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Biomedical subjects

E B Brown

Publications and source records attributed to E B Brown.

At least 55 records · Page 3Linked to original sources
PubMed1976

Intracellular buffering of heart and skeletal muscles during the onset of hypercapnia.

Changes in the total CO2 content of tissues were determined in order to characterize variations in intracellular acid-base parameters during the onset of hypercapnia. Within two minutes after an increasement in the CO2 tension of the inspired air of rats, there were large increases in the intracellular bicarbonate concentrations of both cardiac and skeletal muscles. Greater changes occurred in the heart, and its intracellular pH remained near normal during the first hour of hypercapnia; whereas there was an intracellular acidosis in skeletal muscle. This greater capacity of the heart to buffer excess CO2 has been linked to an increased movement of bicarbonate ions into and/or hydrogen ions out of cardiac cells during hypercapnia (Lai et al., 1973c). Yet, the buffer capacity of the heart was not compromised by metabolic acidosis during which there was a greatly reduced extracellular bicarbonate ion concentration and a greatly increased extracellular hydrogen ion concentration. The intracellular pH of the cardiac ventricle was stable following the imposition of a noncarbonic acid load on normocapnic rats.

Acid-Base Equilibrium↗
PubMed1976

Changes in skeletal muscle cell pH during graded changes in PCO2.

Blood perfusing isolated dog gracilis muscles was equilibrated with CO2 tensions ranging from 30 to 120 mm Hg, resulting in venous P CO2 from 35 to 135 mm Hg. Extracellular pH values ranged from 6.96 to 7.41, and muscle cell pH, calculated from DMO distribution, ranged from 6.64 to 6.94. When intracellular pH was plotted as a function of the corresponding extracellular pH, a linear relationship (r = 0.92) was observed throughout the entire pH range. The slope deltapHi/deltapHe was 0.64, without evidence of a difference in slope at different pH values. These results do not support the previous observations in rat diaphragms that cell pH is not affected by PCO2 changes over a certain extracellular pH range. pHe was 0.64, without evidence of a difference in slope at different pH values. Theses results do not support the previous observations in rat diaphragms that cell pH is not affected by PCO2 changes over a certain extracellular pH range.

Acid-Base Equilibrium↗
PubMed1976

Intracellular and extracellular acid-base changes in hemorrhagic shock.

Each of 21 dogs was bled until mean arterial blood pressure fell to 50 torr; this hemorrhagic shock state was then maintained for two hours. During hemorrhagic shock, the blood lactate concentration increased sixfold. The severe metabolic acidosis in arterial blood was partially compensated by a decreased PCO2 caused by increased ventilation. However, in mixed venous blood, the metabolic acidosis was combined with a respiratory acidosis. This hypercapnia in venous blood was indicative of the increased PCO2 in tissues poorly perfused following hemorrhage. The increase in the PCO2 of the femoral venous blood was greater than that in mixed venous blood, suggesting that some tissue beds were better perfused than those of the hind limb during shock. The intracellular lactate concentration of hind limb skeletal muscle was greatly increased in the shock state, and tissue PCO2 rose. Intracellular pH of skeletal muscle was only slightly decreased and bicarbonate concentration was unchanged during this combined metabolic and respiratory acidosis. This capacity of skeletal muscle to maintain a high HCO-3 concentration in intracellular fluid during metabolic acidosis may be an enhanced response of the mechanism responsible for maintaining (HCO-3)i normally at a level approximately ten times that which would be expected if HCO-3 were distributed passively.

Acid-Base Equilibrium↗
PubMed1976

Studies on pure red cell aplasia. Maintenance therapy with immunosuppressive drugs.

Two patients with pure red cell aplasia, whose marrow cells were capable of increasing their rate of haem synthesis when incubated in vitro with erythropoietin concentrate, had a complete remission associated with the administration of cyclophosphamide and prednisone. Both patients relapsed when the drugs were withdrawn. The patients again went into remission when therapy was reinstituted. Maintenance of normal erythropoiesis was dependent on the continued administration of these drugs. This study provides additional evidence for a causal relationship between immunosuppressive therapy and the resumption of erythropoiesis in patients with this disease and demonstrates the value of this therapy for the maintenance of a remission.

Adult↗
PubMed1976

Allergy: 1976.

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Antigen-Antibody Reactions↗
PubMed1976

Long-term use of disodium cromoglycate in bronchial asthma.

For many patients disodium cromoglycate will retain its usefulness and safety in long-term use. Care should be exercised in employing disodium cromoglycate in chronic corticosteroid users who develop respiratory infection to avoid the development of pneumonia. Disodium cromoglycate may be expected to regain its usefulness following non-use of the drug for varying periods of time.

Adrenal Cortex Hormones↗
PubMed1975

Cell-surface carbohydrates and their interactions. I. NMR or N-acetyl neuraminic acid.

1. The proton nuclear magnetic resonance spectrum of the sialic acid N-acetyl neuraminic acid was measured and completely assigned. The coupling constants for interactions between protons are obtained and the assignments checked by calculating the observed line intensities. 2. It was verified that the pyranose ring exists in the 1C (1-C4) conformation as the alph-D anomer and no mutarotation was detectable. Coupling constants for the glycerol side chain were interpreted to yield its most likely conformation.

Acetates↗
PubMed1975

In vivo evidence for the functional heterogeneity of transferrin-bound iron. I. Studies in normal rats.

