Search

Copyright of Summa, Animali da Compagnia is the property of Point Veterinaire Italie s.r.l. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Tobacco-induced pulmonary vascular disease is partly driven by endothelial dysfunction. The bioavailability of the potent vasodilator nitric oxide (NO) depends on competition between NO synthase-3 (NOS3) and arginases for their common substrate (L-arginine). We tested the hypothesis whereby tobacco smoking impairs pulmonary endothelial function via upregulation of the arginase pathway. Methods: Endothelium-dependent vasodilation in response to acetylcholine (Ach) was compared ex vivo for pulmonary vascular rings from 29 smokers and 10 never-smokers. The results were expressed as a percentage of the contraction with phenylephrine. We tested the effects of L-arginine supplementation, arginase inhibition (by N(omega)-hydroxy-nor-l-arginine, NorNOHA) and NOS3 induction (by genistein) on vasodilation. Protein levels of NOS3 and arginases I and II in the pulmonary arteries were quantified by Western blotting. Results: Overall, vasodilation was impaired in smokers (relative to controls; p < 0.01). Eleven of the 29 smokers (the ED+ subgroup) displayed endothelial dysfunction (defined as the absence of a relaxant response to Ach), whereas 18 (the ED- subgroup) had normal vasodilation. The mean responses to 10-4 M Ach were -23 ± 10% and 31 ± 4% in the ED+ and ED- subgroups, respectively (p < 0.01). Supplementation with L- arginine improved endothelial function in the ED+ subgroup (-4 ± 10% vs. -32 ± 10% in the presence and absence of L- arginine, respectively; p = 0.006), as did arginase inhibition (18 ± 9% vs. -1 ± 9%, respectively; p = 0.0002). Arginase I protein was overexpressed in ED+ samples, whereas ED+ and ED- samples did not differ significantly in terms of NOS3 expression. Treatment with genistein did not significantly improve endothelial function in ED+ samples. Conclusion: Overexpression and elevated activity of arginase I are involved in tobacco-induced pulmonary endothelial dysfunction. [ABSTRACT FROM AUTHOR]

Ureteral obstruction secondary to ureterolithiasis in cats is a challenging situation. Ureteral stenting has recently been introduced to prevent complications that often occurred after ureterotomy or other invasive surgeries. The purpose of this study is to describe the stenting technique and perioperative difficulties, as well as long-term outcome and complications with ureteral stenting in 12 cats with ureteroliths. Fifteen 2.5 Fr soft double pigtail multi-fenestrated ureteral stents were placed in an anterograde fashion under open surgical approaches and with fluoroscopic guidance in 12 cats. Nine cats received a unilateral stent and three received bilateral stents. Ureterotomy or ureteral resection and end-to-end anastomosis were performed in three and four cases, respectively. In six cats, papillotomy was performed to facilitate dilatator and stent placement. All cats recovered well from the surgical procedure, except one cat, which died during the anaesthesia recovery period. Postoperative complications included dysuria (three cases, diagnosed at 15 days, 1 month and 3 months, respectively), urinary tract infection (one case, 1 month after surgery), stent migration requiring stent replacement (one case, 19 months after surgery) and stent obstruction requiring stent removal (three cases with previously end-to-end anastomosis between 2 and 8 months after surgery). Nine cats (75%) were alive at a mean follow-up of 453 ± 194 (123–720) days. The median survival time was >415 days. Stent placement appeared to be a valuable and safe option for treating ureteral obstruction in cats. However, periodic and long-term monitoring of stents is warranted. [ABSTRACT FROM PUBLISHER]

Three Yorkshire terrier dogs (2 males and 1 female) were presented for investigation of chronic dysuria and stranguria. Physical examination was unremarkable except for a poorly filled bladder. Biological tests, urinalysis, ultrasound, and routine radiography detected no significant abnormality, except for intermittent displacement of the bladder in the pelvis. Manual voiding cysto-urethrography showed marked caudal displacement of the bladder without perineal hernia and revealed intermittent, dynamic urethral obstruction. Obstructive kinking of the membranous urethra was observed in male dogs, and the marked caudal displacement of the bladder in the female dog was suspected to induce similar urethral obstruction, although this was not clearly visualized because of the absence of contrast filling of the obstructed urethra. All dogs showed resolution of the clinical signs following cystopexy. Key clinical message: This report documents the diagnostic value of manual voiding cysto-urethrography for the investigation of dynamic voiding disorders, especially in dogs with a pelvic bladder., (Copyright and/or publishing rights held by the Canadian Veterinary Medical Association.)

Persistent pulmonary hypertension of the newborn is a life-threatening condition in which half of infants fail to respond to inhaled nitric oxide. Development of new therapeutic pathways is crucial. The adenosine triphosphate (ATP)-sensitive potassium channels (K(ATP)) may be important in this condition. Concentration-response curves to the K(ATP) channel opener (SR47063) were performed in isolated pulmonary arterial rings from normal newborn lambs (n = 8) and pulmonary hypertensive lambs (n = 7) induced by intrauterine ductus arteriosus ligation. The effect of endothelin (ET) receptor antagonists was analyzed. Expression in the lung of the subunit Kir 6.1 of the K(ATP) channel and of ET were analyzed using Western blot and immunohistochemistry. Relaxation to SR47063 was increased in ligated animals compared with the control group. Endothelium removal enhanced this response in ligated animals (p < 0.01). The inhibitory effect of the endothelium was reversed by the Endothelin-A receptor (ET-A) antagonist BQ 123 (p < 0.01). Kir 6.1 expression was not different between groups and that of endothelin-1 (ET-1) was increased threefold in ligated animals (p = 0.007). In pulmonary hypertensive lambs, vasodilation to K(ATP) channel openers was enhanced compared with controls and further potentiated by ET-A blockade. These data might lead to new therapeutic strategies in infants with pulmonary hypertension.