Coronary artery occlusion alters expression of substance P and its mRNA in spinal dorsal horn in rats.

The painful sensation during acute myocardial ischemia or infarction is a common symptom and results from neural activity in humans. Little is known about the role of neuropeptides in this effect of myocardial ischemia. The aim of the current study was to investigate the role of substance P in mediating the noxious neural signals in spinal cord in acute myocardial ischemia by exploring the change in substance P and its mRNA in thoracic dorsal root ganglia and spinal dorsal horn (T1-T5) after coronary artery occlusion. The experiment was performed with immunohistochemistry, enzyme immunoassay and real time reverse transcription-polymerase chain reaction techniques on rats' hearts. In acute myocardial ischemia (<6 h), substance P and preprotachykinin mRNA were up-regulated in the neurons of the dorsal root ganglia and spinal dorsal horn. The increase in the density of immunoreactive material was mainly observed in small-diameter neurons of the dorsal root ganglia and the superficial laminae (I and II) of the spinal cord. The increase in the expressions was statistically significant compared with the control and the sham surgery groups (P<0.05). The results suggest that substance P is involved in the mediation of the noxious neural signals of acute myocardial ischemia in spinal cord. The pathophysiological role and significance need to be investigated.