摘要:

SummaryThe present study was designed to obtain quantitative data on the extent of portocaval shunting and the time course of closure of the ductus venosus in newborn lambs. Experiments were conducted on eight newborn lambs prepared with chronic portal catheters. The time course of the postnatal closure of the ductus venosus was determined by following the distribution of radiolabelled microspheres injected into the lamb's portal vein 24, 48, 96, and 168 hr after birth. The fraction of the portal blood flow which bypassed the liver was highly variable. In some animals, the ductus venosus was almost completely closed when the first microspheres were injected 24 hr after birth. In others, almost 40% of the portal blood flow bypassed the hepatic circulation at this time. On average, only 77% of the portal blood flow was directed to the liver in the 1‐day lambs. In most cases, closure had occurred by 48 hr after birth, but some animals continued to divert a significant fraction of the portal flow away from the hepatic circulation.SpeculationAt birth, the umbilical perfusion of the liver ceases and the hepatic circulation shifts to a much greater reliance on its portal blood flow. Patency of the ductus venosus during the 1st wk after birth may divert a sizeable fraction of the portal blood flow away from the liver and reduce the hepatic blood flow to levels which limit oxygen exchange and the development of metabolic functions in the postnatal period.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryThe measurement of125I‐insulin binding to erythrocytes from 34 samples of cord blood (% B/T = 11.2 ± 3.8) showed statistically significant differences when compared to adult erythrocytes (% B/T = 6.6 ± 1.7). Preterm erythrocytes (% B/T = 14.7 ± 3.4) bound significantly more insulin when compared to term erythrocytes (% B/T = 10.1 ± 3.2). The negative correlation (r= −0.613;P= 0.001) between insulin binding and gestational age indicates that the trend during the final trimester of gestation is toward the lower binding observed for adult cells.The major differences in binding between adult and term cord blood erythrocytes may be primarily attributed to differences in the number of binding sites per cell. Additionally, there are small differences in both affinity and number of sites per cell in preterm as compared to term and adult erythrocytes.SpeculationThe mechanisms governing insulin release from the pancreas are not maturein utero.Insulin released directly into the circulation from the fetal pancreas may be bound to tissue receptors in relation to the affinity and concentration of specific surface receptors, thereby, providing direct control at the cellular level for rapidly growing fetal tissues. Erythrocyte receptors may serve to transport insulin for this purpose.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryAlterations in pancreatic function and structure were examined in suckling mice infected intraperitoneally with reovirus type 3. The results were compared to pancreatic zymogen enzyme activities and histology in adult mice infected with the same virus. No effect of the reovirus type 3 on the adult mice could be elicited.In contrast, the suckling mice infected by the reovirus type 3 revealed a definite change in pancreatic zymogen enzymes. However, the zymogen enzymes were affected in a nonparallel fashion and three groups of enzymes with different responses were noted. Amylase and lipase activities were significantly diminished (P< 0.001) at 6 days of viral infection. The endopeptidases, trypsin (P< 0.025) and chymotrypsin (P< 0.001) activities were increased significantly in the infected group. The exopeptidases, carboxypeptidase A and B in the infected animals were not changed significantly compared to the control.It seems reasonable that the reovirus type 3 infection in the suckling mouse causes diminished lipase and amylase activities that might contribute to the pathogenesis of viral enteritis.SpeculationStudies on viral enteritis in infants and young animals have primarily implicated changes in the small intestine as the cause of diarrhea. The viral invasion of the intestinal mucosa causes villous cell destruction and as a consequence, the mucosa generated is immature and incapable of handling normal salt and water absorption.In addition, changes in pancreatic function as a result of an extension of the viral infection to the pancreatic parenchyma might contribute to the pathophysiologic mechanisms operating in viral enteritis.In the infected suckling mice, only amylase and lipase activities are diminished to a large extent, while trypsin and chymotrypsin activities are elevated and carboxypeptidase A and B activities remain unaffected. The nonparallel change in pancreatic enzymes toward a viral insult can be explained by a separate effect of the virus on the biosynthesis of each of the zymogen pancreatic enzymes. It is conceivable that amylase and lipase while in a developing stage, are more affected by the virus than the other pancreatic enzymes which are already developed to a certain extent. Another explanation is that lipase and amylase activities are intrinsically more prone to be decreased in response to different disease states affecting the pancreas. Diminished lipolytic and amylolytic activities due to viral gastroenteritis is a possible contributing factor of the diarrhea in infants and children.