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Biomedical subjects

R D Moore

Publications and source records attributed to R D Moore.

At least 181 records · Page 10Linked to original sources
PubMed1983

The preoperative consultation. Response to internists' recommendations.

Preoperative consultations are frequently performed; however, little is known about the way requesters respond to the recommendations offered. For this reason, 90 consecutive preoperative consultations, performed by a general medical unit, were reviewed and compared with 66 consecutive nonpreoperative consultations, performed by the same unit during the same period. Analysis disclosed that recommendations made during preoperative consultation were often not followed and were less likely to be followed than were those made during nonpreoperative consultation (53.9% v 68.9%). Controlling for the type of consultative advice offered and for the type of surgical service requesting the consultation did not alter this relationship. These results highlight the particular importance of consultant follow-up for recommendations made during preoperative consultations.

Consultants↗
PubMed1982

Intracellular pH mediates action of insulin on glycolysis in frog skeletal muscle.

In a glucose-free bicarbonate Ringer (5% CO2 in N2), insulin increased intracellular pH (pHi), as determined by [14C]dimethadione, by 0.12 +/- 0.02 and stimulated glycolysis, as monitored by anaerobic lactate production, by 42.9 +/- 3.5% in paired frog sartorius muscles. The effect of insulin on glycolysis was shown to vary approximately linearly with log [Na+]0, being converted in 0.12 mM Na+ Ringer to a 51.5 +/- 8.4% inhibition of glycolysis. As the Na+ free-energy gradient was varied by decreasing [Na+]0 from 104 to 6.8 mM, the changes in glycolytic flux produced by insulin consistently paralleled the changes in pHi produced by the hormone. The relationship between the change in pHi and percent change in glycolytic flux was the same regardless of whether the effects were produced by insulin or by changing CO2. When glycolysis was either stimulated or inhibited, intracellular levels of fructose 6-phosphate varied inversely with glycolytic flux. This indicates that the effect on glycolysis of either insulin or changes in CO2 is due to a change in the activity of phosphofructokinase. The results support the model that the acute effect of insulin on glycolysis is mediated by a change in pHi, consequent to activation by insulin of Na:H exchange at the plasma membrane.

Animals↗
PubMed1981

Stimulation of Na:H exchange by insulin.

In frog skeletal muscle, the increase of intracellular pH (pHi) induced by insulin is correlated with an increase in intracellular Na+ when the sodium pump is inhibited by ouabain. Reversing the Na+ free energy gradient by substituting either Mg2+ or choline for extracellular Na+ converts the effect of insulin to a decrease in pHi, indicating that the action of insulin upon pHi is determined by the Na+ free energy gradient. Moreover, estimates of the Na+ free energy gradient indicate that both the direction and magnitude satisfy the hypothesis that this is the source of energy for the observed changes in pHi. Both the increase in intracellular pH induced by insulin and the associated increase in intracellular Na+ produced by this hormone in the presence of ouabain are blocked by amiloride. This drug also blocks the decrease in pHi by insulin when Mg2+ is substituted for Na+ in the Ringer. In Ringer containing Na+, the increase in pHi by insulin occurs when both metabolic and atmospheric sources of CO2 are eliminated by using a 100% N2 atmosphere. Thus, the mechanism stimulated by insulin is not a Na+-CO3(2-) cotransport system, but is either an Na:H exchange or a Na+-OH- cotransport system which can be inhibited by amiloride. The suggestion is advanced that the Na:H exchange mechanism is part of the membrane transduction system for insulin.

Animals↗
PubMed1979

Activation by sanguinarine of active sodium efflux from frog skeletal muscle in the presence of ouabain.

1. Applied to intact Na-rich muscle cells, sanguinarine causes an increased 22Na efflux in the presence or absence of extracellular K+ or of ouabain. 2. The increased 22Na efflux does not represent Na:Na exchange as indicated by the fact that it is not associated with an increase in one-way isotopic Na influx nor is it abolished by the absence of external Na+. 3. In both K-free Ringer and K-free Ringer containing ouabain, sanguinarine not only increases one-way efflux of 22Na, it also induces net efflux of Na+ in the face of both an electrical and a concentration gradient. Moreover, the induction of net Na+ efflux occurs in the face of an approximately fourfold increase in PNa. These surprising results lead to the conclusion that, contrary to all experiments, sanguinarine induces active Na+ efflux even in K-free Ringer containing 10(-3) M-ouabain. 4. Sanguinarine depolarizes the Na-loaded muscle to approximately the same value, -54 mV, regardless of the presence or absence of extracellular K+. This depolarization is most likely secondary to the increase in PNa. 5. Sanguinarine causes a net loss of K+, presumably secondary to the depolarization. 6. The stimulation of net Na+ efflux is not correlated with the depolarization. The stimulation in K-free conditions (with or without ouabain), which is associated with the largest depolarization, produces an increment in net Na+ efflux which is not significantly different from the increment in net Na+ efflux in 10 mM-K+ Ringer where the depolarization is smallest. 7. Although sanguinarine increases active Na+ efflux in intact cells, it inhibits the isolated (Na+ + K+)-ATPase, presumably due to interaction with a site on the inner face of the membrane fragment. 8. The surprising stimulation of active Na+ efflux in the presence of 10(-3) M-ouabain must be due to interaction of sanguinarine with a site on the outer face of the membrane, perhaps the K+ activation site. It seems probable that the component of active Na+ efflux induced by sanguinarine is mediated by the Na pump. Sanguinarine may produce a K+-like effect upon the Na pump with consequent unbinding of ouabain.

