The Journal of surgical research
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Enteral nutrition with eicosapentaenoic acid (EPA; 20:5 n-3) and gamma-linolenic acid (GLA; 18:3 n-6) decreased pulmonary inflammation by reducing neutrophil counts and chemotactic factors in bronchoalveolar lavage fluid during acute respiratory distress syndrome (ARDS). We hypothesize that the anti-inflammatory effects of EPA and GLA may be due, in part, to induction of neutrophil apoptosis. The purpose of this study was to determine whether EPA and GLA, alone or in combination, trigger apoptotic cell death in the human promyelocytic leukemia HL-60 cell line. ⋯ Viability was significantly reduced to the same extent with the combination of 50 micromol/L EPA\20 micromol/L GLA compared with 100 micromol/L EPA. These data indicate that EPA and GLA, alone or in combination, reduce cell survival by induction of apoptosis. Thus, induction of apoptosis by select dietary n-3 (EPA) and n-6 (GLA) polyunsaturated fatty acids may be the mechanism of the resolution of pulmonary inflammation in ARDS.
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Although ischemic preconditioning (IPC) has been reported to protect the liver from injury when subjected to continuous hepatic ischemia, whether IPC protects rat livers against ischemia-reperfusion (I/R) injury after intermittent ischemia has not been elucidated. ⋯ IPC exerts a greater protective effect against hepatic I/R injury after intermittent hepatic ischemia than after continuous hepatic ischemia.
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A bolus of 7.5% NaCl-6% Dextran 70 (HSD) is effective in resuscitating hypovolemic shock. Common hemodynamic findings with HSD are restoration of cardiac output, increased blood pressure, and improvement of peripheral circulation. However, the effect of HSD upon cardiac function is still controversial. In our previous study, when HSD did not improve cardiac contractility, it was speculated that it might affect cardiac diastolic function without a change in contractility. Therefore, we studied the effects of HSD on cardiac diastolic function. ⋯ HSD seems to be an effective resuscitation fluid after hemorrhagic shock because the volume of HSD required to maintain circulation is significantly smaller than that of normal saline. However, our data revealed that HSD does not change cardiac diastolic function after hemorrhagic shock.