ABSTRACT
<p><b>BACKGROUND</b>Polymorphonuclear neutrophil (PMN), one of the most important inflammatory cells, functions throughout the initiation, progression and resolution of inflammation. This study aimed at investigating the relationship between PMN apoptosis and the lung injury after chest impact trauma.</p><p><b>METHODS</b>PMNs were purified from rabbits subjected to the chest impact trauma and their apoptosis, necrosis, survival and respiratory burst were detected by flow cytometry. Meanwhile, lactate dehydrogenase and (LDH) [Ca2+]i were measured.</p><p><b>RESULTS</b>The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma, and viable cells increased. Respiratory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2 hours with the peak at 8 hours. Meanwhile, lactate dehydrogenase in bronchoalveolar lavage fluid was higher than that in control (P < 0.05) from 4 hours to 24 hours, and intracellular free Ca2+ in PMN was increased temporarily.</p><p><b>CONCLUSIONS</b>Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances, resulting in tissue injury. The temporary increase of intracellular free Ca2+ may be responsible for the delayed apoptosis of PMN.</p>
Subject(s)
Animals , Rabbits , Apoptosis , Physiology , Lung Injury , Neutrophils , Physiology , Respiratory Burst , Physiology , Thoracic InjuriesABSTRACT
Objective To explore the effect of dexamethasone (Dex) given with the intention of prevention or treatment on endotoxin shock in rabbits and its relationship with tumor necrosis factor (TNF). Methods Fifty-three health rabbits were divided into 4 groups, including normal control (n=13), endoxin shock group (n=16), preventive Dex group (n=12) and therapeutic Dex group (n=12). Except normal control was given with saline, the other 3 groups were administered with lipopolysaccharide (LPS) infusion, and the preventive Dex group was treated with Dex (5 mg/kg body weight) 30 min before LPS infusion and the therapeutic Dex group 20 min after LPS infusion. Mean arterial blood pressure (MABP), survival rate, TNF level in circulatory blood and other parameters were detected. Results In preventive and therapeutic Dex groups, MABP was increased and survival rate was reduced compared with the animals from endoxin shock group (P<0.05, P<0.01), and TNF activity in the circulating blood was significantly suppressed (P<0.01). In addition, dexamethasone administration could alleviate the elevation of plasma glucagon, glucose, lactic acid, and β-glucironidase (P<0.05, P<0.01) in shocked animals. It was also found that administration of dexamethasone in vitro prevented the release of TNF by Kupffer cells. Conclusion These results indicate that the preventive and therapeutic effect of dexamethasone on endotoxin shock, which may relate to its direct inhibition of the release of TNF induced by LPS.
ABSTRACT
Objective To explore the effect of dexamethasone (Dex) given with the intention of prevention or treatment on endotoxin shock in rabbits and its relationship with tumor necrosis factor (TNF). Methods Fifty-three health rabbits were divided into 4 groups, including normal control (n=13), endoxin shock group (n=16), preventive Dex group (n=12) and therapeutic Dex group (n=12). Except normal control was given with saline, the other 3 groups were administered with lipopolysaccharide (LPS) infusion, and the preventive Dex group was treated with Dex (5 mg/kg body weight) 30 min before LPS infusion and the therapeutic Dex group 20 min after LPS infusion. Mean arterial blood pressure (MABP), survival rate, TNF level in circulatory blood and other parameters were detected. Results In preventive and therapeutic Dex groups, MABP was increased and survival rate was reduced compared with the animals from endoxin shock group (P<0.05, P<0.01), and TNF activity in the circulating blood was significantly suppressed (P<0.01). In addition, dexamethasone administration could alleviate the elevation of plasma glucagon, glucose, lactic acid, and β-glucironidase (P<0.05, P<0.01) in shocked animals. It was also found that administration of dexamethasone in vitro prevented the release of TNF by Kupffer cells. Conclusion These results indicate that the preventive and therapeutic effect of dexamethasone on endotoxin shock, which may relate to its direct inhibition of the release of TNF induced by LPS.