncomplicated pregnancies of corresponding gestational ages. Volume blood flow remained unchanged in the fetal descending aorta, and in the umbilical vein during atenolol treatment, whereas the pulsatility index increased in the fetal descending aorta and in the arcuate artery. This suggests that the peripheral vascular resistance, both on the maternal and fetal side of the placenta, increased during short-term antihypertensive treatment with atenolol.
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PMID:Fetal and uteroplacental haemodynamics during short-term atenolol treatment of hypertension in pregnancy. 358 Mar 13

Sodium nitroprusside was administered to 58 neonates, including 11 with severe respiratory distress syndrome, 15 with persistent pulmonary hypertension of the newborn, 28 with clinical shock, three with systemic hypertension, and two with pulmonary hypoplasia, all refractory to conventional intensive therapy. Nitroprusside was infused at 0.2 to 6.0 micrograms/kg/min for periods of 10 minutes to 126 hours. Infants with severe respiratory distress syndrome had increased PaO2 and decreased PaCO2 or peak inspiratory pressure, and nearly all (82%) survived. Infants with persistent pulmonary hypertension of the newborn had variable responses; improvement did not correlate with survival, but survival (47%) was identical to that in an earlier series of infants given tolazoline. Infants in shock had improved perfusion, urine output, and serum bicarbonate levels, and these responses were significantly related to survival. Hypertension was controlled in all three hypertensive infants. Adverse effects were very uncommon. Toxic effects were not observed. Sodium nitroprusside is effective and can be used safely in circulatory disorders in the neonate.
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PMID:Use of sodium nitroprusside in neonates: efficacy and safety. 391 95

Endothelial (e) nitric oxide synthase (NOS) activity modulates pulmonary vascular tone in the normal fetus and decreases pulmonary vascular resistance (PVR) at birth. Mechanisms contributing to sustained elevations of PVR and the failure of postnatal adaptation at birth are uncertain but may include decreased eNOS activity. To test this hypothesis, we studied the effects of chronic intrauterine pulmonary hypertension on lung eNOS content and NOS activity in an ovine model of perinatal pulmonary hypertension and in normal lambs. We measured eNOS mRNA and protein content by Northern and Western blot analyses, respectively. Calcium-dependent and total NOS activities were determined by assaying the conversion of L-[14C]arginine to L-[14C]citrulline from lung homogenates. To determine the effects of intrauterine hypertension on lung eNOS content, fetal lung tissue was harvested 8-12 days after intrauterine closure of the ductus arteriosus (DA) performed at 125-128 days of gestation (term = 147 days). Although positive immunostaining for eNOS persisted in lung vascular endothelium, eNOS protein content was reduced by 48%, as measured by Western analysis (P < 0.001). Chronic hypertension reduced lung eNOS mRNA content by 30% (P < 0.05). Compared with age-matched controls, Ca(2+)-dependent NOS activity was decreased after DA ligation by 75% (P < 0.01). We conclude that chronic intrauterine pulmonary hypertension decreases eNOS in the fetal lung. We speculate that decreased NO production contributes to failure of postnatal adaptation in this experimental model of persistent pulmonary hypertension of the newborn.
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PMID:Chronic intrauterine pulmonary hypertension impairs endothelial nitric oxide synthase in the ovine fetus. 917 68

Cardiac abnormalities in birth asphyxia were first recognised in the 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the newborn (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and, therefore, requires treatment in the form of inotropic and ventilatory support (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses, especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required (v) persistent pulmonary hypertension of the newborn (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory tension and right ventricular failure with systolic murmur of tricuspid, and at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.
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PMID:Cardiac abnormalities in birth asphyxia. 1095 39


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