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Browsing by Author "Córdova, S."

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Asociación entre strain y strain rate auricular izquierdo evaluado por speckle tracking y fibrilación auricular post cirugía de revascularización miocárdica
(2011) Gabrielli, Luigi; Córdova, S.; Enríquez, A.; Mc-Nab Martin, Paul Andrew; Verdejo Pinochet, Hugo; Godoy, I.; Corbalán Herreros, Ramón
Introducción: La fibrilación auricular (FA) es la arritmia más común post cirugía de revascularización miocárdica (CRM) y está asociada a dilatación y disfunción auricular izquierda (AI). El strain y strain rate global longitudinal AI determinado por speckle tracking constituyen herramientas novedosas en la evaluación de la función AI. Objetivo: evaluar el strain y strain rate global longitudinal AI en pacientes con enfermedad coronaria con indicación de CRM y su relación con el desarrollo de FA post operatoria. Métodos: se incluyeron pacientes consecutivos con indicación de CRM, en ritmo sinusal con fracción de eyección > 50%. Se registraron características clínicas y ecocardiográficas con evaluación del strain AI: onda s (LASs) y strain rate: onda a (LASRa), onda s (LASRs) por speckle tracking (pre-cirugía). Se evaluó la ocurrencia de FA en el período post operatorio (una semana) mediante monitorización electrocardiografía continua. Se utilizó t-Student, chi-cuadrado y regresión logística múltiple. Resultados: Se incluyeron 70 pacientes, 26% presentaron FA. LASs, LASRr y LASRa estaban significativamente disminuidos en los pacientes que desarrollaron FA post CRM, LASs (10 ± 1,1 vs 24 ± 1,2%, p < 0,001), LASRa (- 0,6 ± 0,1 vs - 1,8 ± 0,12, p < 0,001) LASRs (0,6 ± 0,007 vs 1,2 ± 0,008, p < 0,001). Los pre-dictores independientes de FA fueron: LASRs OR: 6,1 IC 95% (1,3-15,2); LASRa OR: 2,4 IC 95% (1,1-19,6); volumen AI OR: 4,67 IC 95% (1,5-19,2) y edad > 65 años OR: 2,31 IC 95% (1,1-15,8). Conclusiones: LASs, LASRs y LASRa están disminudos en pacientes que desarrollan FA post CRM y LASRs, LASRa fueron predictores independientes de ésta.
Edad mayor a sesenta años y tabaquismo son predictores de la presencia ecocardiográfica de placa aórtica complicada en pacientes con accidente cerebrovascular isquémico sin cardiopatía
(2012) Ramírez, P.; Córdova, S.; Lindefjeld, Dante; Gabrielli, Luigi; Mc-Nab Martin, Paul Andrew; Braun Jones, Sandra; Godoy, I.; Fernández, M. S.
Introducción: El ACV es la segunda causa específica de muerte en nuestro país, siendo el origen cardioembólico responsable del 20% al 40% de los casos. En pacientes sin patología cardiovascular evidente, clínica o por ecocardiografía transtorácica (ETT), la identificación de la fuente embólica requiere la realización de ecocardiografía transesofágica (ETE), que puede confirmar la presencia de una placa aórtica complicada (PAC) como agente causal de este fenómeno. Objetivo: Evaluar cuales son los predictores clínicos para la presencia de PAC que permitan definir y estratificar aquellos pacientes que más se beneficien de la búsqueda cardioembólica mediante el ETE. Métodos: Se analizaron todos los pacientes con diagnóstico de ACV isquémico ingresados a nuestro hospital entre enero del 2008 a diciembre del 2010, co-!respondientes a 398 pacientes. Se excluyeron 112 por presentar historia de arritmias o tener ETT anormal. A los 286 pacientes restantes se les realizó un ETE, para analizar la presencia o no de PAC. Se compararon características clínicas y ecográficas entre aquellos con y sin PAC. Se utilizó chi-cuadrado, test exacto de Fisher, test U Mann Whitney y regresión logística binaria. Resultados: En los 286 pacientes el ETE detectó placas aórticas en 163 (57%) pacientes; de éstos, 32 (11.19 %) presentaban PAC. Por análisis multivariado se identificaron como predictores independientes de la presencia de PAC a la edad > 60 años (OR 6.232, p 0.001) y al tabaquismo (OR 4.893, p <0.001). Conclusiones: A la luz de estos resultados, se podría sugerir que en casos de AVE/TIA de pacientes en ritmo sinusal y sin cardiopatía evidente por ETT, se debería realizar ETE al menos en fumadores y en pacientes > de 60 años.
