Gaspardone A, Crea F, Tomai F, Iamele M, Crossman D C, Pappagallo M, Versaci F, Chiariello L, Gioffrè P A
Servizio Speciale di Diagnosi e Cura di Emodinamica, Università di Roma Tor Vergata, Italy.
J Am Coll Cardiol. 1994 Aug;24(2):477-82. doi: 10.1016/0735-1097(94)90306-9.
This study investigated whether substance P potentiates the muscular and cardiac pain caused by the intraarterial infusion of adenosine, an autocoid known to induce muscular and cardiac ischemic-like pain in humans.
Substance P is involved in the generation of neurogenic inflammation and causes cutaneous hyperalgesia. Because substance P is present in perivascular nerves it might also cause muscular and cardiac hyperalgesia. To test this hypothesis its effects on adenosine-induced muscular and cardiac pain were investigated in humans.
A randomized, crossover study of the algogenic effects of the intrailiac infusion of increasing scalar doses (from 125 to 2,000 micrograms/min) of adenosine or substance P (11.2 pmol/min) for 3 min, followed by the simultaneous infusion of substance P plus the same doses of adenosine, was carried out in nine patients with no evidence of peripheral vascular disease. A similar protocol was carried out by infusing increasing scalar doses of adenosine (from 50 to 800 micrograms/min) or substance P (11.2 pmol/min) for 3 min, followed by the simultaneous infusion of substance P plus the same doses of adenosine, into the left coronary artery of eight patients with angina. Pain severity, assessed by a visual analog scale, is presented as median. The remaining data are presented as mean value +/- 1 SD.
All patients experienced pain during both adenosine and substance P plus adenosine infusion; no patient experienced pain during the infusion of substance P alone. During intrailiac infusion, all patients experienced pain in the right leg that occurred earlier (207 +/- 152 vs. 321 +/- 154 s, p < 0.05) and was greater (47 vs. 30 mm, p < 0.05) during the simultaneous infusion of substance P plus adenosine than during the infusion of adenosine. Similarly, during intracoronary infusion, all patients experienced chest pain that occurred earlier (409 +/- 242 vs. 596 +/- 210 s, p < 0.05) and was greater (51 vs. 33 mm, p < 0.05) during the simultaneous infusion of substance P plus adenosine than during infusion of adenosine. No patient exhibited electrocardiographic signs of ischemia.
Substance P does not cause muscular or cardiac pain, but it provokes muscular and cardiac hyperalgesia.
本研究调查了P物质是否会增强动脉内输注腺苷所引起的肌肉和心脏疼痛，腺苷是一种已知可在人体诱发肌肉和心脏缺血样疼痛的自身活性物质。
P物质参与神经源性炎症的产生，并引起皮肤痛觉过敏。由于P物质存在于血管周围神经中，它也可能导致肌肉和心脏痛觉过敏。为验证这一假设，研究了其对人体腺苷诱发的肌肉和心脏疼痛的影响。
对9名无外周血管疾病证据的患者进行了一项随机交叉研究，分别以递增的标量剂量（从125至2000微克/分钟）向髂内动脉输注腺苷或P物质（11.2皮摩尔/分钟）3分钟，然后同时输注P物质加相同剂量的腺苷。对8名心绞痛患者的左冠状动脉进行了类似的方案，即分别以递增的标量剂量（从50至800微克/分钟）输注腺苷或P物质（11.2皮摩尔/分钟）3分钟，然后同时输注P物质加相同剂量的腺苷。疼痛严重程度通过视觉模拟量表评估，以中位数表示。其余数据以平均值±1标准差表示。
所有患者在输注腺苷和P物质加腺苷期间均经历疼痛；单独输注P物质时无患者经历疼痛。在髂内动脉输注期间，所有患者在同时输注P物质加腺苷时右腿出现的疼痛更早（207±152秒对321±154秒，p<0.05）且更剧烈（47对30毫米，p<0.05），比输注腺苷时更明显。同样，在冠状动脉内输注期间，所有患者在同时输注P物质加腺苷时出现的胸痛更早（409±242秒对596±210秒，p<0.05）且更剧烈（51对33毫米，p<0.05），比输注腺苷时更明显。没有患者表现出缺血的心电图迹象。
P物质不会引起肌肉或心脏疼痛，但会引发肌肉和心脏痛觉过敏。
