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Purpose: The aim of this study was to evaluate the relationship between serum adiponectin levels and carotid–femoral pulse wave velocity (cfPWV) in hemodialysis (HD) patients. Method: Blood samples were obtained from 120 HD patients. cfPWV was measured with a validated tonometry system (SphygmoCor; AtCor Medical, West Ryde, Australia). Serum adiponectin levels were measured using a commercially available enzyme-linked immunosorbent assay kit. Results: By univariate linear analysis of cfPWV in HD patients, we found that diabetes ( r = .281, p = .002), pre-HD body weight ( r = .194, p = .033), post-HD body weight ( r = .192, p = .036), waist circumference ( r =.210, p = .022), and body fat mass ( r = .194, p = .034) were positively correlated, whereas adiponectin level ( r = −.254, p = .005) was negatively correlated with cfPWV in HD patients. Multivariate forward stepwise linear regression analysis showed that diabetes (β = .274, p = .006) and adiponectin level (β = −.215, p = .016) were independent predictors of cfPWV in HD patients. Moreover, post-HD body weight (β = −.274, p = .041), waist circumference (β = −.311, p < .001), logarithmically transformed triglyceride level (log-TG; β = −.186, p = .031), and log-glucose (β = −.225, p = .008) were negatively associated with adiponectin levels in HD patients after multivariable forward stepwise linear regression analysis. Conclusions: Among HD patients, serum adiponectin level was inversely associated with cfPWV level, and post-HD body weight, waist circumference, log-TG, and log-glucose were negatively associated with adiponectin level.

Rosiglitazone is a peroxisome proliferator-activated receptor (PPAR)-γ agonist. By inhibiting nuclear factor κB (NF-κB), it decreases tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) and has an anti-inflammatory effect. Endotoxin shock can induce the production of several inflammatory mediators such as TNF-α and IL-6, leading to multiple organ dysfunction and death. We investigated the effects of rosiglitazone (.3 mg/kg, intravenous administration) on the physiologic attributes and cytokine levels in endotoxin shock in conscious rats. Endotoxin shock was induced by intravenous injection of Klebsiella pneumoniae lipopolysaccharides (LPSs; 10 mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 24 hr after LPS administration. Levels of biochemical and cytokine parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), lactic dehydrogenase (LDH), creatine phosphokinase (CPK), glucose, TNF-α, and IL-6 were measured at 0, 1, 3, 6, 12, and 24 hr after sepsis. Endotoxin shock significantly increased blood GOT, GPT, BUN, Cre, LDH, CPK, glucose, TNF-α, and IL-6 levels and HR, while also decreasing MAP. Rosiglitazone diminished the increase in HR, decreased the markers of organ injury (GOT, GPT, BUN, Cre, LDH, CPK, glucose) and inflammatory biomarkers (TNF-α, IL-6), and did not affect MAP after LPS. In conclusion, rosiglitazone ameliorated endotoxin shock-induced markers of organ injury and suppressed the release of TNF-α and IL-6 in conscious rats.

Freshwater clam ( Corbicula fluminea), a popular edible shellfish in Asia, is said to have beneficial effects on liver function. However, scientific evidence for such benefit is limited. In this study, the authors aimed to assess the treatment effects of freshwater clam extract (FCE) administration after hemorrhagic shock (HS) in rats. The authors randomly divided animals into three groups. After inducing HS in rats in the HS + FCE ( n = 12) and HS groups, the authors fed 20 mg/kg FCE orally to rats in the HS group only. The authors neither induced HS in nor fed FCE to rats ( n = 8) in the vehicle group. The authors measured the blood levels of white blood cells (WBC), aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and tumor necrosis factor-alpha (TNF-α) at several time points during the experiment. After 48 hr, the authors sacrificed the rats and harvested the livers for hematoxylin and eosin (HE) staining. The HS significantly decreased mean arterial pressure (MAP), increased blood AST, ALT, and LDH levels and induced liver injury in rats. Treatment with FCE increased MAP level and decreased AST, ALT, LDH, and TNF-α levels after hemorrhage. The HE staining showed diminished organ injury in the FCE-treated group. In conclusion, the administration of posttreatment FCE suppressed the release of pro-inflammatory TNF-α production after HS and decreased the levels of markers of liver injury associated with HS in rats. These beneficial effects suggest that FCE is a potential immunomodulator.

Patients with hypertension have higher mortality rates from hemorrhagic shock (HS) than normotensive patients. Several inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10) can be produced by HS and lead to multiple organ dysfunction and death. We investigated the effects of high dose (10 mg/kg/hr) and low dose (1 mg/kg/hr) propofol treatment after HS in conscious spontaneously hypertensive rats (SHRs). By withdrawing 40% of total blood volume from a femoral arterial catheter (6 ml/100 g body weight [BW]) for more than 30 min, HS was induced. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 24 hr after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) were measured 30 min before and 0, 1, 3, 6, 9, 12, 18, and 24 hr after the 30-min blood withdrawal period. Cytokine levels, including TNF-alpha and IL-10 in the serum, were measured 1 hr after HS. The kidney, liver, and lung were removed for pathology assessment at 48 hr after HS. HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-alpha, and IL-10 levels in conscious SHRs. Posttreatment propofol decreased serum TNF-alpha level, increased serum IL-10 level, attenuated the severity of organ damage, and improved survival rate after HS. This treatment protected SHRs against HS-induced organ damage. Moreover, high-dose propofol had a more protective effect than low-dose propofol against HS in conscious SHRs.