• Chao Qin, Jay P Farber, and Robert D Foreman.
• Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73190, USA. chao-qin@ouhsc.edu
• J Pain. 2007 Jun 1;8(6):522-9.

UnlabelledThe aim of this study was to examine whether gastric afferent information converged onto upper thoracic spinal neurons that received noxious cardiac input. Extracellular potentials of single upper thoracic (T3) spinal neurons were recorded in pentobarbital-anesthetized, paralyzed, ventilated male rats. Gastric distension (GD) (20, 40, 60 mm Hg, 20 seconds) was produced by air inflation of a latex balloon surgically placed in the stomach. A catheter was placed in the pericardial sac to administer bradykinin solution (10 microg/mL, 0.2 mL, 1 minute) as a noxious cardiac stimulus. Noxious GD (> or =40 mm Hg) altered activity of 26 of 31 (84%) spinal neurons receiving cardiac input. Twenty-two (85%) gastrocardiac convergent neurons were excited, and 1 neuron was inhibited by both intrapericardial bradykinin and GD; the remainder exhibited biphasic response patterns. Twenty-three of 26 (88%) gastrocardiac neurons also received convergent somatic input from the chest, triceps, and upper back areas. Bilateral cervical vagotomy did not significantly affect excitatory responses to GD in 5 of 5 neurons tested. Spinal transection at the C1 segment after vagotomy did not affect excitatory responses to GD in 3 of 4 neurons but abolished the GD response in 1 neuron. These data showed that a gastric stimulus excited T3 spinal neurons with noxious cardiac input primarily by way of intraspinal ascending pathways.PerspectiveConvergence of gastric afferent input onto upper thoracic spinal neurons receiving noxious cardiac input that was observed in the present study may provide a spinal mechanism that explains stomach-heart cross-organ communication, such as postprandial triggering and worsening of angina pectoris in patients with coronary artery disease.

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