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P Aramendía

Publications and source records attributed to P Aramendía.

At least 19 recordsLinked to original sources
PubMed1987

[Extraintestinal isolation of Salmonella in chickens: epidemiologic study of 3 salmonellosis outbreaks after ingestion of raw eggs].

A taxonomic analysis of the malolactic microflora present in nine grape samples from different zones of Galicia, was carried out. Nineteen strains were isolated and identified as Lactobacillus plantarum (42%), L. brevis (10.6%), L. casei (5.25%), L. hilgardii (5.25%), Streptococcus cremoris (5.25%), Leuconostoc lactis (5.25%), L. oenos (10.6%), and Pediococcus acidilactici (15.8%).

Animals↗
PubMed1986

Papaverine-induced positive inotropism with failure to increase cyclic AMP in rat atria.

Phosphodiesterase inhibition by papaverine is likely to play a minor role in the rat atrial inotropic response because non-significant changes in cyclic AMP were obtained. Isoprenaline however raised the nucleotide levels three-fold and up to seventeen-fold when papaverine was added in a similar preparation. A prominent effect of papaverine was to lengthen relaxation instead of shortening it as did isoprenaline. The results suggest different sites of action, although overlapping effects cannot be excluded.

Animals↗
PubMed1986

Effects of papaverine on calcium efflux and contractility in superfused rat left atria.

The effects of papaverine upon force of contraction, maximal rate of contraction, maximal rate of relaxation and 45Ca efflux were studied in isolated superfused rat left atria electrically driven at 1 Hz. Papaverine (3 X 10(-5) mol/l, increased developed tension (from 5.35 +/- 1.17 mN to 7.18 +/- 1.51 mN) by 1.8 +/- 0.41 mN (+33%, p less than 0.01) and maximal rate of contraction (+T) by 34.5 +/- 13% (p less than 0.05). In all experimental conditions tested, papaverine increased the rate of 45Ca efflux. The amount by which papaverine increased 45Ca efflux was 175 +/- 41 nmoles . g wet wt-1 and 304 +/- 76 nmoles . g wet wt-1, in the presence and in the absence of caffeine, respectively. The plot of changes in 45Ca efflux versus changes in developed tension fitted to a straight line (r = +0.56, n = 17, p less than 0.05), with a slope and intercept of 42 nmoles Ca . mN-1 . g wet wt-1 and -0.47 mN respectively, suggesting an association between the changes induced by papaverine in force development and increased 45Ca efflux.

Animals↗
PubMed1984

Simultaneous analyses of Ca exchange and mechanical parameters in the rat atria.

In the rat left atrium, electrically driven, a superfusion dropping method was developed. The device essentially consisted of a pair of platinum wire electrodes which held one end of the tissue, while the other end was attached to an isometric tension transducer. Either normal or isotopically labeled solutions were poured on the preparation at preset flow rates by means of a minipump. Effluent was collected fractionally in vials for measurement of radioactivity. Several perfusion flows tested led us to the conclusion that higher rates than 2.26 ml/min did not improve contractile performance. Stability of the preparation was found similar to the classical isolated organ-bath method during a 180 min period of observation. Set-up of the superfused atria reproduced paired determinations of 45Ca efflux, together with the contractile parameters. In addition, the frequency of sampling (intervals of 1 min or less) allowed us to detect changes in the washout pattern of exchangeable 45Ca even during early phases of Ca efflux. Therefore, the method reported herein seems to overcome the serious handicap of the scanty tissue employed.

Animals↗
PubMed1983

Antagonism and supersensitivity to phenylephrine-induced chronotropic responses.

Right atria from rats were analyzed for chronotropic responses to phenylephrine in face of various drugs and procedures. Propranolol, 10(-8) M, produced a competitive antagonism against the agonist which concentration-effect curve was closely similar to that obtained from reserpinized animals. Prazosin, but not phentolamine (both 10(-6) M) showed inhibition of the phenylephrine-induced changes in heart rate, as judged by their -log EC50. Either of the alpha-adrenoceptor antagonists exhibited a greater steepness in the curve slope with respect to control. The simultaneous exposure of tissues to phentolamine and propranolol proved to effectively antagonize the chronotropic effect of the agonist. This held true for phentolamine assayed in atria from reserpine-pretreated rats. Previous incubation of tissues with papaverine, 10(-5) M, brought about supersensitivity to phenylephrine which was thoroughly inhibited by either phentolamine or propranolol. These results strongly suggest that beta-adrenoceptor stimulation of heart rate by phenylephrine takes place indirectly via norepinephrine release. There is also alpha 1-adrenoceptor stimulation (blocked by prazosin). Finally, it is hypothesized that supersensitivity develops by papaverine-enhanced Ca2+ influx, since numerous evidences are against a phosphodiesterase inhibition-dependent cAMP accumulation mechanism triggered by papaverine in the presence of phenylephrine.

