Effetto eccitatorio dell'adenosina sull'attività di scarica delle fibre afferenti simpatiche cardiache.

Translated title of the contribution: The excitatory effect of adenosine on the discharge activity of the afferent cardiac sympathetic fibers

N. Montano, F. Lombardi, T. G. Ruscone, M. Contini, M. Guazzi, A. Malliani

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Recent clinical observations suggest that adenosine may produce cardiac pain; even though the mechanisms involved still need defining, one of the most convincing hypotheses seems to be a direct adenosine stimulation of the sympathetic nerve endings present in the myocardium. In 10 decerebrate and artificially ventilated cats, single sympathetic afferent fibres innervating the left ventricle were isolated from the third white thoracic ramus communicans of the left sympathetic chain. After locations of the fibre receptor field on the cardiac surface, we evaluated the effects of the local epicardial application of adenosine (0.1, 1 and 10 mg/ml) on the nervous discharge activity. These results were compared with those obtained by application of bradykinin, a potent natural algogenic substance which activates sympathetic afferents, and by a mechanical stimulus such as a slight increase of systolic arterial pressure (46 +/- 6% from 113 +/- 18 mmHg) induced by partial occlusion of the thoracic aorta. In particular, adenosine (1 mg/ml) elicited a significant increase in impulse activity (from 0.11 +/- 0.02 to 0.36 +/- 0.06 imp/0.1 s) with a latency of 16 +/- 2 s. Bradykinin application (20 micrograms/ml), in the same way, produced a significant increase in impulse activity (from 0.11 +/- 0.01 to 0.86 +/- 0.16 imp/0.1 s) with a latency of 8 +/- 1 s. Neither situation showed significant hemodynamic changes. An increased neural discharge (from 0.11 +/- 0.02 to 0.26 +/- 0.04 imp/0.1 s) was also observed during aortic occlusion. After purinergic receptor blockade by aminophylline (5 mg/kg, iv), the response to adenosine was no longer observed, while responses to bradykinin and aortic occlusion were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Original languageItalian
Pages (from-to)953-959
Number of pages7
JournalCardiologia
Volume36
Issue number12
Publication statusPublished - Dec 1991

Fingerprint

Adrenergic Fibers
Adenosine
Bradykinin
Purinergic Receptors
Aminophylline
Nerve Endings
Thoracic Aorta
Heart Ventricles
Myocardium
Arterial Pressure
Cats
Thorax
Hemodynamics
Blood Pressure
Pain

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Effetto eccitatorio dell'adenosina sull'attività di scarica delle fibre afferenti simpatiche cardiache. / Montano, N.; Lombardi, F.; Ruscone, T. G.; Contini, M.; Guazzi, M.; Malliani, A.

In: Cardiologia, Vol. 36, No. 12, 12.1991, p. 953-959.

Research output: Contribution to journalArticle

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abstract = "Recent clinical observations suggest that adenosine may produce cardiac pain; even though the mechanisms involved still need defining, one of the most convincing hypotheses seems to be a direct adenosine stimulation of the sympathetic nerve endings present in the myocardium. In 10 decerebrate and artificially ventilated cats, single sympathetic afferent fibres innervating the left ventricle were isolated from the third white thoracic ramus communicans of the left sympathetic chain. After locations of the fibre receptor field on the cardiac surface, we evaluated the effects of the local epicardial application of adenosine (0.1, 1 and 10 mg/ml) on the nervous discharge activity. These results were compared with those obtained by application of bradykinin, a potent natural algogenic substance which activates sympathetic afferents, and by a mechanical stimulus such as a slight increase of systolic arterial pressure (46 +/- 6{\%} from 113 +/- 18 mmHg) induced by partial occlusion of the thoracic aorta. In particular, adenosine (1 mg/ml) elicited a significant increase in impulse activity (from 0.11 +/- 0.02 to 0.36 +/- 0.06 imp/0.1 s) with a latency of 16 +/- 2 s. Bradykinin application (20 micrograms/ml), in the same way, produced a significant increase in impulse activity (from 0.11 +/- 0.01 to 0.86 +/- 0.16 imp/0.1 s) with a latency of 8 +/- 1 s. Neither situation showed significant hemodynamic changes. An increased neural discharge (from 0.11 +/- 0.02 to 0.26 +/- 0.04 imp/0.1 s) was also observed during aortic occlusion. After purinergic receptor blockade by aminophylline (5 mg/kg, iv), the response to adenosine was no longer observed, while responses to bradykinin and aortic occlusion were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)",
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