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To determine the effect of humoral factors and theirinteraction on the developement of acute hypoxie pulmonarypressor response (HPPR), we performed studies in 16 mongreldogs. We measured plasma levels of noradrealin (NE),angiotensin Ⅱ(AII), prostaglandin F2 (PGF2),6-keto-prostaglandin FIα (6KPGFIα), thromboxane B2(TXB2), leukotrienc B4 (LTB4) and 5-hydroxytryptamine(5-HT) before, during and after HPPR. Multiple regressionanalysis showed that the changes of pulmonary arterial systolicpressure (PASP) and pulmonary arterial diastolic pressure(PADP) correlated well with those of plasma concentration ofNE, PGF2 and 6KPGFIα, respectively (r were equal to 0.633and 0.668, respectively, P<0.01). The results of orthogonal ex-periment analysis with an injection of exogenous NE, PGF2αand PGI into main pulmonary artery of dogs showed that NEand the interaction of PGF2α and PGI2α increased PASP(P<0.05) and PGI2 attenuated PASP (P<0.01). Theinteraction of PGF2α and PGI2 and of PGF2α and NE in-creased PADP(P<0.
To determine the effect of humoral factors and theirinteraction on the developement of acute hypoxie pulmonary pressor response (HPPR), we performed plasma levels of noradrealin (NE), angiotensin II (AII), prostaglandin F2 (PGF2), Multiple regression analysis showed that the changes of pulmonary arterial systolic pressure (PASP), 6-keto-prostaglandin FIα (6KPGFIα), thromboxane B2 (TXB2), leukotrienc B4 (LTB4) and 5-hydroxytryptamine and pulmonary arterial diastolic pressure (PADP) correlated well with those of plasma concentration of NE, PGF2 and 6KPGFIα, respectively (r were equal to 0.633 and 0.668, respectively, P <0.01). The results of orthogonal ex- periment analysis with an injection of exogenous NE, PGF2αand PGI into the main pulmonary artery of dogs showed that NE and the interaction of PGF2α and PGI2α increased PASP (P <0.05) and PGI2 attenuated PASP (P <0.01). Theinteraction of PGF2α and PGI2 and of PGF2α and NE in-creased PADP (P <0.