Critical care medicine
-
Critical care medicine · Feb 2006
Role of tumor necrosis factor-alpha in myocardial dysfunction and apoptosis during hindlimb ischemia and reperfusion.
Peripheral vascular surgery involving limb ischemia/reperfusion is associated with tumor necrosis factor-alpha production and an increased risk of cardiac complications. The objective of this study was to investigate the role of tumor necrosis factor-alpha in myocardial apoptosis and dysfunction following hindlimb ischemia/reperfusion. ⋯ Tumor necrosis factor-alpha contributes significantly to myocardial dysfunction and apoptosis in hindlimb ischemia/reperfusion. Although a causal link between myocardial apoptosis and cardiac dysfunction is not established, our study does suggest that tumor necrosis factor-alpha may be a potential therapeutic target for cardiac injury in clinical situations involving prolonged remote ischemia/reperfusion.
-
Critical care medicine · Feb 2006
Role of inducible nitric oxide synthase in the reduced responsiveness of the myocardium to catecholamines in a hyperdynamic, murine model of septic shock.
Excess nitric oxide production is a key mediator of hypotension and catecholamine-resistance in septic shock. Although nitric oxide synthase blockade has been shown to restore hemodynamics, conflicting results on myocardial function were reported. Inducible nitric oxide synthase (iNOS) knockout (iNOS-/-) mice showed improved heart function, but these results were obtained during hypodynamic shock characterized by reduced cardiac output. Therefore, we investigated heart function and catecholamine responsiveness in a clinically relevant, murine model of cecal ligation and puncture (CLP)-induced septic shock. ⋯ Our results confirm septic shock-related impaired left ventricular function. Genetic iNOS deletion and pharmacologic iNOS blockade enhanced cardiac norepinephrine responsiveness due to improved systolic function. In contrast, iNOS inhibition seemed to be affiliated with compromised left ventricular relaxation.
-
Critical care medicine · Feb 2006
Effects of N-acetylcysteine plus deferoxamine in lipopolysaccharide-induced acute lung injury in the rat.
Interventions that reduce the generation or the effects of reactive oxygen species exert controversial effects in animal models of lung injury, and these could be secondary to the pro-oxidant effects of antioxidants generally by their interaction with iron. We here describe the effects of N-acetylcysteine, deferoxamine, or both in the treatment of acute lung injury induced by intratracheal lipopolysaccharide injection. ⋯ Our data provide the first experimental demonstration that N-acetylcysteine plus deferoxamine decreases oxidative stress and mitochondrial dysfunction and limits inflammatory response and alveolar pathology induced by lipopolysaccharide in the rat.
-
Critical care medicine · Feb 2006
Editorial CommentStandby...cardiac arrest...standby...cardiac arrest.