Literature DB >> 11826035

Myocardial ischemia recruits mechanically insensitive cardiac sympathetic afferents in cats.

Hui-Lin Pan1, Shao-Rui Chen.   

Abstract

Chest pain caused by myocardial ischemia is mediated by cardiac sympathetic afferents. Although silent nociceptors exist in somatic structures and some visceral organs, their presence in the heart remains uncertain. The present study examined the presence and the functional characteristics of mechanically insensitive cardiac sympathetic afferents using an electrical search technique. Single-unit activity of afferents innervating the left ventricle was recorded from the sympathetic chain in anesthetized cats. Cardiac afferents were identified initially with a stimulating electrode placed on the surface of the heart. Responses of cardiac afferents to mechanical stimuli, 5 min of myocardial ischemia, and topical application of bradykinin (1-10 microg/ml) and lactic acid (10-50 microg/ml) were then determined. Ischemia activated all 38 mechanically insensitive afferents and 17 of 25 mechanically sensitive afferents. The mechanically sensitive afferents typically were spontaneously active and had a smaller receptive field and a slightly faster conduction velocity. On the other hand, the mechanically insensitive afferents were slow conducting C fibers and had a large electrical receptive field on the epicardium. The response of 38 mechanically insensitive afferents to ischemia [2.83 +/- 0.14 (SD) imp/s] was significantly greater than that of 17 mechanically sensitive afferents (from 0.41 +/- 0.05 to 0.74 +/- 0.15 imp/s). The mechanically insensitive afferents also exhibited a greater response to topical application of bradykinin or lactic acid in a concentration-dependent manner. This study provides important new evidence that the heart is innervated by silent sympathetic afferents, which are activated profoundly by myocardial ischemia. These data also suggest that the mechanically insensitive sympathetic afferents may function as cardiac nociceptors.

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Year:  2002        PMID: 11826035     DOI: 10.1152/jn.00506.2001

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.714


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