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Biomedical subjects

M Giles

Publications and source records attributed to M Giles.

64 records · Page 4Linked to original sources
PubMed1976

Potassium release from the rat submaxillary gland in vitro. I. Induction by catecholamines.

Slices of submaxillary gland were incubated in vitro in an enriched Krebs-Ringer-bicarbonate medium gassed with 95% O2-5% CO2 at 37 degrees C and the release of K+ into the medium was monitored after stimulation with alpha and beta adrenergic secretagogues under a variety of experimental conditions. K+ was released by the slice system after addition of norepinephrine, epinephrine or phenylephrine, but not after addition of isoproterenol. The extent of K+ release after norepinephrine depends on the dose of secretagogue and is higher when glucose, adenine and inosine, or all three substrates are absent from the medium. The effect of norepinephrine on K+ release is reversed by phentolamine but not by propranolol. Phentolamine also causes a 9.4-fold shift to the right in the dose-response curve to norepinephrine. Addition of ouabain to the incubation medium results in a higher extent of K+ release and prevents the reversal caused by phentolamine. The response to norepinephrine fails to occur when Ca++ is absent from the medium, either by chelation with ethylene glycol bis (beta-amino-ethyl ether)-N,N'-tetraacetic acid or by elimination from the Krebs-Ringer solution, and shows gradations depending on the Ca++ content of the medium. By itself, however, Ca++ does not induce K+ release from the slice system. The following conclusions are derived from these observations: 1) the release of K+ ions from the submaxillary gland is mediated by alpha adrenergic receptors; 2) the net amount of K+ released is the result of two opposing and almost simultaneous mechanisms, a passive extrusion and an active reuptake; 3) the active reuptake of K+ depends on the availability of energy and is mediated through the ouabain-sensitive Na+-K+ activated adenosine triphosphatase; 4) the reaction is critically dependent on the presence of Ca++ in the incubation medium and probably involves an influx of Ca++ upon stimulation with alpha adrenergic secretagogues.

Adrenergic beta-Antagonists↗
PubMed1975

Abnormal secretory response to parasympathomimetic and sympathomimetic stimulations from the submaxillary gland of rats treated with reserpine.

Rats treated with 0.5 mg/kg of reserpine per day for 7 days were anesthetized and submaxillary saliva was collected and analyzed for Na+, K+, Ca++ and protein concentrations. Salivary secretion was elicited by i.p. injections of carbamylcholine (50-100 mug/kg), phenylephrine (5 mg/kg) and isoproterenol (10 mg/rat). Saliva was also collected from untreated controls. Submaxillary glands were excised from both groups of animals at the termination of the secretory response, homogenized and analyzed. Glands from other animals were removed in the resting state and similarly processed. Pretreatment with reserpine resulted in decreased volumes of salvia and in elevated salivary concentrations of Ca++ and protein. Saliva from the reserpine-treated animals secreted in response to carbamylcholine had higher concentrations of Na+ and K+ than control saliva, particularly at the low rates of flow. Saliva secreted after stimulation with the two sympathomimetic secretagogues had lower concentrations of these two ions. Resting glands from the treated animals showed significant elevations in protein and Ca++ content and a significant decrease in K+ content. At the end of the secretory response to the three secretagogues, glands from treated animals showed a significantly higher Na+ content and a significantly lower K+ content than control glands. It is concluded that pretreatment with reserpine alters the secretory response of the rat submaxillary gland to both parasympathomimetic and sympathomimetic stimulation. This alteration results from a toxic lesion caused by reserpine in the salivary cells, which involves changes in their permeability to ions and in their energy resources. These in turn, result in an abnormal stimulus-secretion coupling mechanism. The possibility that the toxic lesion is related to alterations in Ca++ homeostasis is discussed.

Animals↗
PubMedDate not supplied

Need for albumin adjustments of urgent total serum calcium.

In specimens sent for urgent total calcium measurement, failure to adjust for serum albumin concentration led to errors of diagnosis and treatment. Albumin adjustment is necessary, when measuring total serum calcium, for assessment of true calcium status.

Calcium↗
PubMedDate not supplied

Prostaglandins PGE2 and PGF2 alpha in human fetal lung: immunohistochemistry and release from organ culture.

Immunohistochemical studies in human fetal lung have shown that epithelial and endothelial cells are both strongly and equally reactive for PGE2. In contrast, epithelial PGF2 alpha reactivity varied between fetuses, in some as intense as endothelial staining and in others very much less. As lung organ cultures differentiated, the intensity of PGE2 staining declined in airways and blood vessels, although it was still weakly positive at 10 days. In contrast, epithelial cells rapidly became negative for PGF2 alpha, whereas PGF2 alpha positivity was retained in blood vessels, albeit less obviously. PGF2 alpha and PGE2 were released into the media of organ cultures in decreasing amounts as cultures progressed. Amounts of released PGF2 alpha were greater by 2- to 10-fold than PGE2. Our findings suggest that the endogenous production of prostaglandins by human fetal lung in organ culture has a key role in the self-differentiation process that occurs in the absence of sera or added growth factors or hormones.

Absorption↗
PubMedDate not supplied

Prostaglandin production and metabolism in self-differentiating human fetal lung organ culture.

PGE2 and PGF2 alpha are released into the media of human fetal lung organ cultures in decreasing amounts with time. This decline in PGs is not due to culture failure or loss of synthetic capacity, which can be stimulated by fetal bovine serum, nor is it due to increased catabolism of PGE2 to 13,14-dihydro-15-keto-PGE2 (PGEM) or of PGF2 alpha to 13,14-dihydro-15-keto-PGF2 alpha (PGFM). Immunohistochemically reactive PGs are not retained within lung cells. Antisera against methyl-moximated derivatives of PGEM or PGFM and preceded by derivatization on tissue sections of PGs by methyl-moximation not only demonstrate the localization of PGEM and PGFM in epithelial cells and blood vessels, but also show an overall decline in immunoreactivity with time. In addition electron microscopy of uncultured fetal lung removed directly after termination reveals various degrees of mitochondrial damage and in some cases plasma membrane blebs which resolve during the period in culture and as fetal lung self-differentiates. It is proposed that oxidative and mechanical stresses, occurring during termination of pregnancy or tissue preparation, result in cell damage and increased lung prostaglandin production, which, although decreasing during culture as cells recover, is sufficient to trigger terminal self-differentiation.

Cell Differentiation↗
PubMedDate not supplied

Patient perceptions of rheumatoid arthritis.

Rheumatoid arthritis is rarely seen as a serious public health issue, yet it is the single largest cause of disability in the UK (Badley and Tennant 1993). In this qualitative study patients were interviewed about the physical and social effects of the disease.

Activities of Daily Living↗