Functional heterogeneity of iron atoms bound to transferrin as postulated by Fletcher and Huehns was demonstrated by in vivo studies in rats. Serum transferrin was selectively double-labeled by adding 59Fe to 90 per cent saturation of iron binding capacity, incubation with rat reticulocytes to reduce the saturation to 50 per cent or less, and then adding back 55Fe. Rats were killed at various times after intravenous injection of this double-labeled transferrin, and the ratios of 55Fe to 59Fe were measured in plasma, circulating erythrocytes, bone marrow and spleen heme, whole liver and isolated hepatic Kupffer and parenchymal cells, and in small intestinal segments. Selective uptake of erythroblast-oriented 55Fe was observed in red cells and heme from marrow and spleen; storage-oriented 59Fe was selectively removed by liver cells and small intestine. Greater polarization was achieved by using Fe3+-nitrilotriacetic acid instead of ferrous ammonium sulfate and by injecting transferrin selectively double-labeled at less than 50 per cent saturation. These studies confirm the hypothesis of Fletcher and Huehns that the iron atoms of transferrin are functionally different and support the concept that transferrin plays a selective role in the distribution of iron to tissues in the rat.

Animals↗
PubMed1975

In vivo evidence for the functional heterogeneity of transferrin-bound iron. II. Studies in pregnant rats.

Iron atoms from the two iron-binding sites of transferrin in the maternal plasma were selectively transferred to fetal tissues across the placenta of the pregnant rat. Rat serum transferrin was selectively double-labeled with 55Fe bound to the A-site and 59Fe bound to the B-site and injected intravenously into pregnant rats at 11 to 20 days gestation. Ratios of 55Fe to 59Fe were measured in various maternal and fetal tissues sampled from 30 to 120 minutes after injection. In the maternal tissues preponderance of A-site 55Fe was observed in circulating red blood cells and in heme extracted from bone marrow and spleen; B-site 59Fe predominated in the liver parenchymal cells and proximal small intestine. As predicted by the Fletcher-Huehns hypothesis, placental transfer of radioiron resulted in a selective concentration of A-site 55Fe in all the fetal tissues including the fetal placenta, yolk sac, whole fetus, and in the separately analyzed liver heme and ferritin and in fetal blood. When the placenta was bypassed by direct injection of the selectively double-labeled transferrin into the umbilical vein, a reversal of the 55Fe/59Fe ratios of heme extracted from the fetal liver was observed. These studies confirm the concept of functional heterogeneity of iron atoms bound to transferrin and indicate that the placenta of rats between the eleventh and twentieth day of pregnancy selectively removes erythroblast-oriented iron from transferrin and diverts it to fetal tissues.

Animals↗
PubMed1975

In vivo evidence for the functional heterogeneity of transferrin-bound iron. III. Studies of transferrin at high and low iron saturation.

The functional heterogeneity of the transferrin iron pool of rats was studied by means of selective radioiron labeling of transferrin at high and low iron saturations. A sample of iron-poor plasma transferrin brought to 90 per cent iron saturation by the addition of 59Fe-nitrilotriacetate was mixed with a similarly labeled plasma sample of 55Fe-transferrin at 10 per cent iron saturation. The mixture was injected intravenously into groups of normal rats which were killed after 30 minutes, 3, and 24 hours for measurement of the distribution of the 59Fe and 55Fe in various tissues. 59Fe from diferric transferrin disappeared more rapidly from plasma and was preferentially removed by red blood cells, bone marrow, liver, and spleen. This phenomenon was most apparent at 30 minutes and 3 hours with little difference in the distribution of 59Fe and 55Fe at 24 hours. These studies add further support for the Fletcher-Huehns hypothesis of the functional heterogeneity of the transferrin iron pool in the rat.

Animals↗
PubMed1974

The effects of raising alveolar PCO2 and ventilation separately and together on the sensitivity and setting of the baroreceptor cardiodepressor reflex in man.

1. The effects of changes in ventilation and/or alveolar P(CO2) on the baroreflex control of heart rate have been studied in seven experiments on six young men and women who had been trained to control tidal volume and respiratory frequency at various levels independent of alveolar P(CO2), during hyperoxia.2. Intravenous phenylephrine provoked transient rises of directly measured arterial pressure during which individual systolic pressures (P) were linearly related to the following pulse interval (I). Baroreflex sensitivity was expressed as the slope of the regression of I on P, and reflex setting (I(ref)) as I at a single reference arterial pressure (= mean P for the experiment).3. Voluntary control of breathing had little effect on heart rate and arterial pressure (baroreflex setting), but diminished reflex sensitivity.4. Hypercapnia regularly caused tachycardia at the reference pressure (i.e. baroreflex setting lowered). The response was completely or partly reproduced by change of P(A, CO2) at constant ventilation in four subjects but not in two others; in them change of ventilation at constant P(A, CO2) completely mimicked the effect of free-breathing hypercapnia.5. Values of baroreflex sensitivity were relatively scattered. Hypercapnia caused a fall in baroreflex sensitivity in three subjects whether ventilation was fixed or free to rise. After separating the effect of voluntarily controlling ventilation, ventilation per se was without effect on reflex sensitivity.6. It is concluded that hypercapnia and hyperpnoea have separate effects on the baroreflex, the relative magnitudes of which differ from one subject to another. Baroreflex setting and sensitivity vary independently in response to change of ventilation and of P(A, CO2).

Blood Pressure↗