摘要:

The substrate and oxygen uptake by some organs in intact developing animals has been described, however, the kidney has not been studied. To examine substrate and oxygen uptake by the kidney, we implanted polyvinyl catheters into the renal vein, descending aorta, inferior vena cava, and urinary bladder of 11 fetal sheep (120–125 days gestation) and eight newborn lambs (1 day postnatal). Four days after surgery, blood samples were obtained simultaneously from the renal vein, aorta, and inferior vena cava for determination of oxygen content and saturation, and glucose and lactate concentrations. Renal blood flow was determined by the radionuclide-labeled microsphere method in the fetal lambs and by measuring,14C-inulin clearance in the newborn lambs. The fetal and newborn kidneys consumed oxygen at rates of 123 ± 16 and 785 ± 79 μmol/min/100 g kidney weight (mean ± SEM), respectively. The increase in oxygen consumption from the fetal to the newborn period was accompanied by an increase in oxygen extraction from 25–35%, a large increase in oxygen delivery from 418 ± 38 to 2231 ± 127 μmol/min/100 g, and marked increases in glomerular filtration rate and sodium reabsorprion (measured in six additional fetal sheep and the eight newborn lambs). This suggests that the postnatal increase in renal tubular activity is associated with an increase in oxygen consumption. Lactate was taken up by both fetal and newborn kidneys, and in nine of the 11 fetuses and in four of the eight newborns, there was net glucose release from the kidney.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Cerebrovascular volume and transmural pressure loads accompanying acute increases in cerebral blood flow are implicated in the pathogenesis of periventricular-intraventricular hemorrhage in preterm infants. An acute increase in cerebral blood flow would be expected during acute recovery from asphyxia. Therefore, cerebrovascular hemodynamics, including flow (microspheres), were studied during and after acute recovery from asphyxia in seven newborn dogs in order to study the determinants of these volume and pressure loads. During the acute recovery phase, cerebral hemispheric blood flow was 69.6 ± 10 ml/100 g/min (mean ± SEM) representing a 250% increase from baseline values of 19.9 ± 1.8 ml/100 g/min (p< 0.005), while combined cerebellar-brainstem flow was 204.3 ± 19.3 ml/100 g/min representing a 536% increase from baseline values of 32.0 ± 1.5 ml/100 g/min (p< 0.005). Blood flow to both areas had returned to baseline levels 20 min after the onset of recovery. Associated with this cerebral hyperemia was an acute increase in mean arterial pressure from 21.3 ± 4.5 mm Hg at end asphyxia to 69.5 ± 6.0 mm Hg at peak recovery (p< 0.01), and parallel acute increases in sagittal sinus pressure (from 4.0 ± 0.4 to 14.6 ± 1.9 mm Hg,p±.01) and cerebrospinal fluid pressure (from 3.8 ± 0.4 to 14.3 ± mm Hg,p<1). Central venous pressure fell from 4.3 ± 6 mm Hg at end asphyxia to 1.6 ± 0.5 mm Hg, and thus is not a determinant of the elevation in sagittal sinus pressure. AH of these pressure changes were attained within 20–30 s of the onset of recovery. Assuming that acute changes in cerebrospinal fluid pressure reflect acute changes in cerebrovascular volume via the cranial compliance (volume/pressure) relationship, then the acute (<30s) elevation of cerebrospinal fluid pressure reflects an acute cerebrovascular volume load. Also, the elevated cerebrospinal fluid pressure considerably modifies both the cerebral arterial and venous transmural pressures. The cranial compliance relationship thus plays a key role in determining both volume and transmural pressure loads. We propose that the combination of a high cranial compliance and frequent acute cerebral flow/volume loads may be involved in the pathogenesis of periventricular-intraventricular hemorrhage in premature newborn infants.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

We studied the effect of environmental hypothermia on arterial blood pressure, dorsal aortic blood flow, and vascular resistance in stage 18, 21, and 24 chick embryos. The arterial pressure was measured with a servo-null micropressure system. Mean dorsal aortic blood flow was calculated from pulsed-Doppler measurement of mean dorsal aortic blood velocity and dorsal aortic diameter. Vascular resistance was calculated by dividing mean vitelline arterial blood pressure by dorsal aortic blood flow. Sequential data were obtained at temperatures of 34.7, 31.1, and 34.1° C. At stage 21, the vitelline arterial blood pressure decreased from 0.82 ± 0.03 (&OV0335; ± SEM) to 0.72 ± 0.03 mm Hg on cooling and increased from 0.66 ± 0.05 to 0.87 ± 0.06 mm Hg on rewarming (p < 0.05). At stage 21, mean dorsal aortic blood flow decreased from 0.49 ± 0.02 to 0.33 ± 0.02 mm3/s with cooling and increased from 0.34 ± 0.02 to 0.47 ± 0.02 mm3/s with rewarming. The vascular resistance in stage 21 embryos increased after cooling from 1.68 ± 0.19 to 2.23 ± 0.39 mm Hg/mm3/s (&OV0335; ± 95% confidence interval). The changes were similar in stage 18 and 24 embryos. We conclude that the reduction of vitelline artery blood pressure resulted from a decrease in cardiac output. In addition, we noted that the vitelline arterial vascular bed can constrict in response to hypothermia prior to autonomic innervation. These changes in hemodynamics may be a teratogenic mechanism for hypothermia-induced cardiac defects in the chick embryo.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

