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Biomedical subjects

R Einstein

Publications and source records attributed to R Einstein.

50 records · Page 3Linked to original sources
PubMed1974

Studies on the coronary dilator actions of some adenosine analogues.

1 The cardiovascular actions of 23 adenosine analogues have been examined in anaesthetized open thorax dogs; the analogues were substituted in the 2-position of the purine ring, or in the exocyclic amino group, or were modified in the imidazole or sugar rings.2 The effects of these compounds on coronary blood flow, peripheral blood pressure, and heart rate were compared with those of adenosine.3 9-beta-D-Arabinofuranosyladenine had no cardiovascular action; the other analogues on intra-atrial administration caused an immediate increase in coronary blood flow, the magnitude and duration of which varied with the structures of the analogues.4 2-Fluoro-, 2-bromo-, 2-isobutylthio-, 2-ethylamino-, and 5'-deoxy-5'-chloro- adenosines had coronary dilator potencies equal to or greater than that of adenosine. No relationship was found between the dilator potency of the adenosine analogues and their duration of coronary dilator action.5 The coronary dilator action of adenosine was potentiated by inosine, 9-beta-D-arabinofurano-syladenine, tubercidin, N(6)-methyladenosine and 2-trifluoromethyl-N(6)-methyladenosine.6 There was no correlation between the substrate specificities of the shorter-acting analogues for adenosine deaminase or adenosine kinase and their duration of coronary dilator action.7 It is proposed that in the anaesthetized dog, uptake into tissues is a more important mode of removal of adenosine and adenosine analogues from the vascular system than inactivation by adenosine deaminase, that the duration of coronary dilator action of the analogues is related primarily to their specificity for the carrier which mediates adenosine uptake, and that the adenosine carrier is not associated with kinase action.

Adenosine↗
PubMed1971

Cardiovascular actions of substituted adenosine analogues.

1. The effects of adenosine on systemic blood pressure, coronary blood flow and cardiac contractility and rate were studied in anaesthetized open-thorax dogs.2. The potency and duration of action of substituted adenosine analogues were compared with that of adenosine.3. With the exception of 2-chloroadenosine, in which coronary dilator activity was enhanced, substitution in the 2-position of the adenosine molecule reduced activity.4. In all cases 2-substitution prolonged the duration of the coronary dilator activity of adenosine.5. N(6)-Methylation of adenosine and 2-chloroadenosine reduced their coronary dilator activities, but had no effect on the duration of the response.6. Comparison of the coronary dilator potencies and hypotensive activities of 2-ethylaminoadenosine and 2-methoxyadenosine indicates that these analogues have some specificity for the coronary bed.

Animals↗
PubMedDate not supplied

Effects of restraint stress on responsiveness of atria and vas deferens in Sprague-Dawley rats.

1 The effects of stress in rats were evaluated by measuring changes in body weight and in responsiveness to noradrenaline (NA) in the isolated vas deferens and atria after the animals had been exposed to restraint or restraint and isolation. 2 Animals which were subjected to restraint alone (1 h day-1 for 3, 7 or 28 days) had a significantly reduced rate of body weight gain. This effect was not potentiated by the additional stress of isolation. 3 Restraint alone did not produce significant changes in the responsiveness of the vas deferens to NA. However, adding isolation to restraint, as an additional stress, produced a further leftward shift of the NA dose-response curve for the vas deferens, so that there was a significant increase in sensitivity compared with control. 4 There was a significant rightward shift in the NA dose-response curves or reduction in sensitivity in the atria from animals which had been restrained for 7 or 28 days. Isolation did not produce a further rightward shift in the NA dose-response curve. 5 The results from this study indicate that the stress associated with repeated restraint reduces the rate of weight gain and reduces the responsiveness of the atria to NA. The responsiveness of the vas deferens to NA was increased by stress, but the combined effect of isolation and restraint was required to produce a significant effect. The differences in the effects of stress on these tissues could be associated with differences in presynaptic receptor populations.

Adrenal Glands↗
PubMedDate not supplied

A comparison of the cardiac actions of dopamine and noradrenaline in anaesthetized dogs and guinea-pig atria.

1. The positive chronotropic and inotropic actions of dopamine and noradrenaline have been compared in anaesthetized dogs and isolated guinea-pig atria. 2. Inotropic activity was measured with a strain-gauge arch in vagotomized dogs or estimated from max (dp/dt) in dogs with denervated hearts. 3. The effects of propranolol and haloperidol on the concentration-response curves to both amines were studied in isolated atria. 4. In anaesthetized vagotomized dogs noradrenaline was more potent than dopamine but dopamine appeared to have a selective inotropic action, less apparent with noradrenaline. In denervated hearts, doses of noradrenaline and dopamine which caused similar increases in max (dp/dt) also caused similar increases in heart rate. 5. In isolated atrial preparations, concentrations of dopamine and noradrenaline which produced similar increases in force of contraction also had similar chronotropic effects. 6. Propranolol produced a shift to the right of the concentration-response curves to both dopamine and noradrenaline but the antagonism of noradrenaline was quantitatively greater. Haloperidol had not effct in concentrations below those found to cause general tissue depression. 7. It is concluded that neither dopamine nor noradrenaline show any real difference in their relative inotropic and chronotropic activities in the absence of autonomic innervation.

Anesthesia↗
PubMedDate not supplied

Transient pressure-flow responses in the resting canine hindlimb--analysis as responses to rapid stretching of the resistance microvessels.

The transient hyperaemia caused by sudden elevation of arterial pressure and reactive hyperaemia after interruption of arterial pressure for 3, 5, 10, 20 and 40 s were studied in the perfused resting hindlimb of anaesthetized areflexic dogs. Experiments were performed using steady-state pressures ranging from 50-150 mmHg. The component of the hyperaemia response (delta Q) that was attributable to resistance vessel distension by a sudden rise in pressure (delta P), was measured as the difference between peak hyperaemic flow change and the flow change predicted for that delta P in a system having constant resistance. Over the range of steady-state pressures used, vascular conductance was approximately constant, indicating that steady-state flow autoregulation was weak. delta Q was a linear function of delta P for both the hyperaemia of sudden pressure elevation and reactive hyperaemia, and the delta Q/delta P relationships were independent of steady-state perfusion pressure. The delta Q/delta P relationships for sudden pressure elevation and reactive hyperaemia after 40 s occlusion did not differ significantly. For a given delta P, however, delta Q decreased with decreasing occlusion time. The magnitude of reactive hyperaemia after brief occlusion depended not only on the degree of resistance vessel relaxation achieved during occlusion but also on the pressure step resulting from restoration of pressure. Using data from these experiments in a simple mathematical model of an idealized resistance vessel, a series of distensibility curves were constructed that showed that as active wall tension increased with increasing steady-state pressure, resistance vessel distensibility decreased.

Animals↗