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Biomedical subjects

Z Z Xie

Publications and source records attributed to Z Z Xie.

8 recordsLinked to original sources
PubMed1999

An interactive multimedia training system for advanced cardiac life support.

This paper describes an Advanced cardiac life support (ACLS) training system (ACLSYS) with multimedia and hypertext features for training medical personnel and evaluating their performance during ACLS events. ACLSYS runs in a Windows 95 environment and is written in Visual Basic 4.0 Enterprise Edition and Access 7.0. The system consists of two primary modules: a multimedia training module and a simulation/evaluation module. The training module provides the knowledge and skills required for the appropriate early treatment of cardiopulmonary arrest. The simulation/evaluation module generates randomly an unlimited number of ACLS cases. These cases become part of the training case database and are available for retraining. ACLS certified personnel were included in the validation of the system.

Cardiopulmonary Resuscitation↗
PubMed1998

Effects of vitamin C on myocardial mitochondrial function and ATP content in hypoxic rats.

AIM: To observe the effects of large dose of vitamin C (Vc) on myocardial mitochondrial function, ATP content, and myocardial structure in acute and chronic hypoxic rats. METHODS: Rats were exposed to a simulated altitude 4000 m (barometric pressure = 43 kPa) for 3 and 30 d. Vc (0.75 g.kg-1.d-1) was injected i.p. The heart mitochondrial respiratory function were determined by Clark-type O2 electrode; mitochondrial membrane fluidity (MMF) were assayed through fluorescence polarizative method; the contents of ATP, ADP, and AMP in myocardial tissue were measured with HPLC. RESULTS: After administration of Vc, the ATP content was increased from 35 +/- 3 mg.g-1 to 53 +/- 3 mg.g-1 in acute hypoxic rats (P < 0.01), from 42 +/- 4 mg.g-1 to 48 +/- 3 mg.g-1 in chronic hypoxic rats (P < 0.01); Pa, O2 was increased from 7.2 +/- 1.4 kPa to 9.5 +/- 1.2 kPa in acute hypoxic rats (P < 0.01); mitochondrial respiratory control rate (RCR) was increased from 2.1 +/- 0.6 to 4.7 +/- 0.5 in acute hypoxic rats (P < 0.01), and from 3.3 +/- 0.7 to 4.5 +/- 0.6 in chronic hypoxic rats (P < 0.01); MMF was increased in acute and chronic hypoxic rats (P < 0.05); the degree of myocardial necrosis in vitamin C preventive rats was attenuated as compared with those of acute hypoxic rats. CONCLUSION: Vc is effective on improving myocardial energy metabolism and protecting against myocardial structural injury in hypoxic rats.

Adenosine Triphosphate↗
PubMed1998

Protective effects of Ginkgo biloba extract against lysophosphatidylcholine-induced vascular endothelial cell damage.

AIM: To study the protective effects of Ginkgo biloba extract (GbE) against endothelial cell damage induced by lysophosphatidylcholine (LPC). METHODS: The vasorelaxation response to acetylcholine (ACh) were investigated in the isolated rabbit thoracic aorta. Lipid peroxidation products were determined by measuring thiobarbituric acid reactive substance. RESULTS: GbE attenuated the inhibition of vasorelaxation response to ACh and prevented the LPC-induced increase of malondialdehyde (MDA) content both in thoracic aortae. GbE prevented the leakage of LDH and the increase of MDA content in cultured endothelial cells in a concentration-dependent manner. GbE also markedly increased epoprostenol level in cultured endothelial cells treated with LPC. CONCLUSION: GbE protected endothelial cells against LPC-induced damage due to reduction in lipid peroxidation and facilitation of synthesis and/or release of epoprostenol.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Preventive and therapeutic effects of nitrendipine on hypoxic right ventricular hypertrophy.

AIM: To assess whether nitrendipine (Nit) can be used to prevent and treat the hypoxic right ventricular hypertrophy (RVH). METHODS: Rats were exposed to a simulated altitude of 5000 m (barometric pressure = 54 kPa) for 30-60 d. Nit (10-20 mg.kg-1.d-1) was administered via gavage. The therapeutic efficacy was evaluated with right ventricular weight index (RVWI), right ventricular systolic pressure (RVSP), and myocardial ultrastructure. RESULTS: Chronic intermittent hypoxia for 30 d (8 h.d-1) resulted in an increase of RVSP and RVWI as well as in the changes of RV myocardial ultrastructure. As the hypoxic time was prolonged to 60 d, RVWI and RVSP were not further augmented. Nit (20 mg.kg-1.d-1, i.g.), when administered from the beginning of hypoxia, reduced RVSP (8.1 +/- 1.1 vs 6.0 +/- 1.0 kPa, P < 0.05) and RVWI (1.014 +/- 0.012 vs 0.915 +/- 0.049 mg/g body weight, P < 0.05). After development of hypoxic RVH, Nit (20 mg.kg-1) also decreased RVSP (7.9 +/- 1.0 vs 6.2 +/- 0.8 kPa, P < 0.05) and RVWI (1.02 +/- 0.13 vs 0.88 +/- 0.12 g/kg body weight, P < 0.05). Myocardial blood flow was increased and myocardial ultrastructure became nearly normal in rats treated with Nit. CONCLUSION: Nit prevented and lessened the hypoxic right ventricular hypertrophy.

Animals↗
PubMed1991

[The role of polycythemia in the pathogenesis of hypoxic myocardial hypertrophy].

Either chronic hypoxia or polycythemia induced by CoCl2 injection resulted in an increase of RBC, Hb, Hct and blood viscosity at different shear rate. There was an increase of right ventricular systolic and end diastolic pressure, +/- dp/dtmax, Vmax and right weight index, as compared with the control rats. Chronic hypoxia combined with polycythemia induced by CoCl2 injection further augmented the above parameters except Vmax of RV, and caused an increase of left ventricular weight index. The positive correlation was seen between the RV weight index and Hct. The above results prove that polycythemia might play important role in pathogenesis of hypoxic myocardial hypertrophy.

Animals↗