In vitrodifferentiation of B lymphocytes present in cord blood mononuclear cell preparations into immunoglobulin secreting cells was studied in 126 neonates with gestational ages (GA) ranging from 20 to 44 wk. Eight infants had a GA less than 27.9 wk, 24 had GA 28–32.9 wk, 30 had GA 33–37.9 wk, 51 had GA 38–41.9 wk, and 13 had GA above 42 wk. B cell differentiation in response to pokeweed mitogen plus hydrocortisone was assessed using a plaque forming cell assay. All neonates had a measurable plaque-forming cell response in this assay. An increased plaque-forming cell response was observed in some neonates in all gestational age groups. The magnitude ofin vitroneonatal B cell differentiation underwent a continuous and significant (p< 0.002) reduction as gestational age increased. The influence of intrauterine growth retardation onin vitroB lymphocyte differentiation was studied and compared to gestational age-matched controls with a normal intrauterine growth. Intrauterine growth retardation was not associated with changes in B cell responsiveness. An analysis of perinatal factors revealed that cesarean section, and low 1-min Apgar scores were factors that predisposed cord blood cells to be triggeredin vitroto produce increased numbers of plaque-forming cells.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Hyperglycemia in fetal sheep has been shown to increase the fetal metabolic rate. Fetal venous glucose infusion was performed in eight late gestation, chronically catheterized fetal lambs to assess any changes in substrate uptake by the ovine uterus and conceptus. Fetal glucose infusion (11.9 ± 0.6 mg glucose kg−1min−1) caused a stable increase in fetal plasma glucose concentration approximately 3-fold above baseline. The fetal glucose entry rate increased from 6.6 ± 0.7 to 9.3 ± 0.6 mg kg−1min−1by day 3 of infusion(p< 0.01) despite a net umbilical glucose excretion during the period of fetal hyperglycemia. Due to a concomitant increase in fetal oxygen consumption, no change in fetal glucose/O2quotient was observed. A significant relationship was noted (p< 0.02) between the fetal glucose entry rate and the rate of fetal oxygen consumption. Fetal glucose infusion caused a decrease in uterine glucose uptake as well. No changes were observed in‘ calculated net placental glucose uptake although the relative fetal contribution increased from net placental exit to fetus to a placental uptake amounting to 20.8 ± 5.8% of the total placental glucose uptake (p< 0.01). Although no changes in fetal lactate concentration occurred, both maternal and fetal lactate entry rates increased, the magnitude of increase being significantly related to fetal glucose concentration. Both maternal and fetal insulin concentrations rose during the period of fetal hyperglycemia and were related to the respective increases of maternal or fetal’ substrate uptakes but not to fetal oxygen consumption.I These studies suggest that glucose induces significant stimulation of fetal oxidative metabolism and that fuel needs during this period are met by accelerated fetal glucose entry as well as accelerated placental production of lactate, Superimposed hypoxemia during these circumstances might be expected to have a greater effect on fetal oxygenation and pH than during normoxemic circumstances.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Three children from unrelated families presented in early childhood with hypoglycemia and cardiorespiratory arrests associated with fasting. Significant hepatomegaly, cardiomegaly, and hypotonia were present at the time of initial presentation. Ketones were not present in the urine at the time of hypoglycemia in any patient; however, dicarboxylic aciduria was documented in one patient at the time of the acute episode and in two patients during fasting studies. Total plasma carnitine concentration was low with an increased esterified carnitine fraction. These findings suggested a defect in mitochondrial fatty acid oxidation, and specific assays were performed for the acyl coenzyme A (CoA) dehydrogenases. These analyses showed that the activity of the long-chain acyl CoA dehydrogenase was less than 10% of control values in fibroblasts, leukocytes, and liver tissue. Activities of the medium-chain, short-chain, and isovaleryl CoA dehydrogenases were not different from control values. With cultured fibroblasts, CO2evolution from long-chain fatty acids was significantly reduced, while CO2evolution from medium-chain and short-chain fatty acids was comparable to control values—findings consistent with a defect early in the β-oxidation sequence. Studies of acyl CoA dehydrogenase activities in fibroblasts and leukocytes from parents of the patients showed levels of long-chain acyl CoA dehydrogenase activity intermediate between affected and control values and indicated an autosomal recessive form of inheritance of this enzymatic defect. These results describe a previously unrecognized metabolic disorder of fatty acid oxidation due to a deficiency of the long-chain acyl CoA dehydrogenase which may present in early childhood with disastrous consequences. This diagnosis should be considered in children who present with nonketotic hypoglycemia, carnitine insufficiency, and inadequately explained cardiorespiratory arrests.