Toyofuku T, Kobayashi T, Koyama S, Kusama S
Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Am J Physiol. 1988 Sep;255(3 Pt 2):H434-40. doi: 10.1152/ajpheart.1988.255.3.H434.
Hemodynamic response to an intravenous infusion of platelet-activating factor (PAF; 1 microgram/kg) was studied in conscious sheep with lung lymph fistulas. PAF induced increases in pulmonary arterial pressure and decreases in left atrial and systemic arterial pressures and in cardiac output, together with transient increases in thromboxane (Tx) A2 (as TxB2) and prostacyclin (as 6-keto-PGF1 alpha) values in plasma and lung lymph. There were also transient decreases in circulating leukocytes and platelets. The second infusion of PAF induced a reduced response compared with the first one, but the response to PAF was afterward maintained. Pretreatment with OKY 046, a thromboxane synthase inhibitor, reduced the first pulmonary vasoconstriction in response to PAF to a degree equivalent to that after successive infusions of PAF in control sheep. Pulmonary response to PAF (except on first infusion) and systemic cardiovascular response did not change whether or not TxA2 was produced. We therefore concluded that PAF mediates pulmonary and systemic cardiovascular effects via mechanisms other than TxA2 during successive infusions of PAF and that PAF-induced TxA2 contributes only to the pulmonary response to PAF on first infusion of the latter.
在有意识的、带有肺淋巴瘘的绵羊中，研究了静脉输注血小板激活因子（PAF；1微克/千克）后的血流动力学反应。PAF可导致肺动脉压升高，左心房压、体动脉压及心输出量降低，同时血浆和肺淋巴中的血栓素（Tx）A2（以TxB2表示）和前列环素（以6-酮-PGF1α表示）值出现短暂升高。循环白细胞和血小板也出现短暂减少。与首次输注相比，第二次输注PAF诱导的反应减弱，但对PAF的反应随后得以维持。用血栓素合酶抑制剂OKY 046预处理，可将首次PAF诱导的肺血管收缩反应降低至与对照绵羊连续输注PAF后的程度相当。无论是否产生TxA2，PAF的肺反应（首次输注除外）和全身心血管反应均无变化。因此，我们得出结论，在连续输注PAF期间，PAF通过TxA2以外的机制介导肺和全身心血管效应，且PAF诱导的TxA2仅在首次输注PAF时对其肺反应有贡献。