Alkaloids↗
PubMed1979

Mechanism of insulin action on resting membrane potential of frog skeletal muscle.

At a concentration that stimulates the Na pump, insulin hyperpolarizes the plasma membrane of frog sartorius in the presence of substrate-free Ringer. The hyperpolarization ranged from 3.5 to 7.3 mV and averaged 4.7 mV. Ouabain, 10(-4) M, completely blocked the effect of insulin on the membrane potential. Moreover, ouabain completely reversed the insulin-induced hyperpolarization within 20 min. The hyperpolarization produced by insulin was not associated with a detectable increase in the ratio of K+ permeability to Na+ permeability nor with a detectable increase in the concentration of intracellular K+, although a depletion of K+ near the external surface of the membrane cannot be excluded. The results clearly indicate that the hyperpolarization is secondary to stimulation of the Na pump by insulin.

Animals↗
PubMed1978

Injury and repair of the lung: response to intravenous Freund's adjuvant.

Tissue from the lungs of rabbits was examined at intervals up to 24 weeks after the animals had received a single intravenous injection of Freund's complete adjuvant. Though this is not a conventional method for damaging the peripheral lung, it had the advantage of producing multiple lesions in which most tissue components were altered for a prolonged period. White blood cells were present within the tissue and air spaces of these damaged areas. They persisted for 6 weeks in large numbers and gradually decreased over the next 12 weeks. There was replacement of type A by type B alveolar lining cells. Basement membranes were displaced and lost. Elastic and collagen fibres were distorted and destroyed. Blood vessels were occluded. Epithelioid cell and foreign body granulomas developed. Interalveolar septa disappeared, and air spaces were compressed. Despite all these changes the lungs regained near normal structure by 24 weeks after the initial injury. These results do not support the importance that has been placed on damage to various structural components of the lung as an explanation for chronic pulmonary disease. They do give some insight into the capacity of peripheral lung tissue for regenerationa following a single injury that induces a prolonged inflammatory response.

Animals↗
PubMed1978

Latency of thyroid hormone action on heat production in the rat.

Euthyroid rats had an immediate calorigenic response to L 3-5-3' triiodothyronine (T3) 5 microgram/kg of about +10% lasting 8 hr and a somewhat greater response to T.S.H. Larger doses (50 microgram/kg) of T3 had a latency of 4-5 hr but the response was greater and lasted longer.

Animals↗
PubMed1978

Autoimmunity and tumor resistance. 3-Methylcholanthrene tumorigenesis in New Zealand Black mice.

Skin tumors induced by the subcutaneous injection of 3-methylcholanthrene (3-MC) in New Zealand Black (NZB) mice had a delayed development and lower frequency compared with BALB/c and C57BL mice. In the SJL/J strain, the incidence of tumors was lower than in the NZB, but with the same delayed development. Most of the tumors in the BALB/c, C57BL, and SJL/J strains were sarcomas; more than one third of the tumors in the NZB mice were squamous cell carcinomas. The greatest frequency and most rapid development of tumors in the NZB, as a function of age at the time of injection of 3-MC, occurred at 4 months. Young (3.5 and 7 weeks) and 12-month-old tumor incidence in the 4-month-old NZB was decreased by treatment with antithymocyte serum (ATS). Five hundred rad whole-body x-irradiation accelerated the onset of tumors but did not increase the final incidence. 3-MC injection and the presence of skin tumors had no influence on the development of glomerulonephritis or hematopoietic neoplasms in the NZB mice. Coombs' positive anemia was not influenced by 3-MC injection, but there was an earlier and increased incidence of positive Coombs' tests in tumor-bearing animals. Liver aryl hydrocarbon hydroxylase (AHH) specific activity was low in the young NZB, increased gradually with age, and was higher in the female mice.

Age Factors↗
PubMed1977

Mitosis of type B alveolar cells in the early hyperplastic response to Freund's adjuvant.

Numerous areas of granulomatous inflammation develop in the lungs of rabbits following the intravenous injection of Freund's complete adjuvant (FCA). Within a few days after FCA injection, hyperplasia of type B (type I) alveolar cells is present on the surface of the septa in which an inflammatory reaction is developing. Mitosis of type B cells is detected 12 h after FCA injection and is common over the next 120 h. In addition, there are morphologic changes that are consistent with migration of these cells. The type B cells in mitosis extend across alveolar septa as well as along the alveolar surface. The extension of type B cells through alveolar septa is not limited to cells in mitosis, but is also observed in non-mitotic type B cells. Stimulation of mitosis and hyperplasia of type B cells is discussed in relation to the focal tissue injury and inflammatory response.

Animals↗