摘要:

SummarySuperoxide dismutase (SOD) and glutathione peroxidase (GPx) key enzymes in alveolar macrophages regulating levels of super-oxide anion and hydrogen peroxide, respectively, were observed to fluctuate in response to FIO2of 50 and 85% for 18 to 90 hr. At the lower oxygen tension, SOD rose two-fold and GPx decreased significantly by 18 hr and throughout the exposure periods compared to a delayed increase in SOD activity which was not sustained beyond 66 hr of exposure and a sustained rise in GPx to an FIO2of 85%. Peritoneal macrophages containing lower SOD activity and greater GPx activity than resident alveolar macrophages upon injection into the circulation resulted in a 10-fold accumulation in the lungs during exposure of animals to FIO2of 85% but not at 50%. This study indicates that brief exposure to FIO2of 85% but not 50% resulted in alterations of the vascular integrity of the lungs resulting in the accumulation of circulating macrophages to the alveolar macrophage pool. The delayed rise in SOD activity and the sustained increase in GPx activity in alveolar macrophages from animals exposed to FIO2of 85% could in part be related to this influx of circulating macrophages with enzymatic characteristics observed for peritoneal macrophages.SpeculationToxic concentrations of oxygen not only affect the metabolism and enzyme responses of resident alveolar macrophages but incite the early influx of circulating macrophages into the lung favoring the accumulation of superoxide anion which could propagate the inflammatory reaction.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryThe response to parathyroid hormone (PTH) and calcitonin (CT) was studied in eight children with various bone diseases by determining the serum calcium (Ca) and phosphate (P) concentration, urinary phosphate excretion rate, renal phosphate clearance, the percentage of filtered phosphate reabsorbed by the renal tubule (%TRP), creatinine clearance (Ccr), urinary cyclic adenosine 3′,5′ monophosphate excretion rate (UcAMPV), and urinary cyclic guanosine 3′,5′ monophosphate excretion rate (UcGMPV). Administration of PTH caused no significant change in serum Ca and P values, whereas CT produced a decrease in Ca (Δ Ca, −1.4 ± 0.1 mg/100 ml) and P (ΔP; −1.1 ± 0.1 mg/100 ml). There was an increase in UcAMPV (ΔUcAMPV; 437 ± 74 nmoles/min/100 ml Ccr) without any significant change in UcGMPV after administration of PTH. Phosphaturia was produced by both PTH (Δ TRP, −18 ± 3%) and CT (ΔTRP, −13 ± 2%). However, CT did not elicit any increase in either UcAMPV or UcGMPV.SpeculationParathyroid hormone (PTH) and calcitonin (CT) induce phosphaturia of a similar magnitude whereas PTH alone increased the urinary excretion of cyclic adenosine 3′,5′ monosphosphate (cAMP). The phosphaturia induced by CT may not be mediated by a similar mechanism involving the adenylate cyclase-cAMP system as demonstrated for PTH.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryThe ontogeny of β-adrenergic receptors and the characteristics of catecholamine sensitive adenylate cyclase activity were demonstrated in rat ventricular myocardium. β-Adrenergic receptors were identified by the binding of (—)-[3H]dihydroalprenolol, [(—)-[3H]DHA|, and (±)-[125I]iodohydroxy-benzylpindolol, (±)-[125[I]HYP. Heart weight, protein, and the number of β-adrenergic receptors per cell increased with advancing age; however, binding capacity (Bmax) per nig protein was lower in membrane from the adult rat (220 g body weight) than in membrane from the fetal or neonatal rat, 36.8 ±4.1 and 58.3 ± 6.3 fmoles·mg−1protein, respectively, mean ± SE,P< 0.01. The age-dependent increase in the numbers of receptors per heart correlated well with the increases in ventricular weight. In contrast, protein content, Na+, K+-ATPase, 5′-nucleotidase, and adenylate cyclase content increased more rapidly than ventricular weight, and the developmental increase in [3H]DHA binding sites (per heart) did not keep up with increases in ventricular protein. Although specific activity of (—)-[3H]DHA binding was lower in the adult ventricle, the characteristics of the β-receptor did not vary with age; the subtype was β1determined by classical agonist competition in fetal and adult ventricular membranes and the β1- and β2-adrenergic receptor subtypes were present in the ratio of 75% β1and 25% β2in both fetal and adult samples. Guanine nucleotides decreased agonist affinity for the inhibition of (±)-[125I]HYP binding equally in adult and fetal samples and enhanced the activation of adenylate cyclase by catecholamine. Basal