ARTÍCULO ORIGINAL Evaluación a través de tomografía computarizada del efecto de una infusión endovenosa de ketamina en el desarrollo de atelectasia inducida por anestesia general en perrosEvaluation of an endovenous ketamine infusion through computed tomography on the development of pulmonary atelectasis due to general anesthesia in dogs SUMMARYThe aim of this study was to assess through computed tomography the presence of pulmonary atelectasis in dogs under inhalatory anesthesia and evaluate the effect of an endovenous ketamine infusion upon it. For this purpose 12 dogs separated in two groups (A and B) of 6 dogs each were used. Both groups were subjected to the same anesthetic protocol. The protocol consisted in premedication with xilacine IM, induction with propofol IV and maintenance with inhalatory anesthesia for a period of two hours. The group B received also a ketamine infusion. Computed tomographic images were taken at 0, 60 and 120 minutes, with the purpose of monitoring developments of atelectasis. In 58% of the dogs it was possible to determine the presence of some degree of atelectasis. In these animals atelectasis was observed in all the cases, but only in one lung. Atelectasis was found in 5 animals in the group without infusion of ketamine and in 2 animals in the group with infusion. The collapsed lung zones ranged between 0.13 and 8.03 cm 2 in group A, and 0.07 and 2.10 cm 2 in group B. Results indicated that ketamina infusion did not influence the presentation of pulmonary atelectasis. With regard to the evolution of the atelectasis through time, slight changes were observed in both groups, not being statistically significant (P > 0.05).Palabras clave: atelectasia, anestesia, tomografía computarizada, perro.

Macroautophagy and the ubiquitin proteasome system work as an interconnected network in the maintenance of cellular homeostasis. Indeed, efficient activation of macroautophagy upon nutritional deprivation is sustained by degradation of preexisting proteins by the proteasome. However, the specific substrates that are degraded by the proteasome in order to activate macroautophagy are currently unknown. By quantitative proteomic analysis we identified several proteins downregulated in response to starvation but independently of ATG5 expression. Among them, the most significant was HERPUD1, an ER protein of short-half life and a well-known substrate of the proteasome. We found that increased HERPUD1 stability by deletion of its ubiquitin-like domain (UBL) plays a negative role on basal and induced macroautophagy. Moreover, we found it triggers ER expansion by reordering the ER in crystalloid structures, but in the absence of unfolded protein response activation. Surprisingly, we found ER expansion led to an increase in the number and function of lysosomes establishing a tight network with the presence of membrane-contact sites. Importantly, a phosphomimetic S59D mutation within the UBL mimics UBL deletion on its stability and the ER-lysosomal network expansion revealing an increase of cell survival under stress conditions. Altogether, we propose stabilized HERPUD1 downregulates macroautophagy favoring instead a closed interplay between the ER and lysosomes with consequences in cell stress survival.