Purpose: To evaluate whether the use of balanced salt solution (BSS) or an ophthalmic viscoelastic device (OVD) during hydrophilic acrylic intraocular lens (IOL) implantation variously impacts corneal endothelial cell characteristics in eyes undergoing uneventful phacoemulsifications.
Methods: Prospective nonrandomized observational clinical trial. Patients were assigned either to the BSS plus(®) or to the OVD Z-Celcoat™ group depending on the substance used during IOL implantation. Corneal endothelium cell characteristics were obtained before, 1 week, and 6 weeks after surgery. Intraoperative parameters (eg, surgery time, phacoemulsification energy) were recorded.
Results: Ninety-seven eyes were assigned to the BSS plus and 86 eyes to the Z-Celcoat group. Preoperative corneal endothelium cell density (ECD) and endothelium cell size were 2,506±310 cells/mm(2)/2,433±261 cells/mm(2) and 406±47 µm(2)/416±50 µm(2) (P=0.107/P=0.09). After 1 and 6 weeks, ECD decreased and endothelium cell size increased significantly in both groups (each P<0.001) without significant differences between both groups (each P>0.05). Irrigation-aspiration suction time (30.3±16.6 versus 36.3±14.5 seconds) and overall surgical time (7.2±1.2 versus 8.0±1.4 minutes) were significantly longer in the OVD Z-Celcoat group (each P<0.001). No complications or serious side effects occurred.
Conclusion: Implantation of a hydrophilic acrylic IOL under BSS infusion seems to be a useful and faster alternative in experienced hands without generating higher ECD loss rates.
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http://dx.doi.org/10.2147/OPTH.S90628 | DOI Listing |
Invest Ophthalmol Vis Sci
January 2025
Department of Ophthalmology, National Taiwan University Hospital, Taipei, Taiwan.
Purpose: To investigate the effect of Rho-associated protein kinase (ROCK) inhibitor Y27632 on bioenergetic capacity and resilience of corneal endothelial cells (CECs) under metabolic stress.
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J Am Heart Assoc
January 2025
The Center for Vascular Disease and Translational Medicine, The Third Xiangya Hospital Central South University Changsha Hunan China.
Background: Pulmonary arterial hypertension (PAH) is an incurable disease initiated by endothelial dysfunction, secondary to vascular inflammation and occlusive pulmonary arterial vascular remodeling, resulting in elevated pulmonary arterial pressure and right heart failure. Previous research has reported that dysfunction of type 2 bone morphogenetic protein receptor (BMPR2) signaling pathway in endothelium is inclined to prompt inflammation in PAH models, but the underlying mechanism of BMPR2 deficiency-mediated inflammation needs further investigation. This study was designed to investigate whether BMPR2 deficiency contributes to pulmonary arterial hypertension via the NLRP3 (NOD-like receptor family protein 3)/GSDME (gasdermin E)-mediated pyroptosis pathway.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Institute of Experimental Hematology and Transfusion Medicine, University Hospital Bonn, Germany.
Background: Clinical expressivity of the thrombophilic factor V Leiden (FVL) mutation is highly variable. Recently, we demonstrated an increased APC (activated protein C) response in asymptomatic FVL carriers compared with FVL carriers with a history of venous thromboembolism (VTE) after in vivo coagulation activation. Here, we further explored this association using a recently developed ex vivo model based on patient-specific endothelial colony-forming cells (ECFCs).
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Metabolic and Immune Diseases Department, Biomedical Research Institute Sols-Morreale (IIBM), National Research Council (CSIC), Autonoma University of Madrid, Spain (T.A.-G., S.M.-T., R.C.-M., S.U.-B., S.M.-P.).
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View Article and Find Full Text PDFAnnual epidemics of influenza result in 3-5 million cases of severe illness and more than 600 000 deaths. Severe forms of influenza are usually characterized by vascular endothelial cells damage. Thus, influenza A viruses, including subtypes A(H1N1)pdm09, A(H3N2), as well as highly pathogenic avian influenza viruses, can infect the vascular endothelium, leading to activation and subsequent dysfunction of these cells.
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