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

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.

The effect of diethylcarbamazine (DEC), an inhibitor of leukotrienes (LTS) synthesis or indomethacin, an inhibitor of prostaglandins (PGs) synthesis was investigated in chronic hypoxic pulmonary hypertension and reactivity of pulmonary vessels in different strains of rats. The results showed that in Wistar rats, DEC could prevent chronic hypoxic pulmonary hypertension and right ventricular hypertrophy. (?)pa and PVR were reduced, (?)pa from 3.2?0.04kPa to 2.4?0.05kPa; PVR from 76271?3274 dyno?s?cm~(-5) to 35948?3182 dyn?s?cm~(-5) respectively (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.

AIM and METHODS: In situ hybridization and image-analysis system were used to investigate the expression of NOSⅢ mRNA in cultured porcine pulmonary artery endothelial cells (PAEC) under normoxic or chronic hypoxic conditions. RESULTS: The expression of NOSⅢ mRNA were increased by 48%, 125%, 119% respectively in the 2nd, 4th, 6th subculture of normoxic PAEC after expouse to acute hypoxia for 12 hours while in chronic hypoxic group,the expression of Ⅲ NOS mRNA were increased by 92%, 245%, 565% separately. The increase was more apparent in chronic hypoxic group than in normoxic group and became more significant following the prolonging duration of hypoxia. CONCLUSION: Chronic hypoxia increased the expression of NOSⅢ gene in PAEC in response to acute hypoxia. Nitric oxide may play an important role in the decrease of hypoxic pulmonary vasoconstriction caused by chronic hypoxia.

In order to clear up the mechanism of changes in hypoxic pulmonary vasoconstriction(HPV) during hypothermia, arterial plasma concentrations of norepinephrine, thromboxane B_2, 6-keto-PGF_(1?), 5-HT and 5-hydroxyindoleacetic acid(5-HIAA) were measured before and after hypothermia. The results showed that during acute alveolar hypoxia HPV enhanced significantly in hypothermic dogs, the percentage change of PVR increased from baseline 34.7?5.80% to 57.6?6.8% (P

Abstract Making a "thoracic window" on the right thoracic wall of an animal, changes of the surface pulmonary microcirculation in Wistar rats (n=60) in vivo were observed during acute alveaolar hypoxia (Fi=0.1,3minutes), by using intravital microscopic-video recording TV system. The data showed that: (1). Internal diameter (ID) of pulmonary arterioles (20-90?m) decreased markedly, ID of group Al (≥60?m), A2 (40-59?m), and A3 (20-39?m), were decreased by 18.00%, 15.10%, and 9,59%, respectively, and ID of venules (20-100um) were decreased by 12.43% during hypoxia (P

The effect of dietary oils on pulmonary vasoreactivity and chronic hypoxic pulmonary hypertension were assessed in rats fed on soybean oil, pig oil, soybean oil plus pig oil or regular diets for two months before the start of normobaric hypoxia(10?0.5%O_2 ventilation, 8 hours per day, 14 days). Mean pulmonary arterial pressures and pulmonary vasoreactivity to acute hypoxia were higher in the chronically hypoxic rats fed on 15% soybean oil than in the rats fed on 15% pig oil, 7.50% soybean oil plus 7.5% pig oil or regular diets. Hypertrophy of the right ventricle in the rats fed on 15% soybean oil were more serious as well. Blood viscosity and hematocrit were not different among the four groups of chronic hypoxia. The findings suggest that dietary soybean oil can potentiate hypoxic pulmonary vasoconstriction, and thereby promote the development of pulmonary hypertension and right ventricular hypertrophy.