ABSTRACT
BACKGROUND: Acute kidney injury (AKI) is associated with a high mortality. This study was undertaken to detect the factors associated with the prognosis of AKI. METHODS: We retrospectively reviewed 98 patients with AKI treated from March 2008 to August 2009 at this hospital. In these patients, 60 were male and 38 female. Their age ranged from 19 to 89 years (mean 52.4±16.1 years). The excluded patients were those who died within 24 hours after admission to ICU or those who had a history of chronic kidney disease or incomplete data. After 60 days of treatment, the patients were divided into a survival group and a death group. Clinical data including gender, age, history of chronic diseases, the worst laboratory values within 24 hours after diagnosis (values of routine blood tests, blood gas analysis, liver and renal function, levels of serum cystatin C, and blood electrolytes) were analyzed. Acute physiology, chronic health evaluation (APACHE) II scores and 60-day mortality were calculated. Univariate analysis was performed to find variables relevant to prognosis, odds ratio (OR) and 95％ confidence interval (CI). Multiple-factor analysis with logistic regression analysis was made to analyze the correlation between risk factors and mortality. RESULTS: The 60-day mortality was 34.7％ (34/98). The APACHE II score of the death group was higher than that of the survival group (17.4±4.3 vs. 14.2±4.8, P<0.05). The mortality of the patients with a high level of cystatin C>1.3 mg/L was higher than that of the patients with a low level of cystatin C (<1.3 mg/L) (50％ vs. 20％, P<0.05). The univariate analysis indicated that organ failures≥2, oliguria, APACHE II>15 scores, cystatin C>1.3 mg/L, cystatin C>1.3 mg/L+APACHE II>15 scores were the risk factors of AKI. Logistic regression analysis, however, showed that organ failures≥2, oliguria, cystatin C>1.3 mg/L +APACHE II>15 scores were the independent risk factors of AKI. CONCLUSION: Cystatin C>1.3 mg/L+APACHE II>15 scores is useful in predicting adverse clinical outcomes in patients with AKI.
ABSTRACT
OBJECTIVE@#To evaluate the effect of intrathecal pumping tramadol on cell-mediated immunity in rats with formalin inflammatory pain.@*METHODS@#Thirty-two Sprague-Dawley adult male rats weighting 250 approximately 300 g were randomly divided into 4 groups (n=8 in each group):Saline group (NS) and 3 tramadol groups (T1,T2,and T3). The rats were anesthetized with intraperitoneal chloral hydrate (300 approximately 350)mg/kg. Microspinal catheter was inserted into the subarachnoid space at the lumber region according to modified Yaksh techniques. In the tramadol groups,after 5 days tramadol was continuously infused through the spinal catheter at 50 (T1),25 (T2), and 12.5 microg/h (T3) for 7 days. In the NS group normal saline was continuously infused instead of tramadol. On Day 7 formalin (5%, 50 microL) was injected into the plantar surface of the left hindpaw. The number of flinches, lickings and total time of licking was recorded for 60 min.Pain intensity scoring(PIS)(0 approximately 3;0= no pain, 3=severe pain) was used to assess the antinociceptive effect of intrathecal tramadol. The rats were killed after the evaluation of pain intensity. Body weight and spleen weight were measured and spleen index (spleen weight/body weight) was calculated. T-lymphocyte function was evaluated based on Concanavalin-A(ConA) induced splenocyte proliferation. A modified lactic acid dehydrogenase(LDH) release assay was done to assess the NK cell activity. Phenotypic expressions of cell surface markers of T lymphocyte subsets (CD3+, CD3+ CD4+, CD3+ CD8+, and CD4+/ CD8+) and NK cell(CD161+) in the spleen were analyzed by flow cytometry.@*RESULTS@#The PIS scores were significantly lower in the T1,T2,and T3 groups than those in the NS group. The spleen index and splenocyte proliferation induced by ConA were significantly suppressed in the T1 group,and the phenotypes of T lymphocyte subsets were significantly changed,but no significant difference was found in the T2 and T3 groups compared with the NS group. There were no differences in NK cell activity in the 3 tramadol groups from the control group.@*CONCLUSION@#Intrathecal pumping tramadol has significantly antinociceptive effect. Intrathecal pumping higher dosage tramadol (50microg/h) suppresses T lymphocyte proliferation and alteres T lymphocyte subset phenotype but does not affect NK cell activity. General analgesic dosage tramadol (25 and 12.5 microg/h) has no effect on the immune function.
Subject(s)
Animals , Male , Rats , Analgesics, Opioid , Pharmacology , Dose-Response Relationship, Drug , Formaldehyde , Injections, Spinal , Killer Cells, Natural , Allergy and Immunology , Pain , Allergy and Immunology , Pain Measurement , Rats, Sprague-Dawley , T-Lymphocyte Subsets , Allergy and Immunology , Tramadol , PharmacologyABSTRACT
OBJECTIVE@#To investigate the effect of lidocaine on LPS induced apoptosis of cultured adult rat alveolar Type II (AT-II) cells.@*METHODS@#Cultured cells were exposed to LPS and lidocaine for 24 hours. Apoptosis and necrosis rates of cells were detected by flow cytometry and electron microscope. The activity of lactic dehydrogenase (LDH) was analyzed by using LDH kits.@*RESULTS@#LPS induced the AT-II cell injuries by increasing not only the necrosis and apoptosis rates but also the LDH release of cultured AT-II in vitro. Lidocaine decreased the necrosis and apoptosis rates of AT-II cells.@*CONCLUSION@#Lidocaine can directly inhibit the apoptosis and necrosis induced by LPS in cultured AT-II cells.