Pulmonary Circulation最新文献

Current in vivo imaging techniques for cardiopulmonary vascular evaluation in Sprague-Dawley (SD) rats face limitations, including structural disruption, inadequate contrast filling, and invasiveness. This study developed a reliable, minimally invasive computed tomography angiography (CTA) technique via jugular vein catheterization for enhanced cardiopulmonary vascular imaging in live SD rats. Jugular vein catheterization was performed in 22 anesthetized healthy male SD rats (320-480 g), followed by dual-source CT angiography with iopamidol contrast. Three-dimensional vascular reconstruction was performed, and pulmonary artery width alongside left and right ventricular diameters was measured. CT-derived measurements were compared with ultrasound data using Bland-Altman analysis. CTA achieved clear visualization of pulmonary arteries, cardiac chambers, and aortic structures, demonstrating complete contrast filling and anatomical detail. Three-dimensional reconstructions precisely delineated mediastinal and vascular relationships. Pulmonary artery widths measured by CT and ultrasound showed strong agreement (p > 0.05), validating reliability. Jugular catheterization enabled stable contrast delivery with minimal trauma. Jugular vein catheterization combined with CT angiography provides a safe, accurate, and minimally invasive method for in vivo cardiopulmonary vascular imaging in SD rats. This technique offers high anatomical resolution, compatibility with hemodynamic assessments, and reduced experimental trauma, establishing this approach as a valuable tool for cardiopulmonary disease model research. CT-derived measurements were compared with ultrasound data using Bland-Altman analysis. CTA achieved clear visualization of cardiac chambers and pulmonary arteries, demonstrating complete contrast filling and anatomical detail. Three-dimensional reconstructions precisely delineated mediastinal and vascular relationships. Pulmonary artery widths measured by CT and ultrasound showed strong agreement (p > 0.05), validating reliability. Jugular catheterization enabled stable contrast delivery with minimal trauma. Jugular vein catheterization combined with CT angiography provides a safe, accurate, and minimally invasive method for in vivo cardiopulmonary vascular imaging in SD rats. This technique offers high anatomical resolution, compatibility with hemodynamic assessments, and reduced experimental trauma, establishing this approach as a valuable tool for cardiopulmonary disease model research.

This letter to the editor revisits the origins of high-dose calcium channel blocker use in pulmonary arterial hypertension (PAH) in light of bedside vasoreactivity testing, reaffirming its present-day relevance for a selected subgroup. Integrating historical insights with modern tools, the authors highlight: the "responder" phenotype as an expression of precision medicine; ion channels as pathobiological targets; the value of real-world registries and benchmarks for high-quality care pathways; attention to special contexts (interstitial lung disease in connective-tissue diseases, and sex differences in diastolic dysfunction/HFpEF). In sum, we propose a personalized approach that pairs careful high-dose titration in appropriate candidates with molecular phenotyping and standardized follow-up.

Acute chest syndrome in sickle cell disease (SCD) carries high morbidity and mortality, with up to 15% of patients requiring invasive mechanical ventilation. However, the rates and mechanisms of ventilator-induced lung injury (VILI) in SCD remain poorly understood. We hypothesized individuals with SCD are protected from VILI in a caveolin-1 (Cav-1) dependent manner. SCD mice and control littermates underwent either spontaneous tidal breathing or high tidal volume mechanical ventilation for 4 h (VILI model), or received intratracheal Escherichia coli-derived lipopolysaccharide (LPS) or sterile phosphate-buffered saline and recovered for 16 h (LPS model). Bronchoalveolar lavage (BAL) samples were analyzed for inflammatory cytokine profiles and lung tissues were used for histology and Western blot. SCD mice were protected from VILI but were more susceptible to LPS-induced lung injury, as evidenced by higher BAL fluid total protein concentrations, polymorphonuclear cell infiltration and total cell count. Inflammatory cytokine profiles differed significantly in BAL fluid: IL-6, KC and MIP-2 levels were attenuated in the SCD-VILI model, while TNF-α levels were significantly increased after LPS exposure. Cav-1 expression was reduced at baseline in SCD mice and further decreased after exposure to VILI when compared to control animals. Phosphorylated Cav-1 expression increased, leading to depletion of total Cav-1 in the SCD-VILI model. These data suggest SCD mice are protected from VILI, but not LPS-induced lung injury. These differences appear to be mediated by distinct inflammatory cytokine profiles and expression of Cav-1. Further studies are needed to explore differences in lung injury patterns in patients with SCD.

Platelets have emerged as immune-inflammatory cells that may contribute to the pathogenesis and prognosis of pulmonary arterial hypertension (PAH), although their clinical relevance remains uncertain. We retrospectively evaluated platelet indices in 243 patients with PAH from a tertiary referral center and compared them with 50 normopressoric controls undergoing right heart catheterization. Platelet count, mean platelet volume (MPV), and survival outcomes were analyzed. PAH patients exhibited significantly lower platelet counts compared with controls (203,666 ± 90,466 vs. 246,025 ± 126,778/µL; p < 0.001). MPV was also reduced in idiopathic PAH compared with controls (9.8 ± 1.68 vs. 10.44 ± 1.25 fL; p < 0.05). Survival analysis demonstrated that PAH patients with platelet counts within the normal range (150,000-450,000/µL) had significantly better outcomes than those with thrombocytopenia (p < 0.05). These findings suggest that alterations in platelet indices may reflect disease severity and prognosis in PAH. While exploratory and subject to potential confounders such as connective tissue disease, the results reinforce the potential role of platelets as biomarkers in pulmonary vascular disease and highlight the need for further mechanistic and longitudinal studies.