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Biomedical subjects

C F Ryan

Publications and source records attributed to C F Ryan.

49 records · Page 3Linked to original sources
PubMed1980

Enhanced adsorptive capacity of activated charcoal in the presence of magnesium citrate, N.F.

In a series of experiments to determine the effect of magnesium citrate solution, NF, on the adsorption of sodium salicylate onto charcoal, salicylate adsorption was shown to be enhanced in the presence of citrate ion and, to a lesser extent, magnesium ion. Additional in vitro and in vivo studies with sodium salicylate, as well as other drugs, will be necessary to fully assess the potential clinical implications of these findings.

Adsorption↗
PubMed1979

Quantitation of isoproterenol-induced myocardial necrosis with 3H-tetracycline.

Methods currently used to quantitate myocardial damage and necrosis produced by chemicals are usually time consuming and subjective. These studies were conducted to evaluate the utility of 3H-tetracycline as a means of quantitating myocardial necrosis produced by isoproterenol. Male, Sprague-Dawley derived rats (180-200 g) were treated with (+/-)-isoproterenol HCl (0.1-100 mg/kg, s.c.) or equivalent volumes of saline. After 90 minutes, all rats received 50 uCi/kg of 3H-tetracycline. Rats were sacrificed 3 hours after 3H-tetracycline administration and the hearts were removed and rinsed free of blood. The degree of radioactivity of the heart as determined by liquid scintillation counting was directly proportional to the dose of isoproterenol. Propranolol pretreatment decreased the accumulation of radioactivity in a dose-dependent fashion. Determination of 3H-tetracycline accumulation appears to be a rapid and reliable method for quantitating isoproterenol-induced myocardial necrosis.

Animals↗
PubMed1975

Hypothermic response following administration of 2-amino-4-pentenoic acid (allylglycine).

Intraperitoneal administration of allylglycine resulted in a hypothermic response in rats. At a dosage of 90 mg/kg, a significant decrease in temperature was noted at 4 and 8 hr after administration, but no significant difference was noted at 12 hr. The same dose administered intraperitoneally to decapitated rats did not result in a hypothermic response, and intraventricular administration resulted in a rapid onset of hypothermia after 1 hr. These findings are indicative of a central site of action for the allylglycine-induced hypothermia. Quantitative assay of hypothalamic monoamines (norepinephrine, serotonin, and dopamine) did not show any significant changes at 4, 8, and 12 hr postadministration when compared to controls. A significant decrease in hypothalamic gamma-aminobutyric acid was noted at each of these time points when compared to controls. These data suggest an important role for gamma-aminobutyric acid in mammalian thermoregulatory control.

Allyl Compounds↗
PubMed1975

Studies on the temperature-dependent sensitivity of mouse atria to adrenergic drugs.

The sensitivity of mouse atria (chronotropic response) to beta-adrenergic receptor antagonists was examined at 37 and 26 degrees C under various experimental conditions. When isoproterenol was used as agonist, at 37 degrees C, the pA2 value (from pA2 plots) for propranolol was 8.86 and the slope of the regression line was 0.54. At 26 degrees C, the pA2 value for propranolol was 9.2 and the slope was 0.7. In the presence of tropolone, 10-5 M, the values for pA2 and slope of the regression lines were, respectively, 9.0 and 0.90 at 37 degrees C and 9.17 and 0.98 at 26 degrees C. In other words, decreasing antagonism was prevented by low temperature and tropolone. Isoproterenol was potentiated by tropolone and low temperature, but the effects of low temperature were reduced by tropolone. With sotalol as antagonist, there was greated blockade (dose ratios) of the effects of isoproterenol at 26 than at 37 degrees C. When nylidrin, a non-catecholamine, was used as agonist there was no temperature-dependent sensitivity to sotalol. Furthermore, nylidrin was not potentiated by low temperature. The data show that the observed degree of beta-receptor antagonism can be altered by changing the bath temperature and suggest that this effect is related to COMT activity or an influence of agonist disposition in the tissue.

Adrenergic beta-Antagonists↗
PubMed1975

Influence of temperature and cocaine on responses of the isolated mouse vas deferens to adrenergic amines.

Lowering the bath temperature from 37 degrees C to 20 degrees C resulted in supersensitivity of the isolated mouse was deferens to norepinephrine. Dose-response curves to norepinephrine were shifted to the left along the log dose axis (enhanced potency) and the maximum degree of contraction that could be elicited was increased. The effect of cocaine on norepinephrine effects was qualitatively the same as hypothermia. Both treatments enhanced the potencies of other alpha receptor agonists that are substrates for the adrenergic neuronal membrane uptake mechanism. Neither treatment enhanced the potency of methoxamine, which is not taken up by adrenergic neurons, but hypothermia increased the methoxamine-induced maximum contractile height. Uptake of 14C-norepinephrine by the vas deferens was abolished by cocaine and low temperature. The data suggest that enhanced potency of adrenergic amines by hypothermia results from an inhibition of uptake by adrenergic neurons. Increased height of maximum contraction at low temperature may be partly due to decreased neuronal uptake, but other mechanisms are also likely to be involved in this effect.

Animals↗