Comparative study of the efficacy and safety of bromfenac, nepafenac and diclofenac sodium for the prevention of cystoid macular edema after phacoemulsification.

AIM: To compare the efficacy, tolerability and safety of bromfenac 0.09%, nepafenac 0.1% or diclofenac 0.1% for the prophylaxis of the cystoid macular edema (CME) after phacoemulsification. METHODS: Group sequential observational comparative study. After phacoemulsification, patients received two months for topical treatment of either diclofenac sodium, bromfenac or nepafenac. All patients received concomitant topical tobramycin 0.3% and topical prednisolone 1%. We measured CME using optical coherence tomography (OCT) central foveal thickness, macular thickness and total macular volume. RESULTS: We enrolled 243 patients from January to June 2015, and 35% received diclofenac, 32.9% bromfenac and 32.1% nepafenac. When we compared pre-operative to three weeks to two months, bromfenac was more effective in reducing foveal volume (21.3 and 35.4 mm3, respectively), compared with the diclofenac (1.3 and 11.5 mm3, respectively), and the nepafenac group, became more edematous 6.4 and 5.3, respectively. Totally 133 patients completed the post-surgical satisfaction questionnaire. Patients complained of eye stickiness in 13.8% whom we gave nepafenac, versus 10.3% whom we gave diclofenac sodium, and in 0 whom we gave bromfenac. CONCLUSION: Bromfenac is the best tolerated and is more effective than diclofenac and nepafenac in reducing CME after phacoemulsification.

Intracoronary angiotensin II causes inotropic and vascular effects via different paracrine mechanisms.

We hypothesized that Angiotensin II (Ang II), like other circulating hormones, acts exclusively intravascularly. To activate or block solely intravascular Ang II receptors, Ang II and its peptide receptor blocker saralasin (Sar) were covalently coupled to a inert polymer (POL, MW >4000 kD) forming Ang II-POL and Sar-POL. These two nonpermeable polymers, Ang II and Sar, were intracoronarily administered into the isolated, saline-perfused rat hearts. Ang II-POL and Ang II caused a dose-dependent ventricular positive inotropic (+I) and vasoconstrictor effects (+V) which were blocked by Sar. Sar-POL blocked their +I but not their +V. Thus, Ang II and Ang II-POL act on endothelial luminal receptors through paracrine mechanisms. +I were blocked solely by purinoceptor antagonists and paralleled by augmented venous release of ATP degradation products (adenosine, inosine and hypoxanthine). In contrast, +V were blocked solely by aspirin, indomethacin or a thromboxane A2 receptor antagonist. Intracoronary administration of ATP-gamma-S and U46169, a purinergic, and TXA2 agonists, respectively, mimicked +I and +V. The results indicate that ATP is the paracrine inotropic mediator while thromboxane A2 is the vasoconstrictor mediator. Thus, the +I and +V distinct effects by intracoronary Ang II indicate that its diverse mechanism of action along the coronary vascular tree may be due to a functionally heterogeneous endothelium.