Asunto(s)
Insuficiencia Cardíaca/prevención & control , Contracción Miocárdica/efectos de los fármacos , Sepsis/complicaciones , Estilbenos/farmacología , Transactivadores/metabolismo , Vasodilatadores/farmacología , Animales , Masculino , Coactivador 1-alfa del Receptor Activado por Proliferadores de Peroxisomas gamma , Resveratrol , Factores de TranscripciónAsunto(s)
Calcio/metabolismo , Lipopolisacáridos/farmacología , Mitocondrias Cardíacas/metabolismo , Retículo Sarcoplasmático/metabolismo , Sepsis/fisiopatología , Animales , Gasto Cardíaco/efectos de los fármacos , Mitocondrias Cardíacas/efectos de los fármacos , Contracción Miocárdica/efectos de los fármacos , Retículo Sarcoplasmático/efectos de los fármacos , ATPasas Transportadoras de Calcio del Retículo Sarcoplásmico/efectos de los fármacos , ATPasas Transportadoras de Calcio del Retículo Sarcoplásmico/metabolismo , Sepsis/metabolismo , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
Sepsis has high incidence and mortality rates around the world. The role of cardiac depression in myocardial dysfunction during sepsis remains to be elucidated. This review attempts to summarize our understanding of the anatomical, histopathological, and pathophysiological mechanisms behind cardiac dysfunction. Biomarkers to detect cardiac depression have been used to recognize developing problems, but the actual impact of these tools remains unclear.
RESUMEN
Since the ancient Greeks, we have learned that the pathophysiology of the human diseases relies on blood-borne humoral factors. This was the case with the sepsis myocardial depression, whose associated morbidity and mortality remained untouched during the last decades. Despite the growing knowledge of the possible involved mechanisms, our understanding of this serious condition is still in its infancy. Controversies have surrounded the real origin of septic-induced myocardial dysfunction, and it has been ascribed to inflammatory mediators, NO generation, interstitial myocarditis, coronary ischemia, calcium trafficking, endothelin receptor antagonist, and apoptosis. Although not fully understood, myocardial injury/depression remains a challenge for critical care practitioners.