Effect of Early Normotension with Olmesartan on Rho-kinase Activity in Hypertensive Patients
(2020) Cantin, C; Jalil Milad, Jorge; Bulnes, JF; Novoa, Ulises; MacNab, P; Godoy, I.; Córdova, S.; Gabrielli, Luigi; Ocaranza Jeraldino, M. Paz; Cantin, C; Jalil Milad, Jorge; Bulnes, JF; Novoa, Ulises; MacNab, P; Godoy, I.; Córdova, S.; Gabrielli, Luigi; Ocaranza, María Paz
Hendidura de velo posterior que simula una válvula mitral de tres velos
(2015) Vega, J.; Kanacri, A.; Gabrielli, Luigi; Córdova, S.; Olivares, G.
Reportamos el caso de una mujer de 55 años, que completo terapia antibiótica por una periodontitis con buena respuesta clínica. Posteriormente, presentó fiebre y dolor lumbar, hospitalizándose para estudio. Destacaban parámetros inflamatorios elevados y hemocultivos positivos para Streptococcus Viridans. Estudio de imágenes confirmaron espondilodiscitis de L5-S1. Se efectuó un Ecocardiograma transesogáfico (ETE), que mostró una válvula mitral de aspecto tricúspide, con prolapso del velo posterior (P2-P3) e insuficiencia severa, más una endocarditis mural auricular izquierda por lesión de jet. Se efectuó cirugía cardíaca con reparación mitral. Los hallazgos intraoperatorios mostraron el aparato subvalvular y músculos papilares habituales. Por lo tanto, el aspecto de la válvula mitral fue interpretado como una hendidura profunda del velo posterior.
Insuficiencia mitral causada por cuerpo extraño
(2015) Córdova, S.; Gonzáles, R.; Zalaquett Sepúlveda, Ricardo
Introducción: Hombre de 21 años con antecedentes de una valvuloplastía aórtica transventricular a los 3 meses de edad y de una aortoventriculoplastía anterior (operación de Konno-Rastan) con reemplazo valvular aórtico con prótesis de St Jude número 17, a los 10 meses de edad. En el año 2006, a los 16 años, fue re-operado por una estenosis subvalvular aórtica, efectuándose una ampliación del Konno con pericardio bovino y un reemplazo de la prótesis aórtica St Jude 17 por una número 23. Asintomático hasta 3 meses previo a su ingreso en que inicia disnea progresiva. Se efectuó en esta oportunidad un ecocardiograma transesofágico el que demostró una regurgitación periprostética aórtica severa y la presencia de un catéter que entraba a la aurícula izquierda a través de la vena pulmonar superior derecha, dirigiéndose a la válvula mitral (Fig 1-A, flechas). El velo mitral anterior y el aparato subvalvular mitral estaban retraídos alrededor del catéter, lo que originaba una insuficiencia mitral moderada (Fig 1-B, flechas).Al momento de la cirugía se confirmaron los hallazgos ecocardiográficos, encontrándose este catéter completamente adherido al velo mitral anterior, cuerdas tendíneas y músculo papilar, como se puede observar en la pieza quirúrgica (Fig 1-C y D, flechas). En esta cuarta operación se reconstruyó el Konno con Dacron y se reemplazó la válvula mitral con una prótesis de St Jude número 27. En su último control el paciente estaba asintomático.
Mayor actividad de rho kinasa en leucocitos circulantes se asocia a estrés oxidativo y rigidez arterial en hipertensos diabéticos
(2011) Gabrielli, Luigi; Berkovitz, A.; Mora, I.; Novoa, Ulises; Godoy, I.; MacNab, P.; Córdova, S.; Padilla, I.; Rigotti, P.; García, L.; Lavandero, S.; Ocaranza Jeraldino, M. Paz; Jalil Milad, Jorge; Gabrielli, Luigi; Berkovitz, A.; Mora, I.; Novoa, Ulises; Godoy, I.; MacNab, P.; Córdova, S.; Padilla, I.; Rigotti, P.; García, L.; Lavandero, S.; Ocaranza, María Paz; Jalil Milad, Jorge
Introducción: La vía intracellular de RhoA/Rho kinasa es activada por agonistas de receptores acoplados a proteínas G pequeñas unidas a membrana. Su activación está relacionada al remodelado cardiovascular patológico. Previamente hemos observado aumento de actividad de Rho kinasa (ROCK) en pacientes con hipertensión arterial (HT) e hipertrofia ventricular izquierda como daño de órgano blanco. Pero su activación en relación a la diabetes no ha sido explorada en estos pacientes. Objetivo: Evaluar activación de Rho kinasa y parámetros de estrés oxidativo en pacientes hipertensos con diabetes tipo II (DMII). Métodos: Estudio comparativo entre pacientes con HT sin tratamiento, HT con DMII y hemoglobina glicosi-lada Alc > 7,5% y un grupo control normotenso. Se realizó ecocardiograma de superficie. Se midió activación de ROCK en leucocitos circulantes midiendo MYPT1 fosforilado/total (p/t) por Western blot y la velocidad de pulso carotídeo-femoral (PWV) para estimar distensibilidad arterial. El stress oxidativo se estimó midiendo ma-londialdehído (MDA) y 8-isoprostano (8-ISO) en suero. Resultados: Se incluyeron 21 pacientes hipertensos con DMII, 38 pacientes hipertensos sin DMII y 34 controles normotensos. La edad promedio fue 51 ± 0,9; 48 ± 0,9 y 52 (p: NS) ± 1,1 y el 47%, 50% y 52% (p: NS) eran mujeres respectivamente. Los pacientes HT con DMII presentaron MYPTl p/t (5,6 ± 1,3; 3,6 ± 0,4; 2,1 ± 0,1 p< 0,01), MDA (1,8 ± 0,4/
