AIM: To investigate the role of K + channels in the decreased hypoxic pulmonary vasoconstriction(HPV) in chronic hypoxic rats. METHODS: Blockers of three kinds of K + channels, 4-AP(voltage dependent K + channel blocker), TEA(Ca 2+ activated K + channel blocker)\, GLIB(ATP sensitive K + channel blocker) were used in isolated perfused rat lungs to detect the role of K + channels in HPV. RESULTS: In normal rats, 4-AP and TEA, but not GLIB, both elicited a significant increase in pulmonary artery baseline pressure, and also potentiated the acute hypoxic pulmonary vasoconstriction. In chronic hypoxic rats, the HPV is significantly decreased, while 4-AP, TEA, GLIB all elicited a significant but smaller increase in pulmonary artery baseline pressure. Additionally, all these three blockers potentiated the HPV stronger in chronic hypoxic rats than in control rats. CONCLUSION: The opening of Kv, K Ca , K ATP might modulate the hypoxic pulmonary vasoconstriction in isolated rat lungs, and the increase in this modulation by potassium channel in chronic hypoxic rats might play a role in its decrease in HPV.

AIM and METHODS: To determine the role of different K +-channels in attenuation of vasoreactivity of intrapulminary artery rings induced by chronic hypoxia. RESULTS: ①Acute hypoxia-induced pulmonary vasoconstriction(HPV) could be significantly attenuated by chronic hypobaric hypoxia for 15 days and for 30 days. ②HPV could be significantly potentiated by ATP-sensitive K +-channel (K ATP ) blocker or Ca 2+ -activated K +-channel (K Ca )blocker, and the potentiated scope in chronic hypoxic group was much higher than that observed in control group. ③ Delayed rectifier K +-channel (K DR )blocker showed no effect on HPV in both control group and chronic hypoxic group.CONCLUSIONS: Both K ATP and K Ca play an important modulating role in HPV and it's potentiation may be a critical mechanism for the attenuated vasoreactivity to acute hypoxia; following chronic hypobaric hypoxia.

AIM: To investigate the effect of simulated high altitude hypoxia on rat brain mitochondrial translation activity. METHODS: Animals were continuously exposed to simulated 4 000 m high altitude in hypobaric chamber for three days and forty days. Mitochondria of rat brain were isolated by homogenizing brain tissue and following centrifuging program. Protein translation activity in isolated mitochondria in vitro was measured with -Lencine incorporation method. Products labeled with -methionine in isolated mitochondrial protein synthesis system in vitro were separated on SDS-PAGE and identified by autoradiography. RESULTS: Mitochondrial translation activity in vitro in acute hypoxia exposure were significantly lower than control( P

AIM: To detect the role of cyclic nucleotides in the alleviation of hypoxic pulmonary vasoconstriction (HPV) in chronic hypoxic animals. METHODS: The intracellular cAMP and cGMP of the cultured porcine pulmonary arterial smooth muscle cells (PASMC) and endothelial cells (PAEC) were assayed by RIA. The length of single PASMC during acute hypoxia was measured by imaging analysis system. RESULTS: The basal levels of cAMP and cGMP in PASMC and cGMP in PAEC of Chronic hypoxic groups decreased remarkably compared with normoxic groups ( P

AIM: To study the changes in myocardial blood flow (MBF), capillarization and cardiac function in the rat during acclimation to hypoxia. METHODS: Myocardial capillary density (CD) and capillary/myocyte ratio (C/M) was assayed by alkaline phosphatase histochemistry. Biomicrosphere method was used to determine MBF in the rat after 5, 15 or 30 days hypobaric hypoxic exposure (5 000 m). RESULTS: In the course of hypoxia, MBF and cardiac function increased in the right ventricle. However, in the left ventricle, acute hypoxia caused an increase in MBF and a decrease in cardiac function. Both returned to the control level on continued hypoxic exposure. Neovascularization occurred after 15 day or 30 day of hypoxic exposure in both ventricles, judged from the significant increment of C/M ratio albeit the CD remained unchanged in the right ventricle. CONCLUSION: Our findings indicate that adaptive changes in rat heart during acclimation to hypoxia include: ① persistent increase in MBF, hypertrophy associated with increase in capillarity and enhanced cardiac function of the right ventricle; ② increase in MBF and depression of cardiac function at first, then followed by recovery of MBF and increase in capillarity accompanied with recovery of left ventricular function.