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryWhen amino acids were infused at a rate of 4 g/kg/day, an infant with hypoglycemia, metabolic acidemia and chronic regurgitation showed hypersarcosinemia and excreted abnormal amounts of sarcosine, isovalerylglycine, isobutyrylglycine, &agr;‐methylbutyrylglycine, and &bgr;‐hydroxyisovaleric, glutaric, &agr;‐hydroxyglutaric, methylsuccinic, and &agr;‐hydroxyisobutyric acids in urine. On all other occasions, when protein intake was lower and lipid intake higher, urine organic acids were dominated by methylsuccinic, ethylmalonic, and &agr;‐hydroxyglutaric acids, and hypersarcosinemia was absent. Autopsy showed severe fatty changes in liver, kidneys, and skeletal muscle. A previous female sibling had died with similar autopsy findings at 4 days of age. While activity of glutaryl‐CoA dehydrogenase was completely deficient in liver and almost completely so in kidney, it was normal in cultured fibroblasts in the presence of flavin adenine dinucleotide (FAD) and only marginally low in its absence. Incorporation of d‐(2‐14C) riboflavin into flavin mononucleotides (FMN) and FAD by kidney tissue was normal.The authors conclude that this disorder is not due to generalized deficiency of glutaryl‐CoA dehydrogenase or to a defect in FAD synthesis. The amino and organic acid abnormalities noted are most consistent with a defect in the flavoprotein which transfers electrons from the FAD of sarcosine and acyl‐CoA dehydrogenases into the respiratory chain, although a defect in intercompartmental transfer of C4‐5 acyl CoA esters across cell membranes is not excluded.The variability of the organic aciduria, which possibly reflects changes in protein and fat intake, suggests that a previous name for this disorder,i.e., glutaric aciduria type II, is inappropriate and should be replaced, perhaps by “multiple acyl‐CoA dehydrogenase deficiency.”SpeculationWhat appears to be simultaneous deficiency of several acyl‐CoA dehydrogenases may be caused by a number of different primary gene defects; the presence of hypersarcosinemia and/or sarcosinuria may delineate a subtype due to deficiency of an electron carrier flavoprotein. Further, the presence of organic aciduria may define a form of hypersarcosinemia more likely to be associated with phenotypic abnormalities than isolated deficiency of the sarcosine dehydrogenase apoenzyme.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryPancreatic juice was collectedin vivofrom control and reserpine‐treted rats after stimulation with pilocarpine (0.2 mg/100 g body weight), dopamine (6‐7 mg/100 g body weight), caerulein (90‐100 pmole total dose) or with a combination of caerulein and secretin (6 u/100 g body weight) and the volume, amylase, bicarbonate and chloride outputs were compared. The results indicate that the secretory response to the three secretagogues was significantly reduced in the drug treated animals. Thus, the volumes of pancreatic juice were 57.0, 60.5, and 15.7% of those obtained in control rats after stimulation with, respectively, pilocarpine, dopamine, and caerulein. Amylase output was 63.8, 67.1, and 21.0% and bicarbonate output was 29.9, 46.8, and 6.2% of those observed in untreated rats after the same stimulants. Fluid secretion increased in the treated animals to 71.3% of that of controls when both caerulein and secretin were administered together and amylase output became greater than in control rats (151%). However, bicarbonate output was still 55.2% of that of controls with this combined stimulation. It is concluded that chronic reserpine administration impairs exocrine pancreatic secretion and that this effect involves both the acinar and ductal portions of the gland. This impairment involves the physiologic responses of these two segments of the glandular epithelium to both neural and hormonal stimulants. These findings suggest that the exocrine pancreatic disturbance in reserpine‐treated rats may be similar to that observed in cystic fibrosis (CF), and because the treated rat has been proposed as a model for the human disease, they suggest the use of this model as a test system for the study of the pancreatic secretory abnormality in CF.SpeculationRats treated in a chronic fashion with reserpine secrete significantly smaller amounts of fluid, amylase, and bicarbonate in pancreatic juice than control animals, whether secretion is elicited by hormonal or neural stimulants. The abnormality in exocrine pancreatic function induced by the drug treatment involves, therefore, the acinar and ductal segments of the gland and is similar to the alteration seen in patients with CF.