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Zhang F.,Peking University | Li X.,Peking University | Ochs T.,Northwestern University | Chen L.,Peking University | And 5 more authors.
Journal of the American College of Cardiology | Year: 2012

Objectives: This study was designed to explore the predictive value of the midregional fragment of pro-adrenomedullin (MR-proADM) in assessing the therapeutic efficacy of midodrine hydrochloride for children with postural orthostatic tachycardia syndrome (POTS). Background: Midodrine hydrochloride is an important therapeutic option for children with POTS. However, there has not been any method to predict response to the drug. The MR-proADM is produced in equimolar amounts to adrenomedullin (ADM), and directly reflects levels of the rapidly degraded active peptide, ADM. Methods: Fifty-seven children with POTS were designated as the POTS group. Twenty healthy children served as the control group. The children in the POTS group received midodrine hydrochloride treatment. The plasma concentration of MR-proADM was measured, using a sandwich immunoluminometric assay. A receiver-operating characteristic curve was used to explore the predictive value of MR-proADM. Results: Plasma levels of MR-proADM were significantly higher in children with POTS (75.0 [62.5 to 96.0] pg/ml) than in the control group (58.5 [50.3 to 69.0] pg/ml). Plasma levels of MR-proADM in responders to midodrine hydrochloride was significantly higher than that of nonresponders (76.0 [66.0 to 91.0] pg/ml vs. 59.0 [54.0 to 65.5] pg/ml, p < 0.01]. A receiver-operating characteristic curve on the predictive value of MR-proADM showed that the area under the curve was 0.879 with a 95% confidence interval of 0.761 to 0.997. Using a cutoff value for MR-proADM of 61.5 pg/ml produced both high sensitivity (100%) and specificity (71.6%) in predicting the efficacy of midodrine hydrochloride therapy for treating POTS. Conclusions: MR-proADM can help guide midodrine hydrochloride therapy in the management of POTS in children. © 2012 American College of Cardiology Foundation. Source


Zhang F.,Peking University | Li X.,Peking University | Stella C.,University of San Diego | Chen L.,Peking University | And 5 more authors.
Journal of Pediatrics | Year: 2012

Objective: To explore the predictive value of plasma hydrogen sulfide (H 2S) in differentiating between vasovagal syncope (VVS) and postural orthostatic tachycardia syndrome (POTS) in children. Study design: Patients were divided between the POTS group (n = 60) and VVS group (n = 17) by using either the head-up test or head-up tilt test. Twenty-eight healthy children were selected for the control group. Plasma concentrations of H 2S were determined for children in all groups (POTS, VVS, and control). Results: Plasma levels of H 2S were significantly higher in children with VVS (95.3 ± 3.8 μmol/L) and POTS (100.9 ± 2.1 μmol/L) than in children in the control group (82.6 ± 6.5 μmol/L). Compared with the VVS group, the POTS group had plasma levels of H 2S that were significantly increased. The receiver operating characteristic curve for the predictive value of H 2S differentiation of VVS from POTS showed a H 2S plasma level of 98 μmol/L as the cutoff value for high probability of distinction. Such a level produced both high sensitivity (90%) and specificity (80%) rates of correctly discriminating between patients with VVS and patients with POTS. Conclusion: H 2S plasma level has both high sensitivity and specificity rates to predict the probability of correctly differentiating between patients with VVS and patients with POTS. Copyright © 2012 Mosby Inc. All rights reserved. Source


Jin H.F.,Peking University | Wang Y.,Peking University | Wang X.B.,Peking University | Sun Y.,Peking University | And 3 more authors.
Nitric Oxide - Biology and Chemistry | Year: 2013

