Biomedical subjects

B Blattberg

Publications and source records attributed to B Blattberg.

17 recordsLinked to original sources

PubMed1980

The effects of cocaine, chlorpheniramine and tripelennamine on the cardiac responses to sympathetic nerve stimulation.

The effects of cocaine (COC), chlorpheniramine (CHL), and tripelennamine (TRI) on the cardiac responses to sympathetic neural stimulation were compared in open-chest, anesthetized dogs. The amplitudes of the chronotropic responses were not significantly altered by any of these drugs. Similarly, the amplitudes of the inotropic responses were not affected significantly by either COC or TRI, but they were increased moderately by CHL. All three drugs prolonged the inotropic and especially the chronotropic responses. CHL and TRI, in addition to being antihistaminics, are inhibitors of the neuronal uptake of norepinephrine. Therefor, the similarity of the effects of CHL, TRI, and COC on the cardiac responses to sympathetic stimulation is probably ascribable to their inhibitory activities on the neuronal uptake mechanism.

Animals↗

PubMed1978

The influence of cocaine and desipramine on the cardiac responses to exogenous and endogenous norepinephrine.

In open-chest, anesthetized dogs, cocaine and desipramine potentiated the pressor, chronotropic, inotropic and coronary sinus blood flow responses to norepinephrine (NE) infusions. The chronotropic and inotropic responses were also prolonged, the former more markedly than the later and the extraction of exogenous NE from the coronary blood stream was diminished. Cocaine and desipramine also potentiated the pressor and coronary sinus blood flow responses, but not the chronotropic or inotropic responses, to stimulation of the left ansa subclavia. The inotropic response was slightly prolonged, however, and the chronotropic response was markedly prolonged. The overflow of NE into the coronary sinus blood was not increased by either neuronal uptake blocking agent. It is proposed that cocaine and desipramine, at the doses employed, diminish the release of NE from the cardiac nerve endings at the same time that they inhibit reuptake of the neurotransmitter. Their mechanisms of action and their side effects on the circulatory system do not appear to differ significantly.

Animals↗

PubMed1977

Correlation of the mechanical responses of the heart with the norepinephrine overflow during cardiac sympathetic neural stimulation in the dog.

The changes in heart rate and right ventricular contractile force were measured in anaesthetised dogs during stimulation of each ansa subclavia, and the responses were correlated with the overflow or norepinephrine (NE) into the coronary sinus blood. The increase in heart rate was considerably greater during stimulation of the right than of the left ansa subclavia. Conversely, left ansa stimulation had a slightly greater effect on right ventricular contractile force than did right-sided stimulation. The changes in norepinephrine overflow into the coronary sinus blood paralleled the alterations in contractile force; during stimulation at 2 and 4 Hz, the rates of norepinephrine overflow were 50 and 34% greater, respectively, with left-sided than with right-sided stimulation. On both the right and left sides, stimulation of the anterior limb of the ansa subclavia produced greater increments in heart rate and contractile force than did stimulation of the posterior limb. Similarly, the rates of norepinephrine overflow during anterior ansal stimulation were 100 and 75% greater than during posterior ansal stimulation for the right and left sides, respectively. Thus, both limbs of the two ansae subclaviae innervate the myocardial regions drained by the coronary sinus, but the greatest innervation arises from the anterior limb on the left side.

Animals↗

PubMed1976

Progressive reduction in norepinephrine overflow during cardiac sympathetic nerve stimulation in the anaesthetized dog.

The left ansa subclavia was stimulated at supramaximal intensity at a frequency of Hz in open-chest, anaesthetized dogs for periods of about 10 min. Arterial blood pressure, myocardial contractile force, and coronary sinus blood flow reached peak values after 1 or 2 min of stimulation, and then declined gradually throughout the remainder of stimulation. In hearts that averaged 159 +/- 10 (SEM) g, the norepinephrine (NE) overflow rose to a peak value of 470 +/- 128 ng/min at the end of 1 min of sympathetic stimulation in the control animals. By the 10th min of stimulation, the NE overflow had diminished to 97 +/- 24 ng/min. In animals pretreated with cocaine (5 mg/kg) or with phenoxybenzamine (5 mg/kg), the peak NE overflow rates were 288 +/- 62 and 980 +/- 148 mg/min, respectively, and the rate of NE overflow declined to levels of 104 +/- 39 and 128 +/- 30 ng/min, respectively by the 10th min of stimulation. Since there was a profound, progressive diminution in the rate of NE overflow during sustained cardiac sympathetic stimulation regardless of whether or not NE reuptake was suppressed, it is concluded that the reduction in NE overflow reflects a curtailment of neuronal release of NE rather than an acceleration of reuptake.

Animals↗

PubMed1976

Effect of vagal stimulation on the overflow of norepinephrine into the coronary sinus during cardiac sympathetic nerve stimulation in the dog.

In anesthetized dogs with the chest open, supramaximal stimulation of the left cardiac sympathetic nerves at 2 and 4 Hz produced an increase of 40-50% in ventricular contractile force (CF) and of 40-65% in coronary sinus blood flow. At these frequencies of stimulation, norepinephrine (NE) overflow into the coronary sinus was 29.8 +/- 5.1 (SE) and 54.9 +/- 13.2 ng/min, respectively. Concurrent, supramaximal vagal stimulation, at a frequency of 15 Hz, had no significant effect on coronary sinus blood flow, but caused a 25% reduction in CF and a 30% decrease in NE overflow. The changes in CF and NE overflow evoked by vagal stimulation were prevented by atropine. These results are consistent with the hypothesis that there are muscarinic receptors on the postganglionic sympathetic terminals in the walls of the ventricles. Acetylcholine released during vagal stimulation combines with these receptors, causes a reduction in the liberation of NE, and thereby attenuates the positive inotropic response.

Animals↗

PubMed1976

The effect of the pattern of cardiac sympathetic activity on myocardial contractile force and norepinephrine overflow in the dog heart.

The left of right cardiac sympathetic nerves in open-chest, anesthetized dogs were stimulated at mean frequencies of 2 or 4 Hz. The stimuli were applied intermittently, in patterns with repetition rates or either 60/min or 15/min, to simulate the spontaneous patterns of sympathetic neural activity that occur synchronously with the cardiac or respiratory cycles, respectively. With either repetition rate, intermittent stimulation of the left sympathetic nerves was about 10-20% less effective in enhancing myocardial contractile force (CF) and about 10% less effective in increasing coronary sinus blood flow than was steady stimulation at the same mean frequency. With right-sided stimulation, there was no appreciable difference between steady and intermettent stimulation patterns with respect to the effect on heart rate. With either left-or right-sided stimulation, the rate of norepinephrine (NE) overflow into the coronary sinus blood was 20-40% less with intermittent than with steady stimulation. Cocaine administration did not materially affect this difference in NE overflow. It was concluded that the higher instantaneous frequencies that prevail during intermittent stimulation result in a reduction in the rate of NE release at the sympathetic postganglionic nerve endings in the heart.

Animals↗

PubMed1972