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryBecause cholesteryl esters with very long chain fatty acids accumulate in Schilder adrenoleukodystrophy, the ability of extracts of such fibroblasts to hydrolyze [14C]cholesteryl lignocerate was examined. Hydrolytic activity was detected at pH 3.0, and this activity was impaired by sulfhydryl inactivating agents. Cholesteryl lignocerate hydrolysis was deficient in cells from patients with cholesteryl ester storage disease or Wolman disease due to acid lipase deficiency, but was in the control range for adrenoleukodystrophy fibroblasts. This suggests that cholesteryl lignocerate hydrolysis can be carried out by acid lipase.SpeculationDeficiency of a specific lysosomal lipase is probably not the genetic defect in Schilder adrenoleukodystrophy. A defect in long chain fatty acid metabolism may be more likely.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryLiposomes prepared with phosphatidylcholine (PC) labeled with [1‐14C]‐dipalmitoyl‐PC, dicetylphosphate, cholesterol (molar ratio 7:2:1) were injected into the right ear vein of 2‐month‐old male rabbits. At 5, 60, and 120 min after injection, organs were removed and analyzed for [14C]‐PC. Lung, liver, and spleen took up the [14C]‐PC by 5 min. Spleen accumulation of [14C]‐PC increased steadily, liver plateaued from 1‐2 hr, and lung fell rapidly. The uptake of liposomal [14C]‐PC by lung and liver was dependent on the concentration of iv injected liposomal [14C]‐PC. All lung subcellular fractions (lamellar bodies, mitochondria, and microsomes) took up [14C]‐PC. Lamellar body [14C]‐PC was highest at 5 min, and then decreased. Still, on a nmole/mg protein basis, uptake of [14C]‐PC by lamellar bodies was higher than other organelle fractions. Of the radioactivity in lung, 95% was [14C]‐PC even after 2 hr, whereas by 1 hr, 28% of liposomal PC absorbed by liver had been degraded.SpeculationNeonatal respiratory distress syndrome (RDS) is clearly related to alveolar lining surfactant deficiency. PC is quantitatively the principal phospholipid of that surfactant. If iv injected PC in the form of liposomes (large multilamellar concentric bilayer vesicles) can be taken up by lung lamellar bodies, it is possible that this PC will then be available for release to the alveolar surface. This potentially might become a unique biochemical approach in the therapy of neonatal RDS.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SpeculationDuring recovery from protein energy malnutrition, the augmented insulin release and metabolic rate that occurs with increased energy intake induces rapid rates of weight gain.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryThe relationship between pulmonary function and the migration of meconium to distal airways was determined in 10 rabbits (mean weight 2.6 kg) after insufflation of a meconium‐saline mixture (1‐2 ml/kg). Animals were anesthetized, cannulated, intubated, and mechanically ventilated with 100% oxygen. Lung mechanical dysfunction was most severe during the early phase of meconium migration, 15 min postinsufflation. Substantial increases in inspiratory lung resistance (RI) and expiratory lung resistance (RE) suggest that the site of obstruction at 15 min was the large airways. A decrease in dynamic lung compliance with unchanged static compliance characterizes the obstruction as partial. At 15 min and throughout the migration process, REwas greater than RI, demonstrating a check‐valve effect. This phenomenon was substantiated by an increased functional residual capacity (FRC) in all rabbits, presumably due to gas trapping. Secondary to these changes, marked hypoxemia, hypercapnea, and acidosis developed in spite of assisted ventilation with 100% oxygen. At 60 and 120 min postinsufflation, both RIand REdecreased as compared to 15 min. This suggests that the predominant site of obstruction shifted to medium and small airways concomitant with the migration of meconium. Widespread and uneven distribution of meconium still produced significant frequency dependence of lung compliance. Static compliance remained unchanged, indicating that meconium does not affect surface‐active or tissue properties of the lung within 120 min postinsufflation. These data suggest that effective respiratory management after meconium aspiration is dependent on the degree of meconium migration, as reflected by pulmonary mechanics.SpeculationSignificant effects of meconium aspiration on lung function are attributable to migrating obstructive phenomena, which result in a more severe lung dysfunction in earlier stages postinsufflation of meconium than in progressively later stages. It is appealing to speculate that noninvasive pulmonary function measurements made in newborn infants may quantitate the degree of mechanical obstruction and meconium migration in the airways. This information would provide guidelines for effective respiratory management of infants with meconium aspiration syndrome (MAS). Based on the present animal model, elevated oxygen therapy should be employed early to offset the severe hypoxemia. In addition, the check‐valve effect (RE> RI) indicates the use of a low I/E ratio in assisted ventilation. It has been shown that continuous positive airway pressure improves arterial oxygen tension in some newborns with MAS. However, in light of the mechanical dysfunction resulting in an increased FRC, caution is recommended in the use of end distending pressure within 2 hr after meconium aspiration.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID