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Medium-chain acyl coenzyme A (CoA) dehydrogenase deficiency was demonstrated in fibroblasts and/or mononuclear leukocytes from 14 patients, most of whom initially presented early in childhood with a Reye-like syndrome associated with hypoketotic hypoglycemia, dicarboxylic aciduria, and low levels of plasma carnitine. Parents of these patients had intermediate levels of medium-chain acyl CoA dehydrogenase activity, consistent with their being heterozygous for an autosomal recessive trait. All patients had normal levels of long-chain acyl CoA dehydrogenase activity, but had reduced short-chain acyl CoA dehydrogenase activity. Fatty acid oxidation was examined in cultured fibroblasts from five of the patients, using a series of14C-labeled fatty acids of different chain length (palmitic, octanoic, and butyric). Oxidation of [l-14C]-octanoic acid was less than 20% of control levels: [l-,14C], [6-,4q-, [16,4q-, and [14C(U)]-palmitic acid oxidation rates were 88, 51, 13, and 42% of control rates, respectively. [l-14C]-butyric acid was oxidized normally. These data extend our previous findings of medium-chain acyl CoA dehydrogenase deficiency in liver tissue from three of these patients. They demonstrate the value of cultured fibroblasts and leukocytes in the diagnosis and evaluation of inherited disorders of fatty acid oxidation.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The transepithelial potential difference (PD) is raised across cystic fibrosis (CF) respiratory epithelia. This raised voltage reflects active sodium absorption across a relatively chloride impermeable membrane. Because relatively little is known about the regulation of the rate of sodium absorption across mammalian airways, we assessed the possible contribution of aldosterone to the PD in normal and CF respiratory epithelia. Aldosterone excretion in five CF patients was 12.2 ± 0.9 μg/24 h, a mean value not different from normal control subjects (13.6 ± 1.5 μg/24 h,n= 5). Despite similar aldosterone excretion rates, nasal PD was more than 2-fold greater in the CF patients (-53.6 ± 6.4 mV) than normal subjects (-21.3 ± 1.4 mV). The effect of an aldosterone antagonist, spironolactone, on aldosterone excretion and nasal and rectal PD was evaluated in four CF patients and five normal subjects. During spironolactone administration, aldosterone excretion increased (2− to 4-fold) and rectal PD decreased in both groups. However, nasal PD was unchanged in each group (CF = −52.1 ± 4.3 mV pre, −53.6 ± 1.4 mV during; normal = −21.2 ± 3.1 mV pre, −21.6 ± 3.2 mV during). We conclude that neither increased aldosterone secretion rates nor organ sensitivity to aldosterone can account for the abnormally raised PD that characterizes the respira.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The aim of the present work was to study whole body protein synthesis and breakdown, as well as energy metabolism, in very low birth weight premature infants (< 1500 g) during their rapid growth phase. Ten very low birth weight infants were studied during their first and second months of life. They received a mean energy intake of 114 kcal/kg day and 3 g protein/kg day as breast milk or milk formula. The average weight gain was 15 g/ kg day. The apparent energy digestibility was 88%, i.e. 99 kcal/kg-day. Their resting postprandial energy expenditure was 58 kcal/kg-day, indicating that 41 kcal/kg day was retained. The apparent protein digestibility was 89%, i.e. 2.65 g/kg-day. Their rate of protein oxidation was 0.88 g/kg-day so that protein retention was 1.76 g/kg-day. There was a linear relationship between N retention and N intake (r= 0.78,p< 0.001). The slope of the regression line indicates a net efficiency of N utilization of 67%. Estimates of body composition from the energy balance, coupled with N balance method, showed that 25% of the gain was fat and 75% was lean tissue. Whole body protein synthesis and breakdown were determined using repeated oral administration of15N glycine for 60–72 h, and15N enrichment in urinary urea was measured. Protein synthesis averaged 11.2 g/kg-day and protein breakdown 9.4 g/ kg day. Muscular protein breakdown, as estimated by 3-methylhistidine excretion, contributed to 12% of the total protein breakdown. There was a positive correlation (r= 0.68,p< 0.05) between protein synthesis and protein gain, as well as between resting energy expenditure and protein gain (r= 0.58,p< 0.01). The slope of the regression line indicated that 1 g of protein gain required the synthesis of five times more protein (5 g) and resulted in an extra energy expenditure of 10 kcal. Thus, the net cost of protein synthesis in these very low birth weight infants was 2 kcal/ g.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

This report describes the development of superoxide dismutase, glutathione peroxidase, and catalase activities in fetal (days 16–22) and neonatal (day 2 postpartum) lungs of normal rats. Each of the enzymes showed an individual pattern of development in the perinatal period. Glutathione peroxidase activity increased by 135% (p< 0.001) during the last 3 days before birth, catalase activity by 105% (p< 0.01) during the first 2 postnatal days, and the activity of superoxide dismutase by 52% (p< 0.05) from gestational day 19 to 2 days after birth. Contamination by superoxide dismutase from blood in the lung samples accounted for less than 2% of the activity. In contrast, not less than 10–30% of glutathione peroxidase.

ISSN:0031-3998    

出版商:OVID    

年代:1985

数据来源: OVID