RESUMEN
Chronic pain is defined as pain lasting longer than six weeks and is one of the main complaints in elderly subjects. Frailty is a pathological condition that increases an individual's vulnerability by diminishing their homeostatic reserve, and it is considered a mortality risk factor. We examined the association between chronic pain and frailty in subjects who were recruited from a check-up clinic in Mexico City. Chronic pain and frailty were evaluated in 131 subjects through validated questionnaires. Descriptive and analytical statistics were performed. Of the participants, 41.9% presented with chronic pain, and 12.2% were frail. The unadjusted OR for the presence of frailty in subjects with chronic pain was 14.3 (95%CI 3.0-67.8), and the phi coefficient showed a weak positive correlation between the variables (Φ=0.352, p<0.001). In conclusion, chronic pain is associated with a higher risk of frailty. Well-timed diagnosis and treatment of chronic pain can help prevent dependency in these individuals.
Asunto(s)
Actividades Cotidianas , Dolor Crónico , Anciano Frágil/estadística & datos numéricos , Anciano , Dolor Crónico/complicaciones , Dolor Crónico/diagnóstico , Dolor Crónico/epidemiología , Dolor Crónico/terapia , Estudios Transversales , Intervención Médica Temprana/métodos , Femenino , Evaluación Geriátrica/métodos , Humanos , Masculino , México/epidemiología , Persona de Mediana Edad , Factores de Riesgo , Estadística como AsuntoRESUMEN
Airway smooth muscle (ASM) membrane depolarization through KCl opens L-type voltage dependent Ca2+ channels (Ca(v)1.2); its opening was considered the cause of KCl contraction. This substance is used to bypass intracellular second messenger pathways. It is now clear that KCl also activates RhoA/Rho kinase (ROCK) pathway. ROCK isoforms are characterized as ROCK1 and ROCK2. Because ROCK1 seems the most abundant isotype in lung, we studied its participation in KCl stimulated bovine ASM. With methyl-beta-cyclodextrin (MbetaCD) we disrupted caveolae, a membrane compartment considered as the RhoA/ROCK assembly site, and found that KCl contraction was reduced to the same extent (~26%) as Y-27632 (ROCK inhibitor) treated tissues. We confirmed that KCl induces ROCK activation and this effect was annulled by Y-27632 or MbetaCD. In isolated plasmalemma, ROCK1 was localized in non-caveolar membrane fractions in Western blots from control tissues, but it transferred to caveolae in samples from tissues stimulated with KCl. Ca(v)1.2 was found at the non-caveolar membrane fractions in control and MbetaCD treated tissues. In MbetaCD treated tissues stimulated with KCl, contraction was abolished by nifedipine; only the response to Ca(v)1.2 opening remained as the ROCK component disappeared. Our results show that, in ASM, the KCl contraction involves the translocation of ROCK1 from non-caveolar to caveolar regions and that the proper physiological response depends on this translocation.