AIM：To investigate the roles of nitric oxide (NO) and endothelin-1(ET-1) in regulation of coronary vascular reserve (CVR) during hypoxia.METHODS： CVR were measured with 99m TC radiolabelled frog RBC, the changes of NO-2，ET-1 contents， nitric oxide synthase(NOS) activity and the myocardial morphometry were observed. RESULTS： (1) Acute hypoxia caused an increase in left and right ventricular myocardial blood flow，myocardial NO-2，ET-1 contents，NOS activity，but CVR in the left and right ventricle were decreased compared with the control group.(2) Intermittent hypobaric hypoxia for 90 days did not lead to significant change in left ventricular CVR，myocardial ET-1/NO-2 ratio. However, right ventricular myocardial ET-1 contents，ET-1/ NO-2 ratio were increased，right ventricular CVR and myocardial NO-2 contents were decreased. We also observed that perivascular collagen，arterial wall thickness in right ventricle， hematocrit，RV weight index were augmented. CONCLUSION： Rest myocardial blood flow was increased，CVR was decreased；The decreased coronary vascular reserve during chronic hypoxia might be resulted from the increased hematocrit，arterial wall thickness，perivascular collagen，ET-1 content, the decreased NO content and right ventricular hypertrophy

Objective To investigate the effects and mechanisms of all-trans retinoic acid(ATRA)on the proliferation and cell cycle of lung carcinoma cell line A549.Methods The A549 cells were treated with ATRA at the dosages of 5,10,50 ?mol/L for 1-7 d.The proliferation of A549 was assessed by MTT method and cell cycle was analyzed by flow cytometry.The expressions of CDK4,Rb and p-ERK1/2 were assessed by Western blotting.CyclinD1 mRNA was analyzed by SYBR-PCR amplification.Results ATRA obviously inhibited the proliferation of A549 cells,and the cell cycle was arrested in G0/G1 phase.The expression of p-ERK1/2 protein and CyclinD1 mRNA on A549 cells were decreased.Conclusion ATRA might inhibit the proliferation of A549 cells through down-regulating p-ERK1/2 protein and CyclinD1 mRNA.

AIM: To explore the mechanism of ET-1, NO and PGI 2 release from coronary artery endothelial cells (CAEC) induced by acute hypoxia. METHODS: Bovine coronary artery endothelial cells were cultured and [ 45 Ca 2+ ] was used to investigate the difference of calcium uptake between normoxia group and hypoxia group (3% O 2). The contents of ET-1, NO and PGI 2 in media of normoxia group, hypoxia group and hypoxia + verapamil group were measured 24 h after hypoxia. RESULTS: [ 45 Ca 2+ ] uptake by CAEC in hypoxia group was 1.9 times more than normoxia group ( P

AIM: This study was designed to explore the effect of hypoxia on expression of P450 2C11 mRNA in cultured rat astrocytes. METHODS: Cultured rat astrocytes were randomly divided into 4 groups: glutamate group (G), hypoxic group (H), hypoxia + glutamate group (H+G) and control (C). Cells of control group were exposed to nomorxic (95% air, 5%CO 2) condition,that of G and H+G were incubated with 100 ?mol/L L-glutamate ,then cells of H and H+G exposed to hypoxic conditions (5%CO 2, 95%N 2) at 37℃?Each group had five timepoints which included 0 h, 3 h, 6 h, 12 h, 24 h, respectively. Expression of mRNAs of P450 2C11 were detected with reverse transcription ploymerase chain reaction (RT-PCR). RESULTS: Expression of P450 2C11 mRNA did not change in H and C at all the above mentioned timepoints. While it showed marked and continuous increase from 6 h to 24 h in G and from 3 h to 24 h in G+H. P450 2C11 mRNA expression was significantly higher in G than both in H and C, and it was the highest of all groups in G+H. CONCLUSIONS: Glutamate and hypoxia+glutamate increased the expression of P450 2C11 mRNA in cultured rat astrocytes continuously in 24 hours. Hypoxia alone did not increase the expression of P450 2C11 mRNA but enhanced the effect of glutamate on expression of P450 2C11 mRNA in astrocytes, which is maybe one of the mechanisms of hypoxic-induced cerebral dilation.

