The present study compared the effects of several inhibitors of arachidonic acid metabolism on hypoxic pulmonary vasoconstriction (HPV) in Hilltop and Wistar rats. The results showed that HPV is much higher in Hilltop rats than in Wistar rats. U-60257B, an inhibitor of leukotrienes synthesis, resulted in a 46.7% reduction of HPV in Hilltop rats and 88.7% in Wistar rats. After an injection of U-63557A, an inhibitor of TXA_2 synthetase, HPV was reduced in Hilltop rats and was not changed in Wistar rats, so that the difference of HPV between these two strains of rats was eliminated. Indomethacin, inhibiting the synthesis of both PGI_2 and TXA_2, markedly enhanced the HPV in Wistar rats and diminished the HPV in Hilltop rats. It is suggested that roles of different prostaglandins may be the important factor in relation to the difference of HPV between Hilltop and Wistar rats.

In order to investigate the effects of cigarette smoking on hypoxic pulmonary vasoconstriction(HPV) in piglets, receptor or synthetic enzyme blockers of sympathetic nerve, histamine, prostaglandins(PGs) and leukotrienes(LTs) were used. Results showed that hypoxia increased PVR by adrenergic alpha receptor, LTs and PGs to 72.5%(3min. P

Hypoxia is a commenest pathological process. The cellular oxygen sensors and signal transduction involved in hypoxic responses are so far not fully elucidated. There are many theories. Perhaps the oxygen sensors are different among different kinds of cells, and between acute and chronic hypoxic responses. The mitochondria cytochrom-oxidase-H_2O_2 might be the principal pathway leading to the constrictive response of pulmonary smooth muscle cells to hypoxia. The heme protein - reactive oxygen pathway might mediate the response of glomus cells in carotid body to hypoxia. The NADPH oxidase might be the oxygen sensor in airway chemoreceptor. As for chronic hypoxic responses, the oxygen dependent regulation of hypoxia-inducible factors by prolyl and asparaginyl hydroxylation has been paid great attention in recent years.

The alteration of hypoxic pulmonary vasoconstriction (HPV) induced bycigarette smoking was studied in Wistar rats, piglets and in humans. The percentage changeof pulmonary vascular resistance (△PVR%) and the amplitude of the systolic wave inimpedance pneumorheogram (△H%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats was in-creased (△PVR% from 55. 0?15. 6% to 102. 3?12. 4%), which was mainly mediated byleukotrienes (LTs); whereas HPV in piglets was decreased (△PVR% from 65.2?12. 5%to 55.9?9. 8%), which was mainly mediated by ? adrenergic receptors, and HPV inhumans was also increased (△H% from 20. 6? 2. 6% to 31. 1?4. 1%), in which prostag.landins and leukotrienes may play the role of mediators. However, after one-month ciga- rette smoking, the HPV of rats was significantly lowered (△PVR% 11. 4?1. 6%). Anincrease in vasodilative prostaglandins synthesis and a decrease in leukotrienes synthesismight haye contributed to this alteration of HPV.

The effects of acute intragastric administration of tea on hemodynamicsand acute hypoxic pulmonary hypertension were studied by a catheterization technique inspontaneously breathing dogs. The tea was made by adding 25g tea to 400ml boiling wa-ter and was given to each dog in a dosage of 20ml/kg. Both greentea and black-tea didnot affect the hemodynamics obviously. However hypoxic pulmonary vasoconstriction wasinhibited significantly by black-tea. The increase in the plasma concentration of TXA_2induced by acute exposure to hypoxia was also inhibited by black-tea. Green-tea did notshow any effect on HPV and plasma level of TXA_2 and 6-keto-PGF_1??The findings thatblack-tea can reduce the magnitude of HPV may have therapeutic significance in the pre-vention and cure of pulmonary hypertension, pulmonary heart disease and high altitudeheart disease.

The regulatory effect of endothelial cells of the rabbit pulmonary arteriole(PAECs) on the tone of pulmonary artery was studied. The conditioned medium (CM) ofPAECs, cultivated under normal and hypoxic condition for 24 hours, did not induce con-striction of pulmonary artery ring. The aqueous phase was able to induce the constriction.The constriction of pulmonary artery rings was reduced by the heated aqueous phase, but it was disappeared when the heated aqueous phase was treated with trypsin. The constric-tion caused by heated aqueous phase was stronger in hypoxic endothelial cells than innormal cells. Treatment of PAECs with indomethacin and captoril, and administration ofFPL 55712, BN 52021, chlorpheniramine and prazozin to contraction pool did not affectthe constriction of pulmonary artery rings. It was concluded that PAECs might producelong half-life lipid substances which could induce the dilatation of pulmonary artery.Hypoxia inhibted the release of long half-life aqueous heat-unstable vasoconstrictive sub-stances. but enhanced that of the heat-stable fraction which was probably a peptide.

0.05) found between two groups. Hypoxia did not stimulate ECs to release endothe-lium-derived contracting factors (EDCFs), and the contracting effects of HPEC (16.4%)and HAEC (20%) were similar to that of NPEC and NAEC. These results indicated thatEDCFs released from endothelial cells of pulmonary artery and aorta can induce contrac-tion of PSMC directly and that hypoxia did not increase the release of EDCFs from ECs.

Hypoxic vasoconstriction was studied in isolated rings of pig intrapulmonary(PA) with or without endothelium. Arterial rings were suspended in modified Krebs' bic-arbonate solution for isometric recording. Hypoxia was induced by changing the bubblinggas mixture in the chamber from, 95% O_2-5%CO_2 to 95%N_2-5%CO_2. When PA ringswere prestimulated with phenylephrine (PE, 2?10~(-6) mol/L), hypoxia could induce contrac-ctions in PA (0.86?0.09g, n=12). Removal of the endothelium decreased the hypoxicontractions of PA significantly (tension increment 0.11?0.03g, n=12, P

This study was to localize the position of spinal center of sympathetic nerve which controls the pulmonary circulation in pithed rat model. The sympathetic preganglionic fibers arising from C7-T10 spinal segments were stimulated electrically in succession. During stimulation the pulmonary vascular rcsistance(PVR) was increased in all segments tested, most significantly in C7-T4(about 28% above control value) which was obviously higher than that of Ts-T10. In constract, the systemic vascular resistance(SVR) increased more remarkably when lower segments were stimulated. The higher the stimulated spinal segments, the larger the ratio of APVR/ASVR. The data showed that the spinal center of sympathetic nerve which regulates the vasomotion of pulmonary circulation is located in the segments C7-T4.

The changes of hemodynamics and hypoxic pulmonary vasoconstriction (HPV) inducedby cigarette smoking and the role of prostaglandins(PGs) and leukotrienes (LTs) were studied in rats. During smoking, systemic and pulmonary vascular resistance (SVR and PVR) increased 47% and 39%, respectively. The level of TXB_2 rose by 144% in plasma and 69% in lung tissue. HPV increased two-fold after smoking (△PVR increased from 55% to 102%). LTs receptor antagonist, LY-171883, prevented the smoking-in duced increase of SVR and PVR and augmentation of HPV. Cyclooxygenase inhibitor, in domethacin, prevented partly increase of PVR but not HPV induced by smoking. Our results suggest that smoking leads to pulmonary and systemic vasoconstriction and augmentation of HPV mediated by LTs, the increase of PVR during smoking is also mediated by TXA_2, This study also found that LY-171883 inhibited HPV by 72%, the result indictates that LTs mediate HPV in Wistar rats.