Responses of thoracic spinothalamic neurons to intracardiac injection of bradykinin in the monkey.

Abstract

SUMMARY. Bradykinin stimulates afferent fibers arising in the heart and may be involved in the mediation of anginal pain and the pain associated with myocardial infarction. The sensation of pain requires that noxious information reach the brain. The purpose of the present study was to determine whether the spinothalamic tract is involved in transmitting noxious information from the heart to the brain. Bradykinin was injected (0.3-3.5 jug/kg) into the heart via a catheter in the left atrium while we recorded from single spinothalamic cells in the Cg to T 5 spinal segments. Thirty-one of 41 cells responded to bradykinin. The responses of 12 cells were characterized by both an increase in discharge rate and entrairrment of cell activity with the cardiac cycle. Eighteen cells responded with only an increased rate, and one cell exhibited only entrainment of cell activity with the cardiac cycle. The mean onset of increased cell activity occurred 15 seconds following drug injection, and the average duration of the response was 54 seconds. Thirty cells increased their mean discharge rate from 11 ± 2.5 to 29 ± 4.4 spikes/second. Thus, some spinothalamic cells probably received input from both mechanosensitive and chemosensitive afferents. Tachyphylaxis to repeated doses of bradykinin was observed in 41% of cells. Cells responding to bradykinin had a spontaneous discharge rate that was significantly greater than that of nonresponding cells. Cells did not require input from C-fiber afferents to respond to bradykinin. No statistically significant relationships were found among anatomical locations (laminae and segments) and responses to bradykinin, although cells in lamina I seemed to be less responsive than more ventrally located cells. We conclude that the spinothalamic tract may be involved in the sensation of cardiac pain. (Circ Res 51: 83-94, 1982)

Silent Myocardial Ischemia

“…34,41 Bradykinin when applied to the cardiac surface produces a significant increase in cardiac afferent nerve activity including activation of spinothalamic tract neurons. 42,43 Application of bradykinin, as part of a mixture of agents, to the surface of the heart elicits a pseudoaffective response in rats suggestive of pain; 44 however, when infused intracoronary into conscious dogs, Pagani et al observed hemodynamic effects but no evidence of pain. 45 Gutterman et al 46 also showed that the afferent neural response to epicardial application of bradykinin is an increase in afferent nerve activity, but the pattern of the increased activity differed from that observed during brief periods of myocardial ischemia, suggesting that bradykinin release does not fully explain cardiac pain sensation.…”

Responses of thoracic spinal neurons to activation and desensitization of cardiac TRPV1-containing afferents in rats

“…Physiological and pharmacological studies show that BK activates cardiac nociceptors and sympathoexcitatory responses via kinin B2 receptors located in thinly myelinated A␦ and unmyelinated C-fiber afferent endings in the heart (1,23,39,40). The afferent fibers transmitting the action potentials enter the upper thoracic spinal cord where spinal neurons, spinothalamic tract cells, spinoreticular tract, and other ascending pathway neurons process this information (2)(3)(4)(5)(6)27). However, the signaling mechanisms involved in detection of myocardial ischemia and activation of cardiac sympathetic or spinal afferent nerve endings are not fully known.…”

Neural control of sympathetic nerve response to cardiogenic hypotension in anesthetized cat.

“…Thus, a possible contribution of chemical substances released by coronary occlusion to excite the cardiac afferents cannot be excluded from the present study. Previous studies also suggested that the sympathetic afferent nerves may transmit the sensation of pain during myocardial ischemia to the central nervous system (WHITE, 1957;BAKER et a!.,1980;BLAIR et a!., 1982). Thus, further experiments are required to evaluate the net autonomic response to cardiogenic hypotension determining the central interactions of input from cardiac sympathetic afferents and from arterial baroreceptors and cardiac vagal afferents, and to determine more exact interaction with impaired cardiac function and cardiac sympathetic afferents during the hypotension induced by coronary occlusion.…”