Objective: The aim was to characterise stimulus-response curves for hypoxic pulmonary vasoconstriction and to observe the effects of drugs reputed to enhance it: aspirin (a cyclo-oxygenase inhibitor), and doxapram (a peripheral chemoreceptor agonist).
Methods: Mean pulmonary artery pressure (Ppa) versus fraction of inspired O2 (FIO2) relationships were studied in 18 intact anaesthetised piglets, before and after the intravenous administration, in random order, of either physiological saline, 1 g aspirin, or 20 mg.kg-1 doxapram. Cardiac output (Q) was kept constant, to avoid passive Q dependent changes in Ppa.
Results: A progressive decrease in FIO2 from 100% to 12% was associated with an average increase in Ppa from 19 to 38 mm Hg (p < 0.001). When FIO2 was further decreased to 8%, Ppa decreased to 32 mm Hg (p < 0.01). This stimulus-response curve was unaffected by saline, but displaced in a non-PO2-dependent manner to higher Ppa by doxapram and by aspirin.
Conclusions: The pulmonary vascular response to inspiratory hypoxia in intact anaesthetised piglets is biphasic, with a maximum at an FIO2 of 12%. Neither aspirin nor doxapram affect the shape of this stimulus-response curve, and in particular do not prevent low FIO2 associated inhibition of hypoxic pulmonary vasoconstriction.
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http://dx.doi.org/10.1093/cvr/26.10.944 | DOI Listing |
BMC Anesthesiol
January 2025
Department of Anesthesiology and Reanimation, Faculty of Medicine, Van Yüzüncü Yıl University, Van, Turkey.
Background: Patient safety is important in daily anesthesia practices, and providing deep anesthesia is difficult. Current debates on the optimal anesthetic agents highlight the need for safer alternatives. This study was justified by the need for safer and more effective anesthetic protocols for outpatient hysteroscopic procedures, particularly those conducted outside the operating room.
View Article and Find Full Text PDFSci Rep
January 2025
General Hospital of Xinjiang Military Command, 359 North Friendship Road, Sayibak, Ürümqi, 830000, Xinjiang, China.
The inflammatory response of lung tissue and abnormal proliferation of pulmonary artery smooth muscle cells are involved in the pathogenesis of high-altitude pulmonary hypertension (HAPH). Halofuginone (HF), an active ingredient derivative of Chang Shan (Dichroa febrifuga Lour. [Hydrangeaceae]), has antiproliferative, antihypertrophic, antifibrotic, and other effects, but its protective effects on HAPH remains unclear.
View Article and Find Full Text PDFForensic Sci Int
January 2025
Department of Forensic Medicine, School of Basic Medical Sciences, Fudan University, 131 Dong'an Road, Shanghai 200032, PR China. Electronic address:
Death from mechanical asphyxia (DMA) refers to death from acute respiratory disorder caused by mechanical violence. Due to the absence of characteristic signs in corpses, it has been rather challenging to achieve the precise authentication of DMA. In this research, human pulmonary samples were collected and grouped according to different causes of death in search of potential biomarkers of DMA.
View Article and Find Full Text PDFFront Physiol
January 2025
Department of Health Sciences, Environmental Physiology Group, Mid Sweden University, Östersund, Sweden.
Breath-hold diving performances are typically better in men than in women. However, it is still being determined if there are differences in the physiological responses to breath-holding between the sexes. We conducted a study comparing the maximum breath-hold duration, heart rate (HR) reduction, peripheral oxygen saturation (SpO), and spleen volume and contraction in 37 men and 44 women, all of whom had no prior breath-holding experience.
View Article and Find Full Text PDFJ Ginseng Res
January 2025
The Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Province, Jinzhou Medical University, Jinzhou, China.
Background: Vascular endothelial dysfunction (VED) is one of the main pathogenic events in pulmonary arterial hypertension (PAH). Previous studies have demonstrated that the ginsenoside Rg1 (Rg1) can ameliorate PAH, but the mechanism by which Rg1 affects pulmonary VED in hypoxia-induced PAH remains unclear.
Methods: Network pharmacology, molecular docking and other experiments were used to explore the mechanisms by which Rg1 affects PAH.
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