Acute anesthetized measurements of right ventricular and pulmonary artery pressure in a rat model of pulmonary artery hypertension

Alterations in pulmonary function and in hemodynamics were studied in dogs with high pulmonary blood flow resulting from systemic pulmonary artery shunts. In order to facilitate elevation in pulmonary artery pressure, the vascular bed was reduced in some cases by obstructing branches of the pulmonary artery with Teflon clips or by lobectomy. Results in 30 control dogs and in 30 animals that survived 5–36 months (average 16) following creation of shunts indicated that pulmonary function was not significantly altered by increased pulmonary blood flow until pulmonary artery hypertension developed. When systolic pulmonary artery pressure exceeded 40 mm Hg, there was a decrease in arterial Po2, an increase in venous admixture percentage of cardiac output, and an increase in the A-a O2 difference during three levels of O2 breathing, indicating both abnormal venous admixture and abnormal diffusion. Possible explanations for these findings are presented. Evidence in one dog suggests that these alterations are reversible. Submitted on August 10, 1960

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iTRAQ-based quantitative proteomic analysis of the improved effects of total flavones of Dracocephalum Moldavica L. in chronic mountain sickness

Scientific Reports ◽

10.1038/s41598-021-97091-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Aihaidan Abudouwayiti ◽

Yiliyaer Nijiati ◽

Xiangyang Zhang ◽

Dilinuer Maimaitiyiming ◽

Ainiwaer Aikemu

Keyword(s):

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Rat Model ◽

Metabolic Pathways ◽

Quantitative Proteomics ◽

Serum Levels ◽

Chronic Mountain Sickness ◽

Acid Glycoprotein ◽

Artery Pressure ◽

Mountain Sickness

AbstractTo use isobaric tags for relative and absolute quantification (iTRAQ) technology to study the pathogenesis of chronic mountain sickness (CMS), identify biomarkers for CMS, and investigate the effect of total flavones of Dracocephalum moldavica L. (TFDM) on a rat model of CMS. We simulated high altitude hypobaric hypoxia conditions and generated a rat model of CMS. Following the administration of TFDM, we measured the pulmonary artery pressure and serum levels of hemoglobin (Hb), the hematocrit (Hct), and observed the structure of the pulmonary artery in experimental rats. Furthermore, we applied iTRAQ-labeled quantitative proteomics technology to identify differentially expressed proteins (DEPs) in the serum, performed bioinformatics analysis, and verified the DEPs by immunohistochemistry. Analysis showed that the pulmonary artery pressure, serum levels of Hb, and the Hct, were significantly increased in a rat model of CMS (P < 0.05). Pathological analysis of lung tissue and pulmonary artery tissue showed that the alveolar compartment had obvious hyperplasia and the pulmonary artery degree of muscularization was enhanced. Both pulmonary artery pressure and tissue morphology were improved following the administration of TFDM. We identified 532 DEPs by quantitative proteomics; gene ontology (GO)and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis further revealed that metabolic pathways associated with coagulation and complement play crucial roles in the occurrence of CMS. Immunohistochemistry verified that several DEPs (α-1-acid glycoprotein, collagen, fibulin, haptoglobin, PLTP, and TAGLN2) are important biological markers for CMS. Our analyses demonstrated that TFDM can improve CMS and exert action by influencing the metabolic pathways associated with coagulation and complement. This process relieves pulmonary artery pressure and improves lung function. We also identified that α-1-acid glycoprotein, collagen, fibulin, haptoglobin, PLTP, and TAGLN2 may represent potential biomarkers for CMS.

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