Animals↗
PubMed1982

Papaverine-induced changes on cardiac inotropism with special reference to a D-propranolol antagonism.

Contractile responses were analyzed in the rat paced left atrium. Positive inotropic effects were papaverine dose-dependent with an increase in rate of tension development (dT/dt) and time to peak tension, with prolongation in the total duration of contraction. Reserpinized preparations did not modify papaverine response but several treatments inhibited it, i.e., either doubling or halving [Ca2+]0, as well as the addition of D-propranolol. Incubation of tissues with papaverine (1 hr) changed the usual dose-response curve to isoproterenol into a low, monotonous effect, independent of the agonist dose. Neither high nor low [Ca2+]0 could correct this action. D-propranolol restored the isoproterenol response but significantly blocked it. Under the same conditions, phenylephrine showed similar qualitative effects as above, though no significant differences were found in control vs. the various procedures tested. These results strongly suggest that papaverine provokes an initial calcium release followed by a sustained inhibition. In addition its site of action is the same as that of D-propranolol.

Animals↗
PubMed1979

Effect of the frequency of stimulation on the blocker action of propranolol in isolated rat left atria.

The beta-blocking activity of propranolol was studied on the positive inotropic effect of norepinephrine, epinephrine, isoproterenol, dopamine and ethylephrine, in the left atrium driven at different rates. Dose of the antagonist of 10(-8) and 10(-7) M did not block the norepinephrine dose-response curve at 1 and 2.8 Hz, but a shift to the right was observed at 1.6 Hz. Although epinephrine showed a significant increase in its pD2 (p less than 0.001) at the lower stimulation frequency, the blockade increased progressively the higher the rates. On the other hand, propranolol antagonized isoproterenol at all the frequencies tested, in spite of an increase in the maxima at 2.8 Hz. This latter behavior was also true for dopamine and ethylephrine. Both sympathomimetic amines were blocked by propranolol at 1 and 1.6 Hz. The complex effect of propranolol on Ca2+ movements and its effects on cAMP and ATPase seem to be superimposed to the beta-blocking activity. Thus, the various actions on the sympathomimetic amines change according to the agonist considered and the stimulation frequency employed.

Adrenergic beta-Antagonists↗
PubMed1978

Differential beta-adrenergic sensitivity of atrial tissue assessed by chronotropic and inotropic responses to several sympathomimetic amines.

The relative inotropic and chronotropic activity of epinephrine, norepinephrine, isoproterenol, dopamine, dobutamine and ethylephrine was studied on isolated rat atria at 31 C. Dose-response curves were expressed as a percentage of the maximum response. Both atria were used for testing chronotropic effects. Inotropic dose-response curves were performed on left atria driven at 1 Hz, 1.6 Hz, 2.8 Hz and 6.6 Hz. Epinephrine and norepinephrine had a greater chronotropic action than their inotropic one throughout the range of stimulation employed. Their pD2-values changed from 8.12 +/- 0.06 and 8.05 +/- 0.05 to 7.19 +/- 0.03 and 7.14 +/- 0.05, respectively. Isoproterenol, dopamine and ethylephrine produced the same degree of chronotropic and inotropic stimulation. Dobutamine exerted the same effect on heart rate and developed tension at 1 Hz. pD2-values for dobutamine were significantly lower (p less than 0.01, p less than 0.001, p less than 0.001) when the frequency of stimulation was increased to 1.6, 2.8 and 6.6 Hz. These findings may be due to the influence of the negative staircase phenomenon, the temperature and the distribution of beta 1 and beta 2 receptors.

Animals↗
PubMed1977

Response of the atrial pacemaker to dobutamine.

