Dr. Alvarado-Livacic, Cristobal

La Telemedicina es la entrega remota de servicios de atención médica e información clínica utilizando tecnología de telecomunicaciones. La pandemia de SARS-CoV-2 ha catalizado la adopción de esta estrategia. En esta revisión analizamos su desarrollo local, considerando como modelo la Unidad de Teleprocesos del hospital Las Higueras de Talcahuano (HHT) en conjunto con la Unidad de Neurología (UN). Demostramos alta satisfacción usuaria, reducción en lista de espera de primera consulta, cobertura de la enfermedad neurológica ambulatoria y alto nivel de resolutividad. Esta experiencia ofrece una alternativa para mejorar la resolutividad médica a nivel nacional y mejorar la eficacia del sistema de salud especialmente en los nuevos escenarios causados por la pandemia. Finalmente, exponemos nuestras nuevas acciones centradas en educación, seguimiento de pacientes SARS-CoV-2 positivos y contactos estrechos, ampliación de prestaciones telemédicas a domicilio y creación de plataforma web junto a la comunidad.

On renal ischemia-reperfusion (I/R) injury, recruitment of neutrophils during the inflammatory process promotes local generation of oxygen and nitrogen reactive species, which, in turn, are likely to exacerbate tissue damage. The mechanism by which inducible nitric oxide synthase (iNOS) is involved in I/R has not been elucidated. In this work, the selective iNOS inhibitor l- N6-(1-iminoethyl)lysine (l-NIL) and the NOS substrate l-arginine were employed to understand the role of NOS activity on the expression of particular target genes and the oxidative stress elicited after a 30-min of bilateral renal ischemia, followed by 48-h reperfusion in Balb/c mice. The main findings of the present study were that pharmacological inhibition of iNOS with l-NIL during an I/R challenge of mice kidney decreased renal injury, prevented tissue loss of integrity, and improved renal function. Several novel findings regarding the molecular mechanism by which iNOS inhibition led to these protective effects are as follows: 1) a prevention of the I/R-related increase in expression of Toll-like receptor 4 (TLR-4), and its downstream target, IL-1β; 2) reduced oxidative stress following the I/R challenge; noteworthy, this study shows the first evidence of glutathione S-transferase (GST) inactivation following kidney I/R, a phenomenon fully prevented by iNOS inhibition; 3) increased expression of clusterin, a survival autophagy component; and 4) increased expression of nuclear factor of activated T cells 5 (NFAT-5) and its target gene aquaporin-1. In conclusion, prevention of renal damage following I/R by the pharmacological inhibition of iNOS with l-NIL was associated with the inactivation of proinflammatory pathway triggered by TLR-4, oxidative stress, renoprotection (autophagy inactivation), and NFAT-5 signaling pathway.