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Research on condition of oxygen deficiency in rats

大鼠缺氧状况的研究

基本信息

批准号：
10670389
负责人：
HISANAGA Kuroki
金额：
$ 1.6万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10670389/
关键词：
Deficiency of Oxygen Rats Carbon Dioxide Sudden Death Nitrogen Helium Gas Physiology Arterial Blood Gas 二酸化炭素

项目摘要

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.

我们研究了Wistar大鼠缺氧的病理生理学。用戊巴比妥（60 mg/kg）麻醉后，对股动脉进行插管，以监测血压、心率并在氮气、二氧化碳或氦气造成的缺氧状态下抽取血液样本。呼吸停止时间（N_2为15.4±1.5秒，CO_2为19.3±1.8秒，He为17.8±2.4秒）比已发表的狗和兔缺氧实验数据（41-120秒）短得多。100%CO_2气体中心脏停搏时间为263±88秒，N_2气体中为246±30秒，He气体中为263±88秒。在N_2或He诱导的低氧状态下，直到呼吸停止时才出现不规则心跳，血压和心率也保持稳定。CO_2诱导的低氧状态引起心率不齐，平均为5.3秒，随后血压迅速下降。在N_2或He状态下的动脉血气数据显示明显的低氧血症，但在呼吸停止时没有酸中毒和高碳酸血症的进展。在CO_2状态下，由于血压迅速下降，很难抽取血样。因此，只有少数数据显示呼吸停止时出现显著的高碳酸血症和致命性酸中毒。我们认为N_2和He是通过显著的低氧血症引起呼吸暂停，CO_2是通过显著的酸中毒引起呼吸暂停，进而影响循环动力学。我们的数据可能解释了人类在缺氧状态下突然死亡的机制。