The action of dobutamine, (+/-)-4- [2- [[3-(p-hydroxyphenyl)-1-methylpropyl]amino]ethyl] pyrocatechol hydrochloride was studied on the pacemaker of the isolated rat atria. The dose-chronotropic response curve showed a typical bell-dome shape of the sympathomimetic amines. Reserpinization of the animals did not change the curve of the agonist. Cocaine (6.7 microgram/ml) induced a decrease of the sensitivity of the rat atria pacemaker for dobutamine (p less than 0.001). Propranolol (3 X 10(-8) and 10(-7) M) provoked a shift to the right of the dose-response curve for dobutamine. Also, the last concentration of the antagonist depressed the maxima (p less than 0.01). Phentolamine failed to prove a possible alpha-adrenergic action of the drug on the pacemaker. The response to dobutamine was not affected when monoaminoxidase was inhibited by pretreatment with pargyline, or when catechol-O-methyltransferase was inhibited by exposure to U-0521 (3,4 dihydroxy-alpha-methylpropiophenone). These results indicate that dobutamine: a) is a beta-adrenergic agent, b) is not a good substrate of MAO, c) is a direct-acting sympathomimetic amine.

Adrenergic beta-Antagonists↗
PubMed1977

Effects of ethylephrine on the rat atrial pacemaker.

Ethylephrine, assayed in isolated rat atria, as a dose-chronotropic response curve showed a typical bell-dome shape of the sympathomimetic amines. Yet, on the same basis, it was less powerful than epinephrine, norepinephrine or isoproterenol. Pretreatment with reserpine provoked supersensitivity and increase in the maximum. As well, previous administration of pargyline to the animals resulted in augmented accelerating effects, either in normal or reserpinized preparations. Cocaine or phentolamine shifted the dose-response curve to the left. On the contrary, propranolol, produced a marked action, decelerating the effects of ethylephrine and also decreased the maxima with higher doses. It is concluded that ethylephrine: a) is a direct-acting sympathomimetic amine; b) it brings beta-receptor stimulation; c) a certain degree of alpha-receptor decelerating effect is also involved; d) it is a good substrate of monoaminoxidase.

Animals↗
PubMed1977

Positive inotropic effect of ethylephrine on the isolated rat atria.

Ethylephrine, a sympathomimetic amine which belongs to the phenolamine group, was assayed on the driven left rat atrium. The frequency response curve was performed for norepinephrine and ethylephrine. The maxima was attained for both compounds at 1 Hz. The agonist under study has an inotropic action less potent than the classical catecholamines. Propranolol (10(-8) and 10(-7) M) produced a parallel shift to the right in the log dose-response curves of ethylephrine with no decrease in the maximal response, indicating that the antagonism was competitive. In the presence of cocaine or with reserpine-pretreatment the sensitivity of the preparation to the amine did not vary. The alpha-blocker, phentolamine (10(-8) to 3.10(-5) M) did not possess an inotropic effect per se. In contrast, phentolamine, delivered to the bath beforehand, did not block the agonist. However at 10(-8) and 10(-7) M increase the maximal response both in normal and reserpinized preparations. It is suggested that ethylephrine is a direct inotropic preparation. It is suggested that ethylephrine is a direct inotropic agent on the driven left rat atrium and its effects are mediated by beta-receptors. The results also indicate the lack of evidence that ethylephrine has any action on the alpha-receptors.

Animals↗
PubMed1976

Metabolic responses to catecholamines.

Isoproterenol and propranolol, in a single dose, caused hyperglycemia after 15 and 30 min, either in the conscious rat or in the anesthetized dog. In this latter species no modifications of the serum potassium were observed. Adrenaline, 5 microgram/kg, iv provoked hyperglycemia at the same intervals and hyperkalemia at min 1st and 2nd with further hypokalemia until 90 min. The beta-adrenergic blocker, sotalol, 5 mg/kg, iv, administered prior to adrenaline suppressed the increase in glycemia and the late decrease in serum potassium, but not the early hyperkalemia. In the isolated hind limb of the dog the intra femoral artery administration of adrenaline, 3 microgram/kg, produced similar hyperglycemia either in the artery or in the femoral vein, starting from the 15 min. Contrarily, the serum concentration of potassium was significantly less in the vein than in the artery at the 1st min. These findings suggest that different receptors are involved in the glucose and potassium response to adrenaline, and the skeletal muscle plays an important role in the regulation of the early hyperkalemia.

Animals↗