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Biomedical subjects

E W Moore

Publications and source records attributed to E W Moore.

At least 73 records · Page 4Linked to original sources
PubMed1976

Inadequate parathyroid response in acute pancreatitis.

We studied nine consecutive hypocalcemic patients with acute pancreatitis to elucidate the mechanism of hypocalcemia. Mean serum ionized calcium, 0.97 mM, was below the normal mean of 1.16 mM (P less than 0.001). Seven of eight patients tested had normal parathyroid hormone levels. All responded to parenteral parathyroid extract by increasing serum ionized calcium and urinary cyclic AMP, indicating parathyroid-hormone-responsive target organs. Calcitonin and glucagon concentrations were increased above normal in some patients, but there was no relation with serum ionized calcium. Parenteral glucagon had no significant effect on serum ionized calcium or calcitonin concentrations. These findings suggest that neither glucagon nor calcitonin was primarily responsible for the hypocalcemia, which did not produce expected increases in serum parathyroid hormone concentrations. Relative parathyroid insufficiency may account for the persistent hypocalcemia frequently observed in patients with acute pancreatitis.

Acute Disease↗
PubMed1976

Comprehensive formal models for pancreatic calcium secretion. With reference to "exchange-diffusion," "two-component," and "unicellular" models of electrolyte secretion.

This is a theoretical paper in which comprehensive formal models are developed for all possible modes of entry of calcium into pancreatic juice. The 15 models include entry via: (1) the chloride-rich secretion, (2) the bicarbonate-rich secretion, (3) protein-bound calcium, and (4) interstitial fluid (ISF), plus the various possible combinations of these. Equations are presented for both calcium-volume and calcium-bicarbonate relationships. Each equation is modified as necessary to conform to the three current models for sodium, chloride, and bicarbonate secretion: (1) "exchange-diffusion," (2) "two-component," and (3) "unicellular" models. We believe the models provide a sound theoretical framework on which to build an understanding of pancreatic calcium secretion. Subsequent papers will be concerned with the physicochemical state of calcium in the juice, the relative contribution of ISF, and the development of an overall model for pancreatic calcium secretion. The long-term objective is to provide a rational approach for the understanding of pancreatic calcification and stone formation.

Bicarbonates↗
PubMed1976

Effect of serotonin on water and electrolyte transport in the in vivo rabbit small intestine.

The influence of intravenously administered serotonin on water and electrolyte fluxes in the in vivo rabbit jejunum and ileum was examined. Animals were divided into four groups: (1) those receiving saline intravenously while a glucose-free isotonic saline solution perfused the jejunum and ileum; (2) serotonin given intravenously while glucose-free intestinal perfusate was used as in group 1; (3) intravenous saline given while a 10 mM glucose-isotonic saline solution perfused the jejunum and ileum; and (4) intravenous serotonin given while the intestinal perfusate was as in group 3. Serotonin administration resulted in highly significant net secretion of H2O and sodium in both jejunum and ileum in the groups with a glucose-free perfusate. In jejunum, serotonin evoked net water and sodium secretion, whereas controls absorbed water and sodium. In ileum, serotonin significantly enhanced secretion. The addition of glucose to the perfusate completely abolished the serotonin effect. Unidirectional 22Na flux analysis revealed a marked diminution in both mucosal to serosal and serosal to mucosal fluxes in serotonin-treated animals. The decrease in mucosal to serosal flux was greater than the decrease in serosal to mucosal flux, thus explaining the enhanced net secretion observed with serotonin in the groups receiving glucose-free perfusate. In spite of its pronounced effect on water and electrolyte transport, serotonin failed to produce any detectable histological alterations in small bowel mucosa, either by light or electron microscopy. We postulate that serotonin may be an important mediator of the diarrhea so frequently noted in the carcinoid syndrome by virtue of its effects on small intestinal H2O and electrolyte transport.

Animals↗
PubMed1970

Ionized calcium in normal serum, ultrafiltrates, and whole blood determined by ion-exchange electrodes.

Ion-exchange calcium electrodes represent the first practical method for the direct measurement of ionized calcium [Ca(++)] in biologic fluids. Using both "static" and "flow-through" electrodes, serum [Ca(++)] was within a rather narrow range: 0.94-1.33 mmoles/liter (mean, 1.14 mmoles/liter). Within a given individual, [Ca(++)] varied only about 6% over a several month period. Consistent pH effects on [Ca(++)] were observed in serum and whole blood, [Ca(++)] varying inversely with pH. Less consistent pH effects were also noted in ultrafiltrates, believed to largely represent precipitation of certain calcium complexes from a supersaturated solution. Heparinized whole blood [Ca(++)] was significantly less than in corresponding serum at normal blood pH, related to the formation of a calcium-heparin complex. [Ca(++)] in ultrafiltrates represented a variable fraction (66.7-90.2%) of total diffusible calcium. There was no apparent correlation between serum ionized and total calcium concentrations. Thus, neither serum total calcium nor total ultrafiltrable calcium provided a reliable index of serum [Ca(++)]. Change in serum total calcium was almost totally accounted for by corresponding change in protein-bound calcium [CaProt]. About 81% of [CaProt] was estimated to be bound to albumin and about 19% to globulins. From observed pH, serum protein, and [CaProt] data, a nomogram was developed for estimating [CaProt] without ultrafiltration. Data presented elsewhere indicate that calcium binding by serum proteins obeys the mass-law equation for a monoligand association. This was indicated in the present studies by a close correspondence of observed serum [Ca(++)] values with those predicted by the McLean-Hastings nomogram. While these electrodes allow study of numerous problems not possible previously, they have not been perfected to the same degree of reliability obtainable with current pH electrodes. The commercial (Orion flow-through) electrode is: (a) expensive. (b) requires periodic replacement of membranes, and (c) has not yet been thermostated. As with blood pH measurements. (d) electrode response is logarithmic, i.e. small potential errors generate rather large [Ca(++)] errors. (e) loss of CO(2) should be prevented, and (f) errors due to other cations must be considered under certain conditions. Despite these limitations, we believe the electrode represents a major advance in calcium metabolism.

Adolescent↗