摘要:

SummaryPlasma aldosterone (A), corticosterone (B), deoxycorticosterone (DOC), progesterone (P), 17‐hydroxyprogesterone (17‐OHP), cortisol (F), and cortisone (E) were measured simultaneously by specific radioimmunoassays in small plasma samples obtained from 174 normal infants and children between 2 hr and 15 yr of age. The significantly elevated neonatal mean levels (ng/ml) of 2.5 (A), 4.1 (DOC), 53.0 (P), and 6.6 (17‐OHP) dropped significantly during infancy reaching prepubertal levels between 3 months and 3 yr of age, with a transient, significant DOC increase between 1‐7 yr. The glucocorticoids F and B declined significantly from means of 68 and 4.4 to 11.4 and 0.28 ng/ml, respectively, during the first weeks of life, then increased significantly reaching adult levels between 1‐3 yr of age. Mean E fell progressively from 74 ng/ml after birth to 10 ng/ml during 1‐5 yr (P<< 0.0001), then slightly increased to adult levels. After age 7 yr, P and 17‐OHP, in contrast to the other steroids, rose significantly in both boys and girls relative to pubertal development.The observed changes are thought to be due to (1) adaptation of the adrenal neocortex to extrauterine life after disruption of the fetoplacental unit, (2) a physiologic lack of corticosteroid binding globulin (CBG) during infancy due to maturation of hepatic CBG biosynthesis, (3) the functional immaturity of the infant kidney compensated by an increased activity of the renin‐angiotensin‐aldosterone system, and (4) gradually increasing gonadal secretion of progestins during puberty.SpeculationFrom birth to adulthood, marked evolutional changes were observed in the basal plasma concentrations of all physiologically important unconjugated corticosteroids and progestins in normal children. Detailed knowledge of the age‐dependent normal plasma steroid pattern reflecting maturational processes of both the hypothalamo‐adrenocortical and the hypothalamo‐gonadal axis, of the renin‐angiotensin‐aldosterone system, and of hepatic and renal function, therefore, is a prerequisite for understanding pathologic conditions in pediatric endocrinology.

ISSN:0031-3998    

出版商:OVID    

年代:1980

数据来源: OVID