Neutral endopeptidase and angiotensin I converting enzyme insertion/deletion gene polymorphism in humans
(2004) Braun, S.; Chamorro, G.; Córdova, S.; Fardella, C.; Godoy, I.; Jalil, J.E.; Lavandero, S.; Michel, J-B.; Oliveri, C.; Ocaranza Jeraldino, María Paz
Neutral endopeptidase (NEP) hydrolyses angiotensins (Ang) I and II and generates angiotensin-(1-7) [Ang-(17)]. In humans, the insertion/deletion (I/D) angiotensin- I converting enzyme ( ACE) gene polymorphism determined plasma ACE levels by 40%. In rats,
Pericarditis Constrictiva, siempre un desafío diagnóstico
(2016) Vega, Julián; Hameau, René; Córdova, S.; Gabrielli, Luigi; Saavedra Madariaga, Rodrigo Alejandro; Mc-Nab Martin, Paul Andrew; Zalaquett Sepúlveda, Ricardo
Rho kinase cascade activation in circulating leukocytes in patients with diabetes mellitus type 2
(2020) Ocaranza Jeraldino, M. Paz; Moya López, Jackeline Trinidad.; Gabrielli, Luigi; Godoy J., Iván; Córdova, S.; MacNab, P.; Farías, Luis.; Jalil Milad, Jorge; Valderas Igor, Juan Patricio; García Nannig, Lorena.; Ocaranza, María Paz; Moya López, Jackeline Trinidad.; Gabrielli, Luigi; Godoy J., Iván; Córdova, S.; MacNab, P.; Farías, Luis.; Jalil Milad, Jorge; Valderas Igor, Juan Patricio; García Nannig, Lorena.
Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.Abstract Background The intracellular ROCK signaling pathway is an important modulator of blood pressure and of cardiovascular and renal remodeling when Rho-kinase activity is increased. Besides, in preclinical models of diabetes, ROCK activation has also a role in abnormal glucose metabolism as well as in subsequent vascular and myocardial dysfunction. In humans, there are a few data assessing ROCK activation in patients with type 2 diabetes mellitus (T2D) and no studies assessing upstream/downstream components of the ROCK pathway. We assessed here levels of ROCK activation and some of the RhoA/ROCK cascade molecules in peripheral blood mononuclear cells (PBMCs) in T2D patients under current treatment. Methods Cross-sectional observational study comparing 28 T2D patients under current antidiabetic treatment with 31 consecutive healthy subjects, matched by age and gender. Circulating levels of malondialdehyde, angiotensin II and inflammatory cytokines IL-6 and IL-8 were determined in all subjects. ROCK activation in PMBCs, upstream and downstream cascade proteins, and levels of the proinflammatory molecules VCAM, ICAM-1 and IL-8 were determined in their PMBCs by Western blot. Results Compared to healthy controls, ROCK activation in T2D patients measured by 2 direct ROCK targets in PBMCs was increased by 420 and 570% (p < 0001) and it correlated significantly with serum glucose levels. p38 MAPK phosphorylation (downstream from ROCK) and JAK-2 (upstream from ROCK) were significantly higher in the T2D patients by 580% and 220%, respectively. In T2D patients, significantly increased PBMC levels of the proinflammatory molecules VCAM-1, ICAM-1 and IL-8 were observed compared to control subjects (by 180%, 360% and 260%, respectively). Circulating levels of Ang II and MDA were significantly higher in T2D patients by 29 and 63%, respectively. Conclusions T2D patients under treatment with glucose-lowering drugs, antihypertensive treatment as well as with statins have significantly increased ROCK activation in their circulating leukocytes along with higher phosphorylation of downstream cascade proteins despite pharmacologic treatment, along with increased plasma angiotensin II and MDA levels. ROCK inhibition might have an additional role in the prevention and treatment of T2D.

Browsing by Author "Córdova, S."

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