The toxic effects of carbon dioxide and acetazolamide in hepatic encephalopathy.
The toxic effects of carbon dioxide and acetazolamide in hepatic encephalopathy.
复制标题
二氧化碳和乙酰唑胺在肝性脑病中的毒性作用。
DOI：
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发表时间：
1960
影响因子：
15.9
通讯作者：
F. Plum
中科院分区：
文献类型：
--
作者：
J. Posner;F. Plum
肝昏迷通常伴随着呼吸气体和血氨水平的显着变化。动脉 pH 值升高，二氧化碳张力降低 (1)。在许多情况下，血氨水平 (2-4) 会升高，并且脑动静脉氨差异较高 (5, 6)。大脑摄氧量降低 (7, 8)。许多肝病伴随的明显碱中毒是否导致脑病尚不清楚。严重的血液碱中毒会损害氧合血红蛋白解离 (9)、降低动脉氧分压并干扰正常受试者的脑功能 (10)。据报道，碱中毒会增强氨毒性 (11-13)。这些影响导致 Roberts 及其同事 (14) 以及其他人 (13) 建议使用二氧化碳吸入来治疗肝昏迷。对我们自己的服务的初步临床观察表明，吸入二氧化碳会使肝病脑病患者病情恶化而不是改善。因此，进行了详细的临床和脑代谢研究，以量化血液和组织二氧化碳张力升高对脑功能的影响。研究结果报告如下。测量对照组和肝硬化患者静息时的脑血流量和脑摄氧量，结果与患者的精神和躯体神经功能相关。基线研究后，选定的患者吸入二氧化碳并重复临床脑代谢观察。随后，为了消除导致观察到的变化的呼吸过度和呼吸困难的不良副作用，在通过快速输注乙酰唑胺（Diamox）提高组织二氧化碳张力之前和之后进行了类似的观察。
Striking alterations in respiratory gas and blood ammonia levels usually accompany hepatic coma. The arterial pH is elevated and the carbon dioxide tension reduced (1). The blood ammonia level (2-4) is increased in many instances and the brain arteriovenous ammonia difference is high (5, 6). The cerebral oxygen uptake is depressed (7, 8). Whether the pronounced alkalosis which accompanies many instances of hepatic comiia contributes to the encephalopathy is unknown. Severe blood alkalosis impairs oxyhemoglobin dissociation (9), lowers the arterial oxygen partial pressure and interferes with cerebral function in normal subjects (10). Alkalosis is reported to enhance ammonia toxicity (11-13). These effects led Roberts and associates (14) as well as others (13) to suggest using carbon dioxide inhalation to treat hepatic coma. Prelimiiinary clinical observations on our own services suggested that inhaled CO2 worsened rather than improved patients with the encephalopathy of liver disease. Accordingly, detailed clinical and cerebral metabolic studies were carried out to quantitate the effects on brain function of raising blood and tissue CO2 tensions. The results of the study are reported here. Cerebral blood flow and cerebral oxygen uptake were measured at rest in control and cirrhotic patients and the results were correlated with the patients' mental and somatic neurological function. Following the baseline study, selected patients inhaled carbon dioxide and the clinical cerebral metabolic observations were repeated. Subsequently, to eliminate the undesirable side effects of hyperpnea and dyspnea as contributing to the observed changes, similar observations were made before and after raising tissue CO2 tensions by rapidly infusing acetazolamide (Diamox).