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虹鳟动脉血中的酸碱失衡

Acid-base disequilibrium in the arterial blood of rainbow trout.

作者信息

Gilmour K M, Randall D J, Perry S F

机构信息

Department of Biology, University of Ottawa, Ontario, Canada.

出版信息

Respir Physiol. 1994 May;96(2-3):259-72. doi: 10.1016/0034-5687(94)90131-7.

DOI:10.1016/0034-5687(94)90131-7
PMID:8059088
Abstract

An extracorporeal blood circulation and a stopflow technique were used to examine the acid-base status of arterial blood in the rainbow trout, Oncorhynchus mykiss. Arterial blood was routed from the coeliac artery through an external circuit in which pH (pHa), partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were monitored continuously. The stopflow condition was imposed by turning off the pump which drove the external loop. A radioisotopic CO2 excretion assay was performed on blood samples collected periodically to evaluate plasma carbonic anhydrase (CA) activity and hence red blood cell (rbc) lysis. An acid-base disequilibrium was found in the post-branchial blood; pHa increased by 0.04-0.06 units, and PaCO2 by 0.03-0.10 Torr, during the stopflow period. The disequilibrium appeared to arise primarily from the slow (uncatalyzed) rate of plasma H2CO3 dehydration. This was confirmed by the intra-arterial injection of bovine CA (22 mg kg-1) prior to the stopflow; the disequilibrium was abolished. When the CA inhibitor acetazolamide (30 mg kg-1) was injected, a negative pH disequilibrium of 0.04 units, accompanied by a rise in PaCO2 of 0.57 Torr, was observed during the stopflow. These results can be explained by the acetazolamide-induced inhibition of rbc CA, which leads to continuing rbc CO2 "excretion" in the post-branchial blood.

摘要

采用体外血液循环和停流技术研究虹鳟(Oncorhynchus mykiss)动脉血的酸碱状态。动脉血从腹腔动脉引出,通过一个外部回路,在该回路中可连续监测pH值(pHa)、氧分压(PaO2)和二氧化碳分压(PaCO2)。通过关闭驱动外部回路的泵来施加停流状态。对定期采集的血样进行放射性同位素二氧化碳排泄测定,以评估血浆碳酸酐酶(CA)活性,进而评估红细胞(rbc)裂解情况。在鳃后血液中发现酸碱失衡;在停流期间,pHa升高0.04 - 0.06个单位,PaCO2升高0.03 - 0.10托。这种失衡似乎主要源于血浆H2CO3脱水的缓慢(无催化)速率。在停流前动脉内注射牛CA(22 mg kg-1)证实了这一点;失衡现象消失。当注射CA抑制剂乙酰唑胺(30 mg kg-1)时,在停流期间观察到负向pH失衡0.04个单位,同时PaCO2升高0.57托。这些结果可以通过乙酰唑胺诱导的红细胞CA抑制来解释,这导致鳃后血液中红细胞持续“排泄”二氧化碳。

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