In cirrhosis, splanchnic vasodilation contributes to portal hypertension, subsequent renal sodium retention, and formation of ascites. Urotensin II(U-II) is a constrictor of large conductive vessels. Conversely, it relaxes mesenteric vessels, decreases glomerular filtration, and increases renal sodium retention. In patients with cirrhosis, U-II plasma levels are increased. Thus, we investigated hemodynamic and renal effects of U-II and its receptor antagonist, palosuran, in cirrhotic bile duct-ligated rats (BDL). In BDL and sham-operated rats, we studied acute effects of U-II (3 nmol/kg; intravenously) and palosuran (10 mg/kg; intravenously) and effects of oral administration of palosuran (30 mg/kg/day; 3 days) on hemodynamics and renal function. We localized U-II and U-IIreceptor (UTR) in livers and portal veins by immunostaining. We determined U-II-plasma levels by enzyme-linked immunosorbent assay (ELISA), and mesenteric nitrite/nitrate-levels by Griessreaction. RhoA/Rho-kinase and endothelial nitric oxide synthase ( P ortal hypertension in liver cirrhosis is mediated by an increased portal tributary blood flow 1 and an increase in intrahepatic resistance to portal flow. 2 The increased portal tributary blood flow is attributable to decreased splanchnic vascular resistance and consecutive splanchnic vasodilation. Consequences of this vasodilation are activation of the renin angiotensin aldosterone system, renal sodium retention, and formation of ascites. 3 This splanchnic vasodilation is mediated by an overproduction of the vasodilator nitric oxide (NO) 4,5 and by concomitant defects in contractile signaling. Thus, we have recently shown that a decrease in RhoA/Rho-kinase signaling contributes to vasodilation in cirrhosis. 6,7 Urotensin II (U-II) is a cyclic oligopeptide with vasoactive potential. [8][9][10][11] By activation of the urotensin II receptor (UTR), U-II might influence different pathways, depending on the cells and vascular compartment where Abbreviations: ⌬C T , the difference in the number of PCR
OCT-A reveals a distinct reduction in CC vessel density and CC decorrelation signal index in eyes affected by RPD, which emphasizes the relevance of the CC layer in RPD pathogenesis.
ABSTRACT.Purpose: To evaluate the efficacy of intravitreal dexamethasone implants in eyes with cystoid macular oedema (CME) secondary to branch retinal vein occlusion (BRVO) or central retinal vein occlusion (CRVO) in the clinical everyday practice, examine the effects of early retreatment and compare the results with the GENEVA study. Methods: The charts of 102 patients (102 eyes) with CME secondary to BRVO (n = 54) or CRVO (n = 48) treated with Ozurdex at 8 centres were retrospectively reviewed. The patients were examined monthly over a 24-week period. Slit-lamp biomicroscopy, measurement of best-corrected visual acuity (BCVA) and measurement of the central retinal thickness (CRT) with spectral-domain optical coherence tomography (SD-OCT) were performed at baseline and at every follow-up examination. The mean CRT at baseline was 740 ± 351 lm and it decreased to 419 ± 315 lm after 4 weeks, 352 ± 261 lm after 8 weeks, 455 ± 251 lm after 12 weeks, 497 ± 280 lm after 16 weeks, 468 ± 301 lm after 20 weeks and 395 ± 234 lm after 24 weeks. The BCVA improvement was statistically significantly better (p < 0.05) compared with baseline in both groups at every follow-up visit. The mean CRT maintained significantly better when compared with baseline in both groups at all follow-up visits. Early reinjection was indicated in BRVO in 40.7% after 17.5 ± 4.2 weeks and in CRVO in 50% after 17.68 ± 4.2. Six eyes (11%) with BRVO received a sectorial laser photocoagulation at a mean interval of 22 ± 5.0 weeks. Seven eyes (15%) with CRVO received a panretinal laser photocoagulation after a mean interval of 18 ± 7.0 weeks. The BCVA improvement and the mean CRT reduction were statistically significant (p < 0.05) compared with baseline in both groups at every follow-up visit. Conclusions: Dexamethasone intravitreal implant resulted in a significant improvement of the BCVA and reduction of CME in patients with BRVO or CRVO. Early retreatment after 16 weeks instead of 24 weeks, like in the GENEVA study, was indicated in 50% to stabilize the improved functional and anatomical results.
Prior to both qualitative and quantitative analysis, OCT-A images must be carefully reviewed as motion artifacts and segmentation errors in current OCT-A technology are frequent particularly in pathologically altered maculae.
Tears of the retinal pigment epithelium (RPE) are most commonly associated with vascularised RPE detachment due to age-related macular degeneration (AMD), and they usually involve a deleterious loss in visual acuity. Recent studies suggest an increase in RPE tear incidences since the introduction of anti-vascular endothelial growth factor (anti-VEGF) therapies as well as a temporal association between the tear event and the intravitreal injection. As the number of AMD patients and the number of administered anti-VEGF injections increase, both the challenge of RPE tear prevention and the treatment after RPE tear formation have become more important. At the same time, the evolution of retinal imaging has significantly contributed to a better understanding of RPE tear development in recent years. This review summarises the current knowledge on RPE tear development, predictive factors, and treatment strategies before and after RPE tear formation.
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