adenylate cyclase activity was significantly higher in weanling, 13.4 ± 1.42, and adult, 14.2 ± 5.8, than in 21-day fetal or newborn ventricular membrane, 8.18 ± 1.5 pmoles cyclic adenosine 3′:5′-monophosphate produced mg−1· min−1(mean ± S.D.). The percent activation by catecholamine (with and without GTP) was also slightly higher in samples from the older rats,P< 0.01. In the adult and weanling heart, both guanine triphosphate (GTP) and guanyl-5′-yl-imidodiphosphate [Gpp(NH)p] were effective in enhancing catecholamine sensitive activity. Maximal catalytic activation of adenylate cyclase was observed in the presence of (—)-epinephrine and Gpp(NH)p and was significantly higher (fold stimulation) in fetal or neonatal ventricular samples as compared to adult or weanling ventricular samples,P< 0.01.SpeculationThe decreased specific activity (per mg protein) of β-adrenergic receptors in adult as compared to fetal and neonatal myocardium may therefore be related to the decreasing proportion of sarcolemmal proteinversustotal and particulate cell protein which occurs during hypertrophic cardiac growth, supporting the hypothesis that sarcolemmal surface area is a major determinant of β-receptor number. In contrast, sarcolemmal activities which mediate cellular functions by regulating the concentration of various substances within the cell, such as Na+, K+-ATPase, and adenylate cyclase, increased to a greater extent than (—)-[3H]DHA binding, and were more directly proportional to cell protein. The function and affinity of these β-adrenergic receptors in the rat myocardium are mediated by guanine nucleotides early in development, and age-dependent differences in the activation of catecholamine sensitive adenylate cyclase by GTP and Gpp(NH)p may relate to developmental differences in the properties of guanine nucleotide-dependent factors which mediate receptor occupancy and cyclic adenosine 3′:5′-monophosphate formation.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryAllometry, defined as the relationship between the growth rates of organs to the weight of the whole body (38), was used to study the effect of age on the degree of compensatory renal growth (CRG) in the mouse. The normal growth of the kidneys relative to body weight (BW) was determined in animals between 5 to 50 days of age. In one group, nephrectomy and sham operations were performed at 5, 15, and 35 days of age. The remaining (“renopri-val”) kidney was removed 15 days postnephrectomy. In a second group, nephrectomy was performed on 5-day-old animals, the renoprival kidney being removed after 30 or 45 days. Regression equations were calculated by least-squares after logarithmic transformation and different groups were compared by analysis of covariance. The regression equation for the control kidney was kidney weight (KW) = 0.0093 BW0.86(r = 0.96). The regression for renoprival kidneys in females was KW = 0.0142 BW0.83(r = 0.96) after 15 days and, in comparison, was not significantly different after 30 to 45 days. The intrval between control and renoprival regressions was equivalent to a difference of ≃43% KW. In male mice, the regression for renoprival kidneys after 15 days was KW = 0.0103 BW0.96(r = 0.98) and was not significantly different after 30 to 45 days. This study suggests that in young mice the time required for complete CRG may be a maximum of 15 days and that the amount of CRG does not depend on the age at operation. After CRG, a new equilibrium is reached which is therafter maintained up to a minimum of 50 days of age.SpeculationUse of allometry to study compensatory renal growth suggests that the renoprival kidney grows rapidly until its mass is 70 to 75% of the normal total renal mass, after which its growth rate reaches an equilibrium with body weight. This precise degree of growth, which is known to occur mostly in the cortex, suggests the existence of a negative feedback loop regulating overall kidney weight when cortical mass (or function) is restored.