AIM: This study was designed to explore the differentially expressed genes between hypobaric hypoxic delayed preconditioning (HHDP) and normal mouse hippocampus. METHODS: HHDP was produced by treating the animals at a 7 000 m high altitude for 2.5 h/d for 3 d. At 36 h after last time decompression, total RNA was isolated from hippocampus. cDNA was synthesized and amplified by SMART PCR. cDNA libraries of differentially expressed gene between HHDP and control hippocampus were constructed. 452 clones from forward (subtracted control from preconditioning) cDNA library and 74 clones from backward (subtracted preconditioning from control) one were screened by reverse Northern hybridization. RESULTS: Screening with subtracted probes, hybridization signal of 85 gene fractions decreased and that of 217 gene fractions increased by more than 2 times in HHDP hippocampus compared with control. Screening with unsubtracted probe, hybridization signal of 44 gene fractions decreased and that of 135 gene fractions increased by more than 2 times in HHDP hippocampus compared with control. Some of the clones had been sequenced. Analysis and comparison with the data of GenBank were performed. The results showed that mouse cytochrome C oxidase subunit 1, NADH dehydrogenase subunit 1 and 6, deleted in split-hand/split-foot 1 region (DSS1) and cDNA corresponding to clone IMAGE: 5251089 of mice cDNA library were increased in hippocampus of HHDP mice. cDNA corresponding to clone IMAGE: 3593193, mus musculus adult male olfactory brain cDNA and mus musculus bladder RCB-0544 MBT-2 cDAN were decreased in hippocampus of HHDP mice. CONCLUSION: Many genes expresses differentially in hippocampus of mice during HHDP. This may be one of the molecular mechanisms of HHDP.

AIM: This study was designed to investigate the protective role of hypobaric hypoxic pretreatment (HHPT) on hippocampal neurons in Babl/c inbred mice. METHODS: HHPT was produced by simulating a 7 000 m high altitude 2.5 h/d for 3 d. At 36 h after last time decompression, three subgroups consisted of both the control and pretreatment mice were subjected to the 12 000 m high altitude hypobaric hypoxia for 4 h, the severe ischemia produced by bilateral common carotid artery occlusion for 18 min, and the severe ischemia/hypoxia produced by permanently ligation of right lateral common carotid artery followed by a 8 000 m high altitude hypobaric hypoxia for 4 h, respectively. The extents of protection to hippocampal CA1 neurons by HHPT were evaluated by accounting the number of intact neurons between HHPT and control group. RESULTS: The results indicated that HHPT protected hippocampal neurons against severe hypobaric hypoxia, severe ischemia, and ischemia combined with hypobaric hypoxia. CONCLUSION: Hypobaric hypoxic pretreatment induces a delayed protection to hippocampal neurons against hypoxic and ischemic injuries.

Aim To observe the improvement of visual-auditory cognitive functions in the human entering high altitude by taking in tea polyphenols.Methods Thirty eight males living at 3 700 m high altitudes for 90 days constantly were randomly divided into two groups: ①group Ⅰ(placebo,40 mg/day); ②group Ⅱ(TP,300 mg/day).Cognitive functions were measured by integrated visual and auditory continuous performance test and the difference between groups was evaluated by the comparisons of post-treatment to pre-treatment.Results Compared with pre-treatment,PruA was significantly higher after taking in TP(P

Proceeding from the requirements of teaching target for postgraduate students,the course of progress in pathophysiology was constructed and administrated.The course objective was defined which combined teaching knowledge with fostering students' ability together,especially the ability to think new ideas and to do scientific research.Aiming at this teaching target,the teaching contents which combined with the direction of scientific research of the department was growing together with scientific development,especially in new knowledge and new technique.Multiple teaching means and several mode of examine were adopted during the process of teaching practice.

OBJECTIVETo explore the effects of hypobaric hypoxia on the apoptosis of germ cells in male rats.

METHODSAdult male Wistar rats were randomly divided into four groups: a control group raised at sea level; a 5 d, a 15 d and a 30 d hypoxic group raised in a hypobaric chamber simulating 5000 m altitude for 5 days, 15 days and 30 days respectively. Flow cytometry and TUNEL were used to evaluate the apoptosis of germ cells in the testis. Bax and Bcl-2 in the testis were measured by Western blot.

RESULTSSeminiferous tubules with apoptotic germ cells were significantly more in the hypoxic groups than in the control (P < 0.01). Most apoptotic germ cells were spermatogonia and spermatocytes. Compared with the control group, apoptotic germ cells detected by PI flow cytometry were significantly increased in the hypoxic 15 d and 30 d groups (P < 0.05); Bax was significantly higher (P < 0.05), and so was the ratio of Bax to Bcl-2 in the hypoxic 30 d group (P < 0.01).

CONCLUSIONHypoxia promotes apoptosis of testicular germ cells in male rats. Chronic hypoxia increases Bax expression in the rat testis.

Animals ; Apoptosis ; Hypoxia ; metabolism ; pathology ; In Situ Nick-End Labeling ; Male ; Random Allocation ; Rats ; Rats, Wistar ; Spermatozoa ; cytology ; Testis ; metabolism ; pathology ; bcl-2-Associated X Protein ; biosynthesis