Effect Of Endogenous NO On Blood Pressure, Heart Rate And Breathing Rate In Rats Exposing To Acute Hypoxia

Objective : Our study monitored the hemodynamic changes continuously and instantaneously in conscious and anesthetic rats exposing to hypoxia and we investigated the related underlying mechanism. In addition, we observed changes of blood pressure in conscious rats suffering hypoxia and discussed the mechanism by treated the selective inducible nitric oxide synthase(iNOS) inhibitors. Hopefully, our research would be available and valuable for the prevention and treatment of the altitude reaction and acute high-altitude diseases.Methods:Rats were treated with aminoguanidine(AG) as an inhibitor in endogenous NO production from iNOS. 48 Sprague–Dawley rats were randomly divided into A-2260-Blank(A-2260-B) group, A-5000-Blank(A-5000-B) group, C-2260-Blank(C-2260-B) group, C-5000-Blank(C-2260-B) group, C-2260-Control(C-2260-C) group, C-2260-AG group, C-5000-Control(C-5000-C) group and C-5000-AG group. The number of rats in each group was 6. Rats were anesthetized with pentobarbital sodium(50 mg/kg, i.p) and two polyethylene catheters were inserted into the left common carotid artery and the right external jugular vein respectively. After the surgical operation mentioned above, rats were taken into a hypobaric chamber in which the simulated high altitude was 2260 m or 5000 m. The system arterial pressure(Psa), central venous pressure(CVP), heart rate(HR) and breathing rate(BR) were directly and continuously displayed and digitally recorded by a High-performance data acquisition(Power Lab 16/35, AD Instruments) at 200 Hz for 30 minutes. Rats in conscious group, the catheters were filled with heparin saline and rats were given penicillin sodium to prevent infection after the same surgical operation in anesthetic condition. Rats in this group were taken into the hypobaric chamber for experiment with the same method after 48 h for recovery. Results:At 2260 m, the MAP, HR and BR were obviously different between conscious and anesthetic rats; in anesthetic rats, the MAP in A-5000-Blank group was significant lower than that in A-2260-Blank group, and there were no evidently difference in HR and BR; in conscious rats, the MAP, CVP and HR in C-5000-Blank group were significant lower than that in C-2260-Blank group. We obtained that MAP showed a significant rise after injection of aminoguanidine(AG) in both C-2260-AG group and C-5000-AG group but the net increase of MAP(△MAP) in C-5000-AG group was significantly greater. Additionally, HR in C-5000-Control and C-5000-AG group were obviously lower than that in C-2260-Control group. Conclusions:The MAP in anesthetic and conscious rats would decrease caused by acute hypoxia. Acute hypoxia would also cause an obvious decrease in HR while there is no significant difference in BR. Compared to anesthetic subjects, the conscious subjects may be able to convey the real effects of acute hypoxia on hemodynamics. Furthermore, the AG, a selective iNOS inhibitor could weaken the lower blood pressure caused by acute hypoxia.