UV light crosslinking regresses mature corneal blood and lymphatic vessels and promotes subsequent high-risk corneal transplant survival.

Immunologic graft rejection is the main complication after corneal transplant into pathologically prevascularized so-called high-risk eyes. The aim of this study was to evaluate whether ultraviolet (UV) light crosslinking can regress pathologic corneal blood and lymphatic vessels and thereby improve subsequent graft survival. Using the murine model of suture-induced corneal neovascularization, we found that corneal crosslinking with UVA light and riboflavin regressed both preexisting blood and lymphatic vessels significantly via induction of apoptosis in vascular endothelial cells. In addition, macrophages and CD45+ cell counts were significantly reduced. Consistently, corneal crosslinking reduced keratocyte density and corneal thickness without affecting corneal nonvascular endothelial cells, iris, and lens depending on the crosslinking duration. Furthermore, using the murine model of corneal transplant, long-term graft survival was significantly promoted (P < .05) and CD4+ CD25+ FoxP3+ T regulatory cells were upregulated (P < .01) in high-risk eyes preoperatively treated with crosslinking. Our results suggest UV light crosslinking as a novel method to regress both pathologic corneal blood and lymphatic vessels and to reduce CD45+ inflammatory cells. Furthermore, this study demonstrates for the first time that preoperative corneal crosslinking in prevascularized high-risk eyes can significantly improve subsequent graft survival and may become a promising novel therapy in the clinic.

The effect of electroacupuncture and tramadol on experimental tourniquet pain.

OBJECTIVES: The hypoalgesic effect of electroacupuncture (EA) was directly compared with the analgesic effect of pharmacological interventions using the submaximum effort tourniquet technique (SETT). METHODS: 125 healthy subjects (mean age 24.44±4.46 years; 62.4% female, 37.6% male) performed SETT at baseline and under one of five experimental conditions (n=25 per group): EA (2 Hz with burst pulses in alternating one-phase-square wave pulses; burst length 180 µs, burst frequency 80 Hz, stimulation time/pulse width 3 s), tramadol (50 mg), ibuprofen (400 mg), placebo pill or non-treatment control. EA was performed at LI4 and LI10 contralaterally with stimulation beginning 20 min before SETT and lasting throughout SETT. The pharmacological interventions were given in a double-blind design 1 h before the SETT assessment. RESULTS: Subjects showed a hypoalgesic effect of the opiate and of the EA for subjective pain rating (EA p=0.0051; tramadol p=0.0299), and pain tolerance index (time/rating) (EA p=0.043; tramadol p=0.047) analysed using analysis of covariance. More subjects reached the strict time limit of 30 min (analysed by logistic regression and adjusted OR as a post-hoc analysis) under EA compared with most other experimental conditions. Only EA and tramadol were not significantly different (95% Wald confidence limits: non-treatment control vs EA 0.011 to 0.542; placebo pill vs EA 0.009 to 0.438; ibuprofen vs EA 0.021 to 0.766; tramadol vs EA 0.065 to 1.436). CONCLUSION: In a laboratory setting, an EA procedure was as effective as a single dose of an orally administered opiate in reducing experimentally induced ischaemic pain.