摘要:

SummaryTo examine the influence of feeding on the chemical control of breathing in neonates, we studied the ventilatory response to 3% CO2in air in nine bottle fed (BOT) and eight breast fed (BR) term infants during feeding while the infants were alert. Control responses were obtained either before or after feeding. &OV0312;E, respiratory frequency, tidal volume, inspiratory time, expiratory time, and sum of inspiratory and expiratory time, VT/Ti, Ti/Ttot, PACO2and slope (S) of CO2response (liter/min/kg/mmHg) were determined. During 3% CO2while resting BR had a lower &OV0312;E, VT, VT/ Ti than BOT and S in BR was 40% of BOT (P< 0.05). During feeding and CO2when compared to resting and CO2there was no difference in either BR or BOT in VT/Ti but Ti/Ttotdecreased in both groups. During feeding, S in BOT was reduced from 0.049 ± 0.012 (mean ± S.E.) to 0.013 ± 0.002 (74% reduction) and in BR from 0.020 ± 0.002 to 0.009 ± 0.002 (55%). Thus, behavioral activity (either BR or BOT) markedly depresses the ventilatory response to chemical stimuli (CO2). This modification is primarily related to changes in “effective” respiratory timing (Ti/Ttot) rather than mean inspiratory flow (VT/Ti).SpeculationThis is the first demonstration in the newborn infant that behavioral activity (feeding) can override the usual ventilatory control mechanisms. The precise mechanism is unknown and requires further study.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryRenal uric acid excretion was examined in 35 mongrel puppies at 1,30,60 and 90 days of age and in seven mature mongrel dogs. Uric acid concentrations in plasma and urine were determined using a uricase fluorometric method. Clearance of inulin increased with postnatal age; however, fractional excretion of uric acid (FEUA) decreased from 83% at birth to 51% at 90 days of age (r= −0.675,P< 0.001). Filtered uric acid and net reabsorption of uric acid increased with postnatal development. The decline in FEUAwith postnatal age was unrelated to binding of uric acid to plasma proteins or to urine flow rate. A direct correlation was observed between clearance of uric acid (CUA) and clearance of sodium (CNa) during early development (r= 0.48,P< 0.001). These data indicate that postnatal maturational patterns of renal urate excretion in mongrel puppies are similar to human newborns.SpeculationThe high FEUAobserved during early postnatal development in the puppy represents decreased tubular reabsorption and/or increased renal tubular secretion of uric acid. In early development, tubular reabsorption of uric acid may be diminished as a result of the high extracellular fluid volume (ECFV). The persistence of high FEUAin puppies at 2 and 3 months of age may be the result of physiologic factors which are different than those in the first day of life. The mongrel puppy appears to be an appropriate animal model for further investigations of renal uric acid transport during human development

