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Effects of hypoxic preconditioning on myocardial mitochondrial energy metabolism during acute hypoxia in rats

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Journal of Medical Colleges of PLA(China) 1998年第1期13卷 22-25页

作者：罗刚刘福玉谢增柱张国斌

The effects of hypoxic preconditioning (HP) on the functions of myocardial mitochondria and ATP content were studiedin the rat. Rats were exposed to a simulated altitude of 4000m (with a barometric pressure of 43 kPa) for 1d. The myocardialmitochondrial respiratory function was determined with the Clark type O2 electrode, mitochondrial membrane fluidity (MMF) wasassayed with fluorescence polarizative method, and the myocardial content of ATP, ADP and AMP were measured with high performance liquid chromatography. It was found that after the administration of HP, the ATP content was increased from 31.89±2.42/mg·g-1 to 60. 55±3.52/mg·g-1 (P<0.01 ), mitochondrial respiratory control rate (RGR) was increased from 1.84 ±0.58 to4. 55 ± 0. 32 (P<0.01), MMF was significantly increased (P< 0.05) and the activities of FO F1 -ATPase and Na+ -K+ -ATPasewere increased by 66% and 25%, respectively. It is concluded that HP is efficacious to improve myocardial energy metabolismthrough the mechanism of the increase of mitochondrial membrane fluidity and the improvement of mitochondrial respiratory function.

关键词： hypoxic preconditioning anoxia mitochondrion adenosine triphosphate membrane fluidity myocardium

Study on neuronal apoptosis induced by hypoxia or traumatic injury in rats

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Chinese Journal of Traumatology 2000年第3期3卷 149-152页

作者：姜曙于如同鞠延贺民毛伯镛 Department of Neurosurgery First Affiliated Hospital West China University of Medical Sciences Chengdu 610041 China.

Objective: To explore the relationship between neuronal apoptosis and hypoxia or traumatic injury. Methods: Rat neurons primarily cultured in vitro were treated with hypoxia (the hypoxia group) or traumatic injury (the trauma group). The neuronal apoptosis was evaluated with microscope, TUNEL (terminal deoxynucleotidyl transferase mediated X dUTPnick end labeling) staining, flow cytometry, agarose gel electrophoresis and immunohistochemistry. Results: Morphological changes of apoptosis appeared in the treated neurons,and the DNA fragmentation showed “ladder” break. The apoptotic index was 10.8% in the hypoxia group and 4.8% in the trauma group, while it was only 1.6% in the control group. The expression of apoptosis associated genes (c myc, fas and fasL) ***: Hypoxia or traumatic injury can induce neuronal apoptosis, and its molecular mechanism is probably related to the expressions of apoptosis associated genes.

关键词： Apoptosis anoxia Wounds and injuries Gene expression

The Effects of Captopril and Cicaprost on Changes of Cardiac Membrane Fluidity and Lipid Peroxidation

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Journal of Chinese Pharmaceutical Sciences 1993年第2期2卷 114-120页

作者：苏志李元建陈修湖南医科大学药理教研室长沙410078

The main purpose of this study was to investigate the protective actions of captopril and cicaprost on changes of membrane fluidity of cultured neonatal rat myocardial cells exposed to anoxia and sugar *** peroxidation level estimated by determining the thiobarbituric acid reactive substance(TBARS)content and lactate dehydrogenase(LDH)released in culture medium was also observed in order to examine other membrane-related changes due to *** fluidity was monitored by measuring changes in the steady state fluorescence anisotropy(r_s)by fluorescence *** r_s value,TBARS level and LDH release were significantly increased after 3 h ***(180 μmol/L),cicaprost(30 nmol/L)and indomethacin(1μmol/L)did not alter r_s, TBARS level and LDH activity of normal cultured neonatal rat myocardial ***,both captopril and cicaprost significantly prevented the increases of r_s,TBARS content and LDH release in those cells exposed to anoxia and sugar *** abolished the actions of captopril on TBARS production and LDH release,but maintained its membrane fluidity *** results indicate that captopril and cicaprost protect membrane fluidity and lipid peroxidation changes in anoxia- injured myocardial *** action mechanism of captopril may be due,in part,to stimulation of prostacyclin synthesis and/or release.

关键词： anoxia Membrane fluidity Lipid peroxidation Captopril Cicaprost Cardiac myocytes