| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Research Abstract |
We examined the patho-physiology of hypoxia in Wistar rats. After anesthetizing with pentobarbital (60 mg/kg), femoral arteries were cannulated for monitoring blood pressure, heart rates and drawing blood samples in a hypoxic state made by nitrogen, carbon dioxide, or helium gas. The time to the respiratory standstill (15.4±1.5 sec in N_2 and 19.3±1.8 sec in CO_2, 17.8±2.4 sec in He) was much shorter than those of the published experimental data of hypoxia using dogs and rabbits (41-120 sec). The average time to the cardiac standstill was 263±88 sec in 100% CO_2 and 246±30 sec in N_2, 263±88 sec in He gas. In N_2 or He induced hypoxic state, we did not recognize any irregular heartbeats until the respiratory standstill, and the blood pressure and the heart rates also remained stable. On the other hand, CO_2 induced hypoxic state caused irregular heartbeats at 5.3 sec on the average, and then the blood pressure decreased rapidly. The arterial blood gas data in a N_2 or He state showed a remarkable hypoxemia but no progress of acidosis and no hypercarbia at the respiratory standstill. In a CO_2 state drawing blood samples is hard because of rapidly falling blood pressure. Therefore, only a few data showed a remarkable hypercarbia and a fatal acidosis at the respiratory standstill. We esteemed that N_2 and He cause the respiratory standstill by a remarkable hypoxemia and CO_2 causes by remarkable acidosis that affects the circulatory kinetics in turn. Our data may explain the mechanism of a very sudden death of human being in an anoxic state.
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