Protective response in renal transplantation: no clinical or molecular differences between open and laparoscopic donor nephrectomy

OBJECTIVE: Prolonged warm ischemia time and increased intra-abdominal pressure caused by pneumoperitoneum during a laparoscopic donor nephrectomy could enhance renal ischemia reperfusion injury. For this reason, laparoscopic donor nephrectomy may be associated with a slower graft function recovery. However, an adequate protective response may balance the ischemia reperfusion damage. This study investigated whether laparoscopic donor nephrectomy modified the protective response of renal tissue during kidney transplantation. METHODS: Patients undergoing live renal transplantation were prospectively analyzed and divided into two groups based on the donor nephrectomy approach used: 1) the control group, recipients of open donor nephrectomy (n = 29), and 2) the study group, recipients of laparoscopic donor nephrectomy (n = 26). Graft biopsies were obtained at two time points: T-1 = after warm ischemia time and T+1 = 45 minutes after kidney reperfusion. The samples were analyzed by immunohistochemistry for the Bcl-2 and HO-1 proteins and by real-time polymerase chain reaction for the mRNA expression of Bcl-2, HO-1 and vascular endothelial growth factor. RESULTS: The area under the curve for creatinine and delayed graft function were similar in both the laparoscopic and open groups. There was no difference in the protective gene expression between the laparoscopic donor nephrectomy and open donor nephrectomy groups. The protein expression of HO-1 and Bcl-2 were similar between the open and laparoscopic groups. Furthermore, the gene expression of B-cell lymphoma 2 correlated with the warm ischemia time in the open group (p = 0.047) and that of vascular endothelial growth factor with the area under the curve for creatinine in the laparoscopic group (p = 0.01). CONCLUSION: The postoperative renal function and protective factor expression were similar between laparoscopic ...

Comparison of the Effects of Propofol and Midazolam on Inflammation and Oxidase Stress in Children with Congenital Heart Disease Undergoing Cardiac Surgery

PURPOSE: To investigate and compare the effects of propofol and midazolam on inflammation and oxidase stress in children with congenital heart disease undergoing cardiac surgery. MATERIALS AND METHODS: Thirty-two ASA class I-II children with congenital heart disease undergoing cardiac surgery were randomly divided into two groups: propofol combined with low dose fentanyl (PF group, n = 16) and midazolam combined with low dose fentanyl (MF group, n = 16). Tracheal extubation time and length of Intensive Care Unit (ICU) stay were recorded. Blood samples were taken before operation (T0), at 2 h after release of the aorta cross-clamp (T3) and at 24 h after operation (T4) to measure interleukin 6 (IL-6), IL-8, superoxide dismutase (SOD) and malondialdehyde (MDA) levels. Myocardium samples were collected at 10-20 min after aorta cross-clamp (T1) and at 10-20 min after the release of the aorta cross-clamp (T2) to detect heme oxygenase-1 (HO-1) expression. RESULTS: Tracheal extubation time and length of ICU stay in PF group were significantly shorter than those of the MF group (p < 0.05, respectively). After cardiopulmonary bypass, IL-6, IL-8 and MDA levels were significantly increased, and the SOD level was significantly reduced in both two groups, but PF group exhibited lower IL-6, IL-8 and MDA levels and higher SOD levels than the MF group (p < 0.05, respectively). The HO-1 expression in the PF group was significantly higher than that in MF group at the corresponding time points (p < 0.05, respectively). CONCLUSION: Propofol is superior to midazolam in reducing inflammation and oxidase stress and in improving post-operation recovery in children with congenital heart disease undergoing cardiac surgery.

Heme oxygenase-carbon monoxide system in patients with cirrhosis: relation to splanchnic hemodynamics

Carbon monoxide [CO], an end product of the heme-oxygnase [HO] pathway,is a potent vasodilator and an important modulator of vascular cell function. The present work was designed to study the HO-1/CO system in patients with cirrhosis in relation to severity of liver disease, blood viscosity and splanchnic haemodynamics. Plasma HO-1 levels and blood carboxyhaemoglobin [COHB] concentration,an index of CO production were measured in 30 patients with liver cirrhosis and variable degrees of hepatic dysfunction and in 15 healthy subjects as a controls group. Both patients and control were non smokers. Blood viscosity was measured using the red blood cell pipette viscometer. The blood volume of the portal vein,superior mesenteric artery and splenic artery as well as pusatility index of the arteries were measured using doppler ultrasonography. Plasma [HO-1] levels and blood carboxy haemoglobin concentration were significantly higher in patients with liver cirrhosis than in healthy subjects [p< 0.001]. Also, patients who had esophageal varices, history of bleeding varices, portal hypertensive gastropathy and ascites showed significant increase in HO-1/COHB levels compared with those who did not have these complications [p < 0.001]. The increases in plasma HO-1 level and COHB level showed positive correlation with Child-Pugh score, blood viscosity and the increases in the blood flow volume of the portal vein, superior mesenteric artery and splenic artery and inverse correlation with the decreases in the pulsatility index and the resistive index of the arteries in patients with liver cirrhosis [P< 0.05]. Increased HO-1 activity with enhanced endogenous CO generation may play a role in the development of splanchnic vasodilation and serious manifestations of portal hypertension in liver cirrhosis

Expression of heme oxygenase-1 in the peripheral blood mononuclear cells from asthmatic patients / 华中科技大学学报（医学）（英德文版）

To explore the expression of heme oxygenase-1 (HO-1) in the peripheral blood mononuclear cells (PBMCs) and its relationship with pulmonary ventilation function in asthmatic patients, 18 asthmatic patients and 18 healthy subjects were selected. HO-1 protein and mRNA levels in PBMCs were measured by immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Blood carbon monoxide Hb (COHb), serum total IgE and pulmonary ventilatory function were observed. Our results showed that the percentage of cells positive for immunohistochemical staining of HO-1 were significantly higher in asthmatic patients (41.72 +/- 7.44) % than that in with healthy subjects (10.45 +/- 4.36) % (P < 0.001) and the optical density of PBMC HO-1 mRNA was higher in asthmatic patients (26.05 +/- 4.14) than that in healthy subjects (10. 82 +/- 4.26) (P < 0.001). The relation analysis showed that PBMC HO-1 protein and mRNA levels had significantly negative relation with FEV1%, PEFR, MEFR50%, respectively (r = -0.51-0.89, P < 0.05-0.001, respectively) and a positive relation with COHb and serum total IgE (r = 0.48-0. 85, 0.05-0.001, respectively). It is concluded that the expression of PBMC HO-1 protein and mRNA increased significantly in asthmatic patients, and HO-1 may play a significant role in the pathogenesis of asthma. The expression of HO-1 may bear a relation with severity of asthma.