RESUMEN
Alcohol intoxication and psychiatric medication overdoses, including antidepressants, are common emergency room events. Heavy alcohol and antidepressant exposure are able to induce changes in cytokines disturbing normal physiology. We examined the inflammatory and physiological effects of selective serotonin reuptake inhibitor (SSRI) medication after heavy alcohol exposure. Rats were randomly divided into Alc (EtOH 5g/kg, intravenous infusion for 3 h), SSRI (paroxetine oral intake) and Alc+SSRI groups. Serum samples were collected to measure blood ethanol, aspartate transferase, alanine transferase, creatine phosphokinase, lactate dehydrogenase, amylase, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels. Lactate dehydrogenase levels in bronchoalveolar lavage fluid were also examined. Liver, pancreas and lungs were removed after sacrifice and any pathological changes were catalogued. Ethanol infusion resulted in blood levels of ethanol of >100 mg/dL after ethanol infusion. Serum levels of aspartate transferase, alanine transferase, creatine phosphokinase, lactate dehydrogenase, amylase, TNF-α and IL-6 in the Alc+SSRI group were lower than in the Alc group. Moreover, pathological damages to the liver, pancreas and lungs were slightly lower in the Alc+SSRI group than in the Alc group. These findings suggested that SSRI is able to decrease the release of pro-inflammatory cytokines and thereby reduce liver and pancreas damage after heavy alcohol exposure.
Asunto(s)
Citocinas/efectos de los fármacos , Etanol/antagonistas & inhibidores , Inflamación/tratamiento farmacológico , Paroxetina/farmacología , Inhibidores Selectivos de la Recaptación de Serotonina/farmacología , Animales , Líquido del Lavado Bronquioalveolar , Citocinas/sangre , Enzimas/sangre , Etanol/toxicidad , Inflamación/inducido químicamente , Interleucina-6/sangre , L-Lactato Deshidrogenasa/sangre , L-Lactato Deshidrogenasa/metabolismo , Hígado/efectos de los fármacos , Hígado/patología , Pulmón/efectos de los fármacos , Pulmón/enzimología , Pulmón/patología , Masculino , Páncreas/efectos de los fármacos , Páncreas/patología , Paroxetina/uso terapéutico , Ratas , Inhibidores Selectivos de la Recaptación de Serotonina/uso terapéutico , Factor de Necrosis Tumoral alfa/sangreRESUMEN
Inflammatory response secondary to hemorrhagic shock (HS) frequently precedes multiple organ failure and death in trauma patients. Researchers have recognized that exercise benefits immune function. However, the effects of exercise on HSinduced death and organ damage are unknown. In this study, the authors aimed to explore the effects of exercise on survival rate and organ injury after HS. Rats were divided into exercise and nonexercise groups. The exercise group received running training 30 min/day five times/week for 4 weeks. After 4 weeks, researchers withdrew 60% of total blood volume in both groups to mimic HS. Levels of blood aspartate transferase (GOT), alanine transferase (GPT), blood urea nitrogen (BUN), creatinine (Cr), lactic acid dehydrogenase (LDH), creatine kinase-myoglobin (CK-MB), blood glucose, and lactate were measured. The survival rate and injury scores for the liver, kidney, and lung were examined 48 hr after HS. Physical activity was measured in surviving rats from the 3rd to the 7th day after HS. Exercise training significantly increased the survival rate (75% for the exercise group vs. 50% for the nonexercise group) after HS and decreased organ injury. In addition, the exercise group was more active than the nonexercise group after HS.
Asunto(s)
Condicionamiento Físico Animal , Choque Hemorrágico/fisiopatología , Animales , Líquido del Lavado Bronquioalveolar , Ratas , Tasa de SupervivenciaRESUMEN
Endotoxin shock is a major cause of death in patients with septicemia. Endotoxin induces nitric oxide (NO) production and causes tissue damage. In addition, the release of oxygen free radicals has also been observed in endotoxin shock and was found to be responsible for the occurrence of multiple organ failure. The purpose of the present study was to evaluate suitable indicators for early and late stages of endotoxin shock. The experiments were designed to induce endotoxin shock in conscious rats by means of an Escherichia coli lipopolysaccharide (LPS) injection. Arterial pressure (AP) and heart rate (HR) were continuously monitored for 72 h after LPS administration. The maximal decrease in AP and increase in HR and nitrate/nitrite level occurred at 9-12 h following LPS administration. The white blood cell (WBC) count had decreased at 3 h. Hydroxyl radical (methyl guanidine, MG) decreased rapidly after LPS administration. Plasma levels of blood urea nitrogen (BUN), creatinine (Cr), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), and glutamic oxaloacetic transaminase increased before the rise of amylase. Our results suggest that changes in AP, HR, WBC, free radicals, and chemical substances (BUN, Cr) can possibly serve as approximate indicators for the early stage of endotoxin shock. Severe multiple organ damage may be caused by amylase release in the late stage of endotoxin shock.