Myocardial dysfunction is well-documented in sepsis even in hyperdynamic state, and may develop and contribute to morbidity and mortality. Nicaraven has been shown to protect the coronary endothelial and myocardial function from ischemia and reperfusion injury due to hydroxy radical scavenging activity. The purposes of present study were to determine the effects of nicaraven on cardiac function in lipopolysaccharide (LPS) induced sepsis.
This protocol was approved by our institutional committee. Following arterial and venous cannulation and tracheostomy, rats (330-350 g) were anesthetized with pentobarbital, and mechanically ventilated with a control mode (TV = 12 ml/kg, RR = 40 rpm). After baseline measurements, rats (n = 20) were administrated with LPS (10 mg/kg, intravenously) and randomly assigned to following two groups: the nicaraven group treated with nicaraven (3 mg/kg/min, intravenously) and the control group treated with saline. The left ventricular pressure and volume were measured with the pressure and conductance catheter every one hour. Cardiac function, including cardiac output (CO), ejection fraction (EF), and maximal elastance of left ventricle (Emax) were analyzed with a computer soft. Arterial blood gas analysis and lactate concentration were also measured. Data were analyzed by repeated measure ANOVA. A p < 0.05 was considerd to be statistically significant.
The CO in the nicaraven group was kept significantly higher than the control group (p < 0.05; Figure 1). The EF and Emax in the nicaraven group were also kept significantly higher than the control group (p < 0.05). Arterial lactate was significantly lower in the nicaraven group versus the control group (P < 0.05).
The current study indicates that nicaraven preserves cardiac function and improves lactic acidosis in septic model.
The present study suggests that nicaraven improves cardiac function and circulation in sepsis. This cardio-protective strategy with nicaraven could be promising against sepsis.
R. Serita, None.