Saijo A, Ishii Y, Kitamura S
Department of Internal Medicine 1, Tokyo Women's Medical Collage Daini Hospital, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1996 Jan;34(1):16-23.
We studied the effect of sensory nerve peptide substance P (SP) and neurokinin A (NKA) in isolated perfused guinea pig lungs. SP and NKA increased pulmonary arterial pressure, capillary pressure, pulmonary venous resistance, and lung weight, but they did not change pulmonary arterial resistance or pulmonary vascular permeability. The effects of SP on pulmonary vascular dynamics were greater than those of NKA. Ozagrel hydrochloride, a thromboxane synthase inhibitor, partially attenuated the effect of SP. This indicates that thromboxane contributes to SP-induced pulmonary vasoreactivity. However, ozagrel hydrochloride did not change the effects of NKA. FK224, an NK-1/NK-2 receptor antagonist, abolished both SP- and NKA-induced pulmonary vasoconstriction. This indicates that SP and NKA acted on the pulmonary vasculature through the NK-1 or NK-2 receptor, or both. Papaverine, a smooth muscle relaxant, abolished the effects of SP. The SP-induced increase in lung weight was caused by a rise in pulmonary hydrostatic pressure, especially that caused by pulmonary venoconstriction.
我们研究了感觉神经肽P物质(SP)和神经激肽A(NKA)对豚鼠离体灌注肺的影响。SP和NKA可升高肺动脉压、毛细血管压、肺静脉阻力及肺重量,但不改变肺动脉阻力或肺血管通透性。SP对肺血管动力学的影响大于NKA。血栓素合酶抑制剂盐酸奥扎格雷可部分减弱SP的作用。这表明血栓素参与了SP诱导的肺血管反应性。然而,盐酸奥扎格雷并未改变NKA的作用。NK-1/NK-2受体拮抗剂FK224可消除SP和NKA诱导的肺血管收缩。这表明SP和NKA通过NK-1或NK-2受体,或两者作用于肺血管系统。平滑肌松弛剂罂粟碱可消除SP的作用。SP诱导的肺重量增加是由肺静水压升高引起的,尤其是肺静脉收缩所致。