Background The study was designed to explore if sulfur dioxide (SO 2) preconditioning increased antioxidative capacity in rat with myocardial ischemia reperfusion (I/R) injury. Methods The myocardial I/R model was made by left coronary artery ligation for 30 min and reperfusion for 120 min in rats. Myocardial infarct size and plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities, plasma superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and glutathione (GSH) changes were detected for the rats. The contents of myocardial hydrogen sulfide (H2S) and nitric oxide (NO) were measured. Myocardial protein expressions of SOD1, SOD2, cystathionine γ-lyase (CSE) and iNOS were tested using Western blot. Results Myocardial infarction developed and plasma CK and LDH activities were significantly increased in I/R group compared with those in control group, but SO2 preconditioning significantly reduced myocardial infarct size, and plasma CK and LDH activities. SO2 preconditioning successfully increased plasma SOD, GSH and GSH-Px levels and myocardial SOD1 protein expression, but decreased MDA level in rats of I/R group. Compared with controls, the myocardial H2S level and CSE expression were decreased after I/R, but myocardial NO level and iNOS expression were increased. With the treatment of SO2, myocardial H2S level and CSE expression were increased, but myocardial NO level and iNOS expression were decreased compared with those in I/R group. Conclusions SO 2 preconditioning could significantly reduce I/R-induced myocardial injury in vivo in association with increased myocardial antioxidative capacity, upregulated myocardial H2S/CSE pathway but downregulated NO/iNOS pathway. © 2013 Elsevier Inc. All rights reserved. Source


Luo L.,Peking University | Chen S.,University of California at San Diego | Jin H.,Peking University | Tang C.,Peking University | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2011

While sulfur dioxide (SO 2) has been previously known for its toxicological effects, it is now known to be produced endogenously in mammals from sulfur-containing amino acid l-cysteine. l-cysteine is catalyzed by cysteine dioxygenase (CDO) to l-cysteinesulfinate, which converts to β-sulfinylpyruvate through transamination by aspartate aminotransferase (AAT), and finally spontaneously decomposes to pyruvate and SO 2. The present study explored endogenous SO 2 production, and AAT and CDO distribution in different rat tissue. SO 2 content was highest in stomach, followed by tissues in the right ventricle, left ventricle, cerebral gray matter, pancreas, lung, cerebral white matter, renal medulla, spleen, renal cortex and liver. AAT activity and AAT1 mRNA expression were highest in the left ventricle, while AAT1 protein expression was highest in the right ventricle. AAT2 and CDO mRNA expressions were both highest in liver tissue. AAT2 protein expression was highest in the renal medulla, but CDO protein expression was highest in liver tissue. In all tissues, AAT1 and AAT2 were mainly distributed in the cytoplasm rather than the nucleus. These observed differences among tissues endogenously generating SO 2 and associated enzymes are important in implicating the discovery of SO 2 as a novel endogenous signaling molecule. © 2011 Elsevier Inc. Source


Luo L.,Peking University | Liu D.,Peking University | Tang C.,Peking University | Tang C.,Key Laboratory of Molecular Cardiology | And 5 more authors.
Biochemical and Biophysical Research Communications | Year: 2013

Pulmonary hypertension (PH) is an important pathophysiological process in the development of many diseases. However, the mechanism responsible for the development of PH remains unknown. The objective of the study was to explore the possible impact of sulfur dioxide (SO2) on the endogenous hydrogen sulfide (H2S) pathway in rats with PH induced by high pulmonary blood flow. Compared with sham group, the systolic pulmonary artery pressure (SPAP) in the shunt group was significantly increased, along with the increased percentage of muscularized arteries and partially muscularized arteries of small pulmonary arteries. Compared with the shunt group, SPAP in the shunt+SO2 group was significantly decreased, and the percentage of muscularized pulmonary arteries was also decreased. Additionally, rats that developed PH had significantly lower levels of SO2 concentration, aspartate aminotransferase (AAT) activity, protein and mRNA expressions of AAT2 in pulmonary tissues. Administration of an SO2 donor could alleviate the elevated pulmonary arterial pressure and decrease the muscularization of pulmonary arteries. At the same time, it increased the H2S production, protein expression of cystathionine-γ-lyase (CSE), mRNA expression of CSE, mercaptopyruvate transsulphurase (MPST) and cystathionine-β-synthase (CBS) in the pulmonary tissue of the rats. The results suggested that endogenous SO2/AAT2 pathway and the endogenous H2S production were downregulated in rats with PH induced by high pulmonary blood flow. However, SO2 could reduce pulmonary arterial pressure and improve the pulmonary vascular pathological changes in association with upregulating endogenous H2S pathway. © 2013 Elsevier Inc. Source

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