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryAllometry was used to study the effect of growth hormone (GH) deficiency on compensatory renal growth (CRG) in a dwarf mouse strain (Little). Nucleic acid and protein estimations were used to assess changes in cellular hyperplasia and hypertrophy. Nephrectomy was performed at 5,15, or 35 days of age with removal of the renoprival kidney 15 days later. Controls underwent sham nephrectomies at 35 days of age. The allometric growth of the normal kidney in the homozygote dwarf (lit/lit) between 8 and 50 days of age was closely related to that of the normal heterozygote (lit/ +). A regression line for the renoprival kidneys in lit/lit animals was parallel to that of the control right kidney (P< 0.001). The interval between the regression lines was equivalent to a constant difference of approximately 40% between renoprival and control right kidneys and was similar to that found in the normal heterozygote (43%). Increases in DNA, RNA, and protein in control animals during CRG indicate that cell division and hypertrophy were occurring in similar proportions. In the GH-deficient mouse, the total amount of DNA in renoprival kidneys was 0.451 mg compared with 0.439 mg in controls (NS). This suggests that cell replication was suppressed. The protein:DNA ratio increased from 20.91 to 24.27 (P< 0.001) and the RNA:DNA ratio increased from 0.732 to 0.912 (P< 0.001), suggesting that cell size was markedly increased. These findings suggest that reduced amounts of GH may produce a dissociation between hyperplasia and hypertrophy, with CRG occurring predominantly by cellular hypertrophy.SpeculationGrowth hormone deficiency does not prevent compensatory renal growth, which occurs to the same extent in control and growth-hormone-deficient animals, both of which have undergone nephrectomy. However, the increase in kidney size is accomplished predominantly by cellular hypertrophy instead of cell replication.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryA 10-year longitudinal study was conducted on 26 prepubescent youngsters who had undergone successful weight reduction. Their ages ranged from 2 to 10 years when the study began. In all subjects, weight reduction proceeded only by a decrease in adipose cell size (from 0.62 ± 0.02 to 0.46 ± 0.02 μg lipid per cell) and resulted in a corresponding 33% decrease (from 177 ± 6 to 144 ± 5%) in percent ideal body weights. Cell numbers did not change appreciably during the period of weight loss (29.4 ± 2.6versus28.7 ± 2.3 × 109total adipocytes). Three years after the start of the study, 14 of 20 youngsters had maintained their reduced percent ideal body weights, including eight who remained below 130% ideal body weight. Ten years later, only four remained below 130% ideal body weight. AH four children had total adipose cell numbers below 20 × 109total adipocytes at the start of the weight reduction program, a value below the lower limit for adult normal weight subjects. Thirteen other children have maintained or decreased their initial percent ideal weights. The remaining nine youngsters have further increased their percent ideal body weights.In vitrometabolic studies of the patient's adipocytes revealed a >50% depression of epinephrine-stimulated lipolysis pre- and immediately postweight reduction; this decrease persisted for the entire period of study, irrespective of the maintenance of a normal percent ideal body weight. At the same time, normal 150% increases in thein vitroproduction of14CO2from [1-14C]glucose in the presence of insulin occurred.SpeculationMaintaining weight reduction long term is generally unsuccessful except in a small minority of very young obese children. Therefore, if the prevalence of obesity and its associated diseases are to be decreased, very early identification of at-risk youngsters is important. Specific enzymatic and metabolic alterations in these children,e.g., depression ofin vitroepinephrine-stimulated lipolysis, appear to be useful for early identification of susceptible individuals. In addition, this study indicates that factors such as genetics and gestation may lay the groundwork for the future development of increased adiposity.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryBecause of lack of acceptability of the previous log-linear model of slope velocity for the assessment of weight and length in children 1 to 36 months of age, a modified method for least squares determination of velocity of growth by slope has been designed. This model uses a compound logarithmic expression of tune and a newly designed graphic scale. The acceptability of the graphic (hand-drawn) line is retained while “goodness of fit” of the model is improved. This improved model makes it possible to revise our standards for velocity of growth of children 1 to 36 months of age.SpeculationWhen applied to clinical situations of abnormal growth, this model shouldhelp in the evaluation of patient growth. Along with the previously developed model for children 3 to 12 yr of age, it will form the basis for new office charts for the practitioner.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID