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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The microvascular architecture of the subependymal matrix in premature infants was studied with microangiography and benzidine stains. This revealed that the subependymal matrix is the end zone or the border zone between cerebral arteries and the collection zone of the deep cerebral veins. Focal hypoxic changes of this subependymal matrix may occur in hypoxemia and ischemia because of the characteristic architecture. The vascular permeability of these vessels was studied in rabbits using three different molecular weights of FITC-dextran. Vascular permeability was increased in the subependymal matrix by hypoxia and especially by hypoxia associated with an increased venous pressure. These findings may be related to the pathogenesis of subependymal hemorrhage in prematurity.
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PMID:Microangiography and vascular permeability of the subependymal matrix in the premature infant. 64 97

The authors present an analysis of the multifocal leucoencephalomalacia in children under 1 year of life based on the material obtained from 2.398 autopsies. It was found that 32 autopsied children suffered from this disease (1.33%). Twenty four of these children were premature. The disease was more frequent in the infants (23 cases) than in neonates (9 cases), and in boys (20 cases) than in girls (12 cases). Multifocal leucoenephalomalacia was manifested mainly as spastic infantile paralysis in the majority of the infants (14 cases). Morphological lesions to the brain most frequently embraced white substance adjacent to the cerebral ventricles (foci of leucoencephalomalacia of 1 cm in diameter) and cerebral vessels. Widening of the ventricular system of the brain was seen in 15 cases. Pathological reaction resulted from the brain anoxia and ischemia in perinatal period (20 cases) or septicaemia (12 cases) while predisposing factors included: prematurity, respiratory failure with hyaline membranes in the lungs and congenital abnormalities of the heart.
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PMID:[Multifocal periventricular leukomalacia in children up to 1 year of life]. 228 78

Impaired excitation-contraction coupling has been suggested as the underlying mechanism of postischemic contractile dysfunction of reperfused myocardium in in-vitro studies. To test this hypothesis in situ, postextrasystolic potentiation (PESP) following an extrasystole with constant prematurity and three different postextrasystolic time intervals (compensated, regular, abbreviated) was analyzed in 12 anesthetized dogs. Changes in regional inotropic state were assessed by comparison of end-systolic wall thickness (sonomicrometry) during PESP to the respective pressure-matched values of an end-systolic pressure/wall-thickness relationship established during brief manual clamping of the aorta. Before ischemia, posterior end-systolic wall-thickness was increased by 0.19 +/- 0.35 (SD) mm during PESP with an abbreviated, by 0.36 +/- 0.42 mm with a regular, and by 0.60 +/- 0.42 mm with a compensated postextrasystolic interval. Baseline systolic wall thickening was decreased from 16.2 +/- 5.4% (before ischemia) to -3.0 +/- 3.4% at the end of 15 min left circumflex coronary occlusion, and to 2.8 +/- 7.5% at 10 min, 7.2 +/- 3.9% at 4 h, and 7.9 +/- 4.1% at 8 h reperfusion. Stepwise increases in regional inotropic state during PESP with increasing postextrasystolic intervals were not different in normal and reperfused myocardium. Thus, excitation-contraction coupling appears not to be impaired during inotropic stimulation of reperfused myocardium in situ.
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PMID:Recruitment of a time-dependent inotropic reserve by postextrasystolic potentiation in normal and reperfused myocardium. 238 19

To study the role of silent ischemia and the arrhythmic substrate in the genesis of sudden cardiac death, 67 patients were studied (mean age 62 +/- 12 years). Of these, 14 patients (Group 1) had an in-hospital episode of ventricular tachycardia or fibrillation while wearing a 24 h Holter ambulatory electrocardiographic (ECG) monitor, 33 (Group II) had a documented episode of sustained ventricular tachycardia or fibrillation, or both, and 20 (Group III) had angina pectoris but no ventricular tachycardia or fibrillation. Eight Group I survivors underwent programmed electrical stimulation or ECG signal averaging, or both. All Group II patients underwent 24 h Holter monitoring and ECG signal averaging to detect late potentials before programmed electrical stimulation. Group III patients underwent both 24 h Holter recording and coronary angiography. The 24 h ECG tapes were analyzed for ST segment changes, prematurity index and characteristics of ventricular premature depolarizations. Any ST depression greater than or equal to 1 mm for greater than 30 s was considered to be a reflection of silent ischemia, and the induction of ventricular tachycardia or fibrillation by programmed electrical stimulation or the presence of late potentials, or both, was considered to be a reflection of the arrhythmia substrate. Silent ischemia preceded ventricular tachycardia in only 2 (14%) of the 14 Group I patients. The prematurity index was less than 1 in only 18% of ventricular tachycardia episodes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of silent ischemia, the arrhythmic substrate and the short-long sequence in the genesis of sudden cardiac death. 258 49

Numerous risk factors for necrotizing enterocolitis (NEC) including prematurity, bowel ischemia, pathogenic bacteria, and hyperosmolar feedings have been proposed. Recent studies have demonstrated feeding intolerance and bowel dysfunction in children with hypoalbuminemia. No association between hypoalbuminemia and NEC has been suggested. The records of 45 patients with NEC and complete documentation of prenatal and birth histories were reviewed. A control (CONT) group of 90 children matched for maternal age (+/- 1 year), parity, gestational age (+/- 1 week), birth weight (+/- 20 g), type of delivery, sex, race, type of initial feeding, and perinatal stress was compiled. While all other measured parameters were similar in the two groups, premorbid albumin was significantly lower in the patients who subsequently developed NEC (P less than .001). These data suggest that newborns with hypoalbuminemia may have an increased risk of developing NEC.
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PMID:Hypoalbuminemia may predispose infants to necrotizing enterocolitis. 275 84

Primary tissue closure of gastroschisis remains controversial. Some surgeons routinely place a silicone rubber sheet silo over the exposed bowel, planning a staged closure. In the past 14 1/2 years, we have cared for 106 newborns with gastroschisis, closing the defect primarily in 80%. The success of this technique depends on enlarging the abdominal cavity and decreasing the volume of bowel that must be replaced in the peritoneal cavity. Thorough preoperative rectal irrigation should evacuate all meconium. After undermining the skin around the abdominal wall defect for only 1 cm, a midline subcutaneous fasciotomy is created from the xiphoid to the pubis. The abdominal wall is then stretched in all quadrants beginning at the flanks. The eviscerated small bowel can often be returned without enlarging the initial skin defect. The skin is closed with subcuticular absorbable sutures reinforced by long skin tapes. The small ventral hernia that results is closed at about 1 year of age. Fascia could be closed primarily in 28% of these patients, and 17% required a prosthetic pouch. The duration of postoperative ileus and length of hospital stay were statistically significantly shorter in the infants who underwent primary closure. Even though more complicated patients were included in the primary closure group, the incidence of mortality and morbidity was not higher than in patients treated with silicone rubber pouches. Deaths were inevitable in five infants with gangrenous bowel, multiple anomalies, and extreme prematurity. Deaths were related to sepsis in three infants and were the result of operative or anesthetic technique in four. Only two preoperative factors were prognostic of morbidity and mortality: gestational age (but not birth weight) and the presence of intestinal ischemia or atresia.
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PMID:Gastroschisis in 106 consecutive newborn infants. 293 43

