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- Deng, Wenjun, et al.
(författare)
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Difference between Supine and Upright Blood Pressure Associates to the Efficacy of Midodrine on Postural Orthostatic Tachycardia Syndrome (POTS) in Children
- 2014
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Ingår i: Pediatric Cardiology. - : Springer Verlag (Germany). - 0172-0643 .- 1432-1971. ; 35:4, s. 719-725
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Tidskriftsartikel (refereegranskat)abstract
- Postural orthostatic tachycardia syndrome (POTS) is common, and has a serious impact on childrens quality of life. Midodrine hydrochloride, an alpha 1-adrenoreceptor agonist, is an effective treatment. The study was designed to examine the therapeutic efficacy of midodrine hydrochloride by quantifying changes in blood pressure during the head-up test (HUT), in children with POTS. Overall, 104 out of 110 children with POTS were treated with midodrine hydrochloride and successfully followed-up. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) changes were analyzed during the HUT. In a retrospective analysis, a receiver operating characteristic (ROC) curve was used to analyze the therapeutic predictive value of pre-treatment changes in SBP, DBP, and a combination of both, from the supine position to standing, in the subjects. The increase of SBP and DBP from the supine position to standing in responders were significantly lower than that of the non-responders. The ROC curve showed that midodrine hydrochloride for children with POTS would be predicted to be effective when the pre-treatment increase of SBP was a parts per thousand currency sign0 mmHg, or when the pre-treatment increase of DBP was a parts per thousand currency sign6.5 mmHg (from the supine position to standing), yielding a sensitivity of 72 % and specificity of 88 %. The area under the curve was 0.744 and 0.809, respectively. Hence, the results suggested that looking at the changes in blood pressure during the HUT was useful in predicting the response to midodrine hydrochloride in children with POTS.
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| 2. |
- Zhu, Mingzhu, et al.
(författare)
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Effect of endogenous sulfur dioxide in regulating cardiovascular oxidative stress
- 2014
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Ingår i: Histology and Histopathology. - : F HERNANDEZ. - 0213-3911 .- 1699-5848. ; 29:9, s. 1107-1111
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Forskningsöversikt (refereegranskat)abstract
- In the middle of the 1980s, nitric oxide received extensive attention because of its significant effects in life science. Then, carbon monoxide and hydrogen sulfide were discovered to be gasotransmitters playing important roles in regulating cellular homeostasis. As a common air pollutant, sulfur dioxide (SO2) can cause great harm to the human body by producing free radicals, which causes oxidative damage to various organs. Recently, endogenous SO2 was found to be produced in the cardiovascular system and might be a bioactive molecule regulating the physiological activities including cardiovascular oxidative stress.
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| 3. |
- Zhu, Mingzhu, et al.
(författare)
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L-Cystathionine Inhibits the Mitochondria-Mediated Macrophage Apoptosis Induced by Oxidized Low Density Lipoprotein
- 2014
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Ingår i: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 15:12, s. 23059-23073
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Tidskriftsartikel (refereegranskat)abstract
- This study was designed to investigate the regulatory role of L-cystathionine in human macrophage apoptosis induced by oxidized low density lipoprotein (ox-LDL) and its possible mechanisms. THP-1 cells were induced with phorbol 12-myristate 13-acetate (PMA) and differentiated into macrophages. Macrophages were incubated with ox-LDL after pretreatment with L-cystathionine. Superoxide anion, apoptosis, mitochondrial membrane potential, and mitochondrial permeability transition pore (MPTP) opening were examined. Caspase-9 activities and expression of cleaved caspase-3 were measured. The results showed that compared with control group, ox-LDL treatment significantly promoted superoxide anion generation, release of cytochrome c (cytc) from mitochondrion into cytoplasm, caspase-9 activities, cleavage of caspase-3, and cell apoptosis, in addition to reduced mitochondrial membrane potential as well as increased MPTP opening. However, 0.3 and 1.0 mmol/L L-cystathionine significantly reduced superoxide anion generation, increased mitochondrial membrane potential, and markedly decreased MPTP opening in ox-LDL + L-cystathionine macrophages. Moreover, compared to ox-LDL treated-cells, release of cytc from mitochondrion into cytoplasm, caspase-9 activities, cleavage of caspase-3, and apoptosis levels in L-cystathionine pretreated cells were profoundly attenuated. Taken together, our results suggested that L-cystathionine could antagonize mitochondria-mediated human macrophage apoptosis induced by ox-LDL via inhibition of cytc release and caspase activation.
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