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryPhotodegradation of bilirubinin vitrohas been investigated by using monochromatic light supplied by an argon ion laser selecting the 457.9, 488.0 and 514.5 nm wavelengths.Bilirubin was examined in chloroform, in aqueous solutions and in human serum under different experimental conditions of concentration, laser power and time of irradiance. Photodecomposition was followed by optical density measurements on the absorption maximum of the electronic band at 460 nm.The rate of degradation of bilirubin was found to be only slightly affected by the wavelength of the exciting lines provided they fall within the absorption band. In particular it was shown that any wavelength, &lgr;, is equally effective if the corresponding absorbance, A&lgr;, exceeds a minimum value of 5–10%. In the aqueous solutions, light with &lgr; > 470 nm has been found to be largely effective in the photodegradation of bilirubinin vitro.SpeculationThe results of bilirubin degradation by wavelengths longer than 470 nmin vitrosuggest the use of green light in the clinical procedure in order to reduce damages to the tissues which can be caused when higher frequency radiations are employed.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryHypoxic ventilatory responses and 100-msec inspiratory occlusion pressures (P100s) were measured at constant alveolar PCO2(normocapnia) in 13 asthmatic [12.5 ± 1.0 (S.E.) years] and in 12 normal children (13.3 ± 0.6 years) to determine the appropriateness of the asthmatics' minute ventilation and ventilatory (inspiratory) drive, respectively. Most asthmatics were well controlled with continuous drug therapy and exhibited only mild pulmonary abnormalities at the time of testing. Hypoxia-induced increases in minute ventilation were quantitated in terms of A-values per m2body surface area. An A-value describes, in numerical terms, the slope of the hyperbolic ventilatory response to progressive alveolar hypoxia. Larger A-values denote greater increases in ventilation. The A-values were not significantly different between the asthmatic (105 ± 14) and normal children (123 ± 24). The occlusion pressures were significantly different, however, and were 2.3 ± 0.2 cm H2O (sub-atmospheric) for the asthmatics and 1.5 ± 0.1 cm H2O for the normal children at an alveolar PO2= 80 mm Hg, and 7.7 ± 0.9 and 5.2 ± 0.8 cm H2O for the respective groups at an alveolar PO2=40 mm Hg (P< 0.05). These findings indicate that asthmatic children with minimal pulmonary abnormalities maintain a normal ventilatory response to alveolar hypoxia by increasing their ventilatory drive, whereas adult asthmatics have been reported to have less than a normal increase in ventilatory drive and hence a diminished ventilatory response during hypoxic exposure.SpeculationAlthough the mechanism(s) which diminishes the hypoxic ventilatory response and drive in asthmatic adults, but not in asthmatic children, is not known, it may relate to hypoxic exposures or advancing age.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryHuman serum opsonins to type III Group B streptococci (GBS) were studied in anin vitroopsonophagocytic assay. Two type III GBS test strains were susceptible (893 and IIINor) and two resistant (891 and 892) to opsonization by the majority of sera from 15 healthy adults. Four individuals with undetectable or low opsonic liters to the test strains were immunized with pneumococcal vaccine; immunization with pneumococcal vaccine induced a titer rise in all but one instance when susceptible GBS strains were tested. In contrast, only a single titer rise was detected when resistant GBS strains were employed in the test. These results indicate that immunization with a cross–reacting antigen (identical to core antigen of type III GBS) fails to induce opsonic antibody to all strains of type III GBS. A resistant strain was made highly susceptible to neutrophil killing in vitro by exposure to neuramindase prior to incubation with opsonic serum. Using a fluorescent lectin–binding assay, this enzyme appeared to remove surface sialic acid, suggesting that sialic acid is an antiphagocytic factor. However, the possibility that other surface moieties may act as antiphagocytic factors cannot be ruled out. Both opsonic susceptible and resistant strains absorbed opsonic antibody from serum, which suggests that the GBS antiphagocytic factors do not prevent binding of antibody to resistant bacteria.These findings indicate that demonstration of serum opsonic activity to one strain of type III GBS may not accurately depict opsonic activity to other strains. In addition, immunization with core antigen did not enhance opsonic activity against all GBS strains. These data also point out the need to use assays which measure functional antibody, since demonstration of antibody binding may not reflect its ability to facilitate bacterial phagocytosis and killing.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryTo study the effect of corticosteroids on postnatal maturation of Na+transport in the small intestine, we studied 10–12-day-old suckling rabbits after they had received cortisone acetate, 20 mg/kg SC on days 3, 4, and 5 of life. When killed, the cortisone-injected animals weighed significantly less than saline-injected controls. In jejunal villus enterocytes isolated from this cortisone-treated group, the specific activities of sucrase and Na+-K+-ATPase were significantly greater than those in control enterocytes. Studied in Ussing chambers, a significant electrical and ion-flux response to glucose was observed hi the jejunal epithelium of the treated group, but not in controls. We conclude that exogenous cortisone, administered early in life, can stimulate the precocious development not only of certain epithelial enzymes but also glucose-facilitated Na+transport in the jejunum of the rabbit.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

摘要:

SummaryFour possible modes of action for the clinically observed effectiveness of sulfamethoxazole/trimethoprim in chronic granulomatous disease were evaluated: (1) inhibition of bacterial catalase, (2) improvement of granulocyte oxygen metabolism, (3) synergism of the antibiotic with nonoxygen-dependent granulocyte killing mechanisms, and (4) a purely antibiotic effect based on uptake and concentration of the antibiotic by and within granulocytes.While the first three mechanisms were excluded, the fourth mechanism is highly probable; sulfamethoxazole was found to reach granulocyte associated concentrations 1.7-fold and trimethoprim 4.1-fold of extracellular levels. Penicillin G, a known non-penetrating antibiotic, reached 0.3-fold, and tetracycline, a known penetrating agent, 7.1-fold the extracellular level. These findings indicate that sulfamethoxazole/trimethoprim is an antibiotic combination uniquely suited for the long-term prophylaxis of infections in patients with defects of intracellular phagocyte killing.SpeculationCell permeable antibiotics that concentrate within the acidic granules and vacuoles of phagocytes are likely to be lipid-soluble weak bases.

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID

ISSN:0031-3998    

出版商:OVID    

年代:1981

数据来源: OVID