ABSTRACT
AIM: To study the changes in capillarity of skeletal muscle during acclimation to high altitude, and explore the effects of a certain extent physical activity under hypoxia on capillary formation and the role of vascular endothelial growth factor (VEGF) in this process. METHODS: 48 Wistar rats were divided into 3 groups: Ⅰ normoxic control; Ⅱ hypoxia and Ⅲ hypoxia+exercise. Rats of Ⅱ and Ⅲ groups were subjected to hypobaric hypoxia for 5 weeks (23 h/d). They were first brought to simulated 4 000 m altitude, where rats of the Ⅲgroup were forced to swim for 1 h/d (6 d/week). Then the animals were ascent to 5 000 m. Biomicrosphere method was used to determine blood flow of skeletal muscle. The mean fiber cross-sectional area (FCSA), capillary density (CD) and capillary/fiber ratio (C/F) of red portion of the lateral head of the gastrocneminus were assayed by myofibrillar ATPase histochemistry. VEGF and its receptor KDR were assayed with immunohistochemistry method.RESULTS: By comparison with the normoxic control, 5-week hypoxic exposure resulted in a decrease in cross-sectional area of skeletal muscle fiber and an increase in CD, but the C/F remained unchanged. The blood supply to the gastrocnemius was not changed. After 5-week-exercise at high altitude, the muscle fibers did not undergo atrophy. CD, C/F, and the blood flow at rest increased significantly. VEGF protein was found primarily in the matrix between muscle fibers; KDR were shown mainly in endothelial cells of capillary. VEGF was more strongly stained in the skeletal muscle of hypoxia-exercise rats.CONCLUSION: Hypoxia itself can not induce neovascularization. While exercise during hypoxic exposure can lead to capillary formation. VEGF and KDR may play roles in it. New capillary formation benefits the blood supply, oxygen delivery and working performance at high altitude.
ABSTRACT
AIM and METHODS: Total RNA was extracted from 6th rat subcultured pulmonary artery smooth muscle cells(PASMC) exposed to continual chronic hypoxia or normoxia and the effects of chronic hypoxia on the changes of Kv1.3,Kv2.1,Kv3.1 mRNA in cultured PASMC induced by acute hypoxia were studied by semiquantitative RT-PCR in vitro. RESULTS:①Kv1.3,Kv2.1,Kv3.1 genes were found to be expressed in PASMC of rats exposed either to hypoxia or normxia.②The expression of Kv2.1 and Kv3.1 in 6th subcultured of PASMC in normaxia group could be upregulated by exposure to acute hypoxia,the levels of Kv2.1 and Kv3.1 mRNA were significantly increased from 0.646?0.092, 0.782?0.104 to 1.059?0.134, 0.985?0.116,respectively (P
ABSTRACT
AIM: To compare the effects of hypoxia on expression of vascular endothelial growth factor (VEGF), iNOS and eNOS mRNA in cultured umbilical vein endothelial cells (UVECs) obtained from Tibetan and Han. METHODS: UVECs were obtained from native Tibetan and immigrant Han, respectively and cultured under hypoxia conditions (0.5% oxygen) for 2 h, 4 h, 12 h, and 24 h and normoxic conditions. VEGF, iNOS and eNOS mRNAs were detected with methods of RT-PCT. RESULTS: VEGF and iNOS mRNAs were up-regulated while eNOS mRNA depressed by hypoxia similarly in Tibetan and Han UVECs. CONCLUSION: Our results suggest that the changes of VEGF, iNOS and eNOS mRNA expression are common pathways in the mechanisms of hypoxic responses.
ABSTRACT
AIM: To investigate the possible role of prostaglandin, NO and potassium channel in the adaptive blunting of hypoxic pulmonary vasoconstriction (HPV) in the high altitude animal (pika). METHODS: The effect of L-NAME, indomethacin and 4-AP on the response of isolated lung strips of pika and Wistar rats instead of pulmonary artery to acute hypoxia were studied. RESULTS: (1) After inhibition of prostaglandins by indomethacin, the percentage increase in hypoxic constriction in lung tissue strip of pikas was greater than that in Wistar rats[(64.7?50.9)% vs (19.7?14.1)%], P
ABSTRACT
Dogs were bled and maintained at the mean arterial pressure(MAP)of 6.67 kPa(moderate shock)or of 5.33 kPa(severe shock)for 2 hours.Then the blood shed was transfused back to the animals and observation on the dogs was carried on for 2 more hours.26 mongrel dogs,weighing 10~16 kg,were randomized into Group I of normoxia and moderate shock(NMS,n=7),Group I of normoxia and severe shock(NSS,n=7).Group I of hypoxia at a simulated alti- tude of 4 000 m and moderate shock(HMS,n=6),and Group IV of hypoxia and severe shock(HSS,n=6).The changes of the cardiovascular function and the oxygen transport were observed in these animals after anesthetization.It was found that the cardiovascular function was similar in HMS and NMS groups.The decrease of VO2 of HMS animals was similar to that of NSS dogs.Decompensation occurred earlier in HSS animals and resulted in high mortality.
ABSTRACT
The effects of zymosan-activated plasma(ZAP) on the lipid peroxides(LPO) content, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) in lung lymph and their relationship to lung injury were studied in control (with normal leukocyte count) and leukopenic goats. In the control goats, after ZAP infusion, LPO production elevated, that was coincided with the increase of lung lymph flow (QL), and the clearence rate of lung lymph protein (LLPC). SOD activity was also elevated, but GSHpx activity was inhibited. In leukopenic goats, ZAP challenge caused an increase in LPO production, but its content was lower than that in control goats. No marked change was observed in QL and LLPC. The results suggest that: (1) Leukocytes and oxygen free radicals are involved in the pathogenesis of lung injury due to ZAP infusion; (2) Leukocytes play an important role in producing oxygen free radicals.
ABSTRACT
Hypoxic pulmonary pressor response (HPPR) was observed witb a preparation of perfused lungs in situ in rats, and the effects of deoxy-2-glucose (2DG), verapamil, and dipyridamole on HPPR were studied.During bypoxia (inhalation of 3% oxygen for 10 minutes) , there was a 50% increase on average in pulmonary arterial pressure in the perfused lungs in situ in rats. 2DG inhibited the first and second but enhanced the seventh and eighth HPPR. Both verapamil and dipyridamole depressed HPPR.On the basis of the results, the author suggests that the mechanism of HPPR might originate from the lungs themselves. There might be a close relation between the glucose-energy metabolism and the occurrence of HPPR, the trans-membranous influx of calcium might play a certain role in the development of HPPR, and adenosine would probably participate in the regulation of HPPR.
ABSTRACT
Eleven male rabbits were divided into 2 groups. Normal saline(NS) group consisted of 5 animals and was treated with 0.9% NaCl solution, and hyperosmotic saline (HS) group consisted of 6 rabbits and was treated with 7.5% NaCl. The animals were exposed to hypobaric hypoxia at a simulated altitude of 4000 m and hemorrhagic shock was inflicted to them through femoral artery bleeding. The mean arterial pressure (MAP) was brought to 6.0 kPa over 10 minutes and kept at that level for 70 minutes. A certain amount of 0.9% NaCl (300 mmol/L) or 7.5% NaCl (2400 mmol/L) was intravenously infused over a 10-minute interval. The volume infused was equivalent to 10% of the total blood shed. It was found that MAP, left ventricular systolic pressure, and LV dp/dt were significantly higher in HS group than in NS group (from 3rd to 20th minute after infusion). Sodium ion concentration was significantly higher in HS (145.8?3.16 mmol/L) than in NS (135.6?2.87 mmol/L) (P