SOME HUMORAL FACTORS AND THEIR INTERACTION ON ACUTE HYPOXIC PULMONARY PRESSOR RESPONSE

To determine the effect of humoral factors and their interaction on the developement of acute hypoxic pulmonary pressor response (HPPR), we performed studies in 16 mongrel dogs. We measured plasma levels of noradrealin (NE), angiotensin Ⅱ (AII), prostaglandin F2α (PGF2α), 6-keto-prostaglandin F1α (6KPGF1α), thromboxane B2 (TXB2), leukotriene B4 (LTB4) and 5-hydroxytryptamine (5-HT) before, during and after HPPR. Multiple regression analysis showed that the changes of pulmonary arterial systolic pressure (PASP) and pulmonary arterial diastolic pressure (PADP) correlated well with those of plasma concentration of NE, PGF2α and 6KPGF1α, respectively (r were equal to 0.633 and 0.668, respectively, P<0.01). The results of orthogonal experiment analysis with an injection of exogenous NE, PGF2α and PGIα into 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). The interaction of PGF2α and PGI2 and of PGF2α and NE increased PADP(P<0.01) and PGI2 attenuated PADP (P<0.01).

Electrical Stimulation of Deep Peroneal Nerve Mimicking Acupuncture Inhibits the Pressor Response via Capsaicin-lnsensitive Afferents in Anesthetized Rats

Objective： To assess the inhibitory modulation of blood pressure by stimulation of the deep peroneal nerve （DPN） and to determine the involvement of nociceptive fibers in the modulation. Methods： All the animals were divided into six groups （A-F）. The rats in groups A and B received no pretreatment. The rats in groups C and D received subcutaneous injection of capsaicin or control vehicle, respectively, near the DPN for 2 days. Those in groups E and F had the DPN exposed to capsaicin or control vehicle, respectively, for 20 min. Subsequently, pressor responses were induced by stimulation of paraventricular nucleus （PVN） either electrically （groups A and C-F） or chemically via injection of glutamate （group B）. After two stable pressor responses （baseline）, all groups were subject to 5-min DPN stimulation followed by PVN stimulation for 10 s. Arterial blood pressure, heart rate, and electrocardiogram were recorded. The pressor response was calculated as the difference in the mean arterial pressure （MAP） before and after PVN stimulation, and changes from baseline in pressor response after DPN stimulation were compared between the groups. Results： Increases of MAP of 22.88 ＋ 2.18 mm Hg and 20.32 ＋ 5.25 mm Hg were induced by electrical （group A） or chemical （group B） stimulation of the PVN, respectively. These pressor responses were inhibited by stimulation of the DPN, and the MAP was reduced to 12.00 _＋ 2.10 mm Hg in group A （n=6, P〈0.01） and 7.00 ＋ 2.85 mm Hg in group B （n=6, P〈0.01）. Subcutaneous injection of capsaicin （125 mg/kg） near the DPN in group C （n=7） had no effect on the inhibitory effect of DPN stimulation compared with the group D （n=9）, and neither did blockade of nociceptive fibers with capsaicin in group E （n=6） compared with group F （n=8）. Conclusion： Stimulation of the DPN mimicking acupuncture has an inhibitory effect on the pressor response, and the effect is mediated by capsaicin-insensitive afferent fibers in the DPN.