Neonatal necrotizing enterocolitis is the most common serious gastrointestinal disorder encountered in neonatal intensive care units. It is a major cause of morbidity and mortality in the newborn, particularly in premature infants. Consistent risk factors are birth weight and prematurity. Polycythemia and hyperviscosity altering blood flow and infectious agents are also implicated. Clinical findings include abdominal distention and diarrhea, and systemic symptoms such as apnea, acidosis, and lethargy. Pneumatosis intestinalis can be demonstrated radiographically. Mucosal ulcerations, hemorrhage, and thrombosis occur early, followed by inflammatory changes. Later still necrosis develops. Ischemia, infection, and enteral feedings are suspected to be involved in the pathophysiology. Eicosanoids, especially thromboxane, platelet-activating factor, and leukotrienes are likely mediators.
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PMID:Neonatal necrotizing enterocolitis. Inflammatory bowel disease of the newborn. 312 29

The electrocardiographic responses to programmed ventricular stimulation and acute posterolateral myocardial ischemia were studied in conscious dogs treated with the resolved optical isomers of sotalol. Studies were conducted 3-7 days after anterior myocardial infarction to determine the relative contributions of beta-adrenergic receptor blockade and direct Class III electrophysiologic actions in the antiarrhythmic and antifibrillatory actions of the isomers. With cumulative i.v. administration of up to 8 mg/kg, both the beta-blocking levorotatory isomer and the dextrorotatory isomer suppressed the induction of ventricular tachyarrhythmias by programmed stimulation in at least 50% of dogs tested. Both isomers produced equivalent 15-20% increases in normal zone ventricular refractoriness, thereby preventing propagation of programmed ventricular extrastimuli of sufficient prematurity to elicit tachyarrhythmias. The levorotatory isomer of sotalol prolonged the PR interval; the administration of the dextrorotatory isomer increased QTc and, in several dogs, was associated with the development of ventricular ectopy. The prior administration of 8 mg/kg of either optical isomer of sotalol prevented the immediate spontaneous development of ventricular fibrillation in response to ischemia at a distance from the previous site of infarction. These results suggest that alterations in ventricular refractoriness may underlie the antiarrhythmic and antifibrillatory actions of the optical isomers of sotalol and of racemic sotalol.
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PMID:Antiarrhythmic and antifibrillatory actions of the levo- and dextrorotatory isomers of sotalol. 608 71

Theory states that the extracellularly recorded potential (epsilon) is determined by spatial and nonspatial factors. Spatial factors include the boundary between areas with different transmembrane voltages (Vm) and the relationship of the boundary to the extracellular electrode. Nonspatial factors include the Vm across the boundary [transmembrane potential gradient (TPG)] and a conductivity term (C sigma). Few studies have investigated the nonspatial factors experimentally due to the difficulty in separating the nonspatial from the spatial determinants. Our model rendered the spatial factors constant, permitted the simultaneous recording of epsilon and Vm, and allowed the manipulation of Vm and C sigma across the boundary. Epsilon and the TPG were related predictably with changes in [K+]o, [Na+]o, temperature, conduction, stimulus rate or prematurity, and hypoxia. In the presence of a constant TPG, epsilon could be affected by a change in C sigma caused by hypoxia and a metabolic poison. The effects of the nonspatial determinants on epsilon could be modeled using electrical circuit analogues. Nonspatial determinants must be considered in studies using electrocardiographic measures as an index of ischemia.
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PMID:Nonspatial determinants of electrograms in guinea pig ventricle. 721 55

Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature neonates that accounts for 3000 to 4000 deaths each year in the United States. The pathogenesis is not well understood, however theories suggest that prematurity, enteral feeding, bacterial colonization, and intestinal ischemia contribute to the intestinal injury. Furthermore, recent studies have shown that platelet activating factor and perhaps other inflammatory mediators mediate bowel necrosis in animals and possibly in humans. Although no specific intervention for NEC treatment exists, preventive therapy using either enteral IgA supplementation, breast milk feeding, antibiotic prophylaxis, or exogenous steroid administration have reduced the incidence of this overwhelming disease in small randomized trials. These modalities and perhaps PAF antagonists or other inflammatory mediator inhibitors may reduce the incidence or severity of NEC in the next several years.
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PMID:Necrotizing enterocolitis: a review of pathogenetic mechanisms and implications for prevention. 851 29


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