【Literature Review】 Anterior Chamber Paracentesis Reduces Intraocular Pressure and Triggers an Immune Response in the Conventional Aqueous Humor Outflow Pathway
Release time:
2026-07-06

1. Research Background:
Anterior chamber injection has become an effective means of delivering agents to anterior segment tissues, including the aqueous humor outflow pathway (i.e., trabecular meshwork, Schlemm's canal) and the corneal endothelium. In mouse experiments, researchers have administered various substances via anterior chamber injection, including drugs, viral vectors, microbeads, and stem cells. However, anterior chamber drug delivery is not without off-target effects. Injection of recombinant adenovirus into the mouse anterior chamber can lead to prolonged macrophage aggregation in the iris and iridocorneal angle, which may alter experimental outcomes and confound data interpretation. Experimental anterior chamber paracentesis can eliminate the confounding effects of drugs or other substances injected into the anterior chamber. Anterior chamber injection is an effective approach for delivering biomedical agents and therapeutics to tissues of the conventional outflow pathway. Nevertheless, the effects of anterior chamber injection on intraocular pressure (IOP) and aqueous humor dynamics have not been fully elucidated and warrant further investigation.
2. Methods:
Anterior chamber paracentesis (ACP, without injection of any substance) was performed on 3–5-month-old wild-type C57BL/6 mice. One eye of each mouse underwent paracentesis, while the contralateral untreated eye served as an internal control. Mice were anesthetized with isoflurane (induction concentration: 2% v/v; maintenance concentration: 1.0%–1.5% v/v) administered continuously via a nose cone. Following paracentesis, IOP, aqueous humor outflow facility, aqueous humor production rate, episcleral vessel diameter, and macrophage density were measured. IOP was measured using the TonoLab rebound tonometer specifically designed for mice and rats (Icare Finland Oy, Helsinki, Finland). Aqueous humor production was measured using a mouse-specific fluorophotometer (Fluorotron Master, Ocumetrics, Mountain View, CA, USA). Conventional aqueous humor outflow facility was measured using the iPerfusion system. ImageJ software was used for quantitative analysis of IBA1-positive macrophages in the ciliary body (CB), the trabecular meshwork (TM) within the conventional outflow pathway, Schlemm's canal (SC), and distal vessels (DV).

3. Results:
On day 1 post-surgery, IOP was significantly reduced by 30% (P < 0.0001, n = 25), while aqueous humor outflow facility (P = 0.31, n = 15) and aqueous humor production rate (P = 0.16, n = 9) showed no significant changes. Furthermore, the filtration area of Schlemm's canal remained unchanged; however, distal vessels were dilated on day 1 post-ACP (P < 0.001). Correspondingly, perivascular macrophage density in the episcleral vessels was significantly elevated on day 1 post-surgery (P < 0.0005). Macrophage density within Schlemm's canal and the trabecular meshwork showed no significant change on day 1 but increased significantly by day 3 (P < 0.0001).
4. Conclusion:
A significant reduction in IOP was observed on day 1 following anterior chamber paracentesis, accompanied by macrophage infiltration into the distal tissues of the conventional aqueous humor outflow pathway and dilation of episcleral vessels, which may have contributed to reduced distal outflow resistance. This study demonstrates that the route of ocular drug administration influences immune responses and conventional outflow pathway homeostasis, a factor that must be taken into consideration in research studies.
5. Publication Information:
Authors: Darren M. Schuman; Maria Fernanda Suarez; Aleksander O. Grimsrud; Megan Kuhn; Daniel R. Saban; W. Daniel Stamer; Katy C. Liu
Journal: Investigative Ophthalmology & Visual Science, November 2025, Vol.66, 54. doi:https://doi.org/10.1167/iovs.66.14.54
Original Article Link: https://iovs.arvojournals.org/article.aspx?articleid=2811139&resultClick=1
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