DIRECT EVALUATION OF ACIDIFICATION BY RAT TESTIS AND EPIDIDYMIS - ROLE OF CARBONIC-ANHYDRASE

DIRECT EVALUATION OF ACIDIFICATION BY RAT TESTIS AND EPIDIDYMIS - ROLE OF CARBONIC-ANHYDRASE
复制标题

DOI:
10.1152/ajpendo.1990.258.1.e143
复制
发表时间:
1990-01-01
影响因子:
--
通讯作者:
DUBOSE, TD
DUBOSE, TD
中科院分区:
其他
文献类型:
--
作者:
CAFLISCH, CR;DUBOSE, TD

文献摘要

被引文献

相似文献

本实验采用微电极技术(pH和PCO_2)和微量热法(总CO_2浓度)来确定大鼠睾丸和附睾部特定结构在对照条件下和给予碳酸酐酶抑制剂乙酰唑胺(20或50 mg/kg)后的酸化参数。生精小管在控制条件下原位pH值(ST;6.96。+-。0.01),近端头(PCP;6.62+-.0.01),中头(MCP;6.59+-.0.01),中间语料库(MCR;7.10+-.0.02)和附睾尾近端(PCD;6.85+-)。0.01),显著高于睾丸动脉(TA;7.36.+-)。0.01)或全身动脉血(SAB;7.40.+-)。0.01),服用乙酰唑胺后无明显变化。TA(52.2.+-.)中原位二氧化碳分压(PCO2)0.6毫米汞柱)、ST(52.3±-.0.4 mm Hg)、PCP(52.9±-.0.4毫米汞柱)、MCP(53.0±-.0.7 mm Hg)、MCR(53.4±-.0.4毫米汞柱)和PCD(52.4±-.0.4毫米汞),但均显著高于SAB二氧化碳分压(39.2.±-)。0.5毫米汞柱)。乙酰唑胺使除MCR外的所有结构的原位二氧化碳分压均显著增加。正常ST液中的总二氧化碳浓度(10.7±-.0.5 mm)显著高于“原发”液体(6.9±-)。0.3 mm),这两个值都远低于TA(26.9±-)。1.3 mm)或SAB(24.6.+-.0.4 mm)总二氧化碳浓度。附睾部的总二氧化碳浓度与原始液中的值无明显差别。总而言之,乙酰唑胺对管腔酸化的明显缺乏与支持细胞中缺乏这种酶是一致的,并表明与以前的研究相反,附睾酸化不依赖碳酸酐酶。
The present experiments have employed microelectrode techniques (pH and PCO2) and microcalorimetry (total CO2 concentration) to define parameters of acidification in specific structures of the rat testis and epididymis during control conditions and after administration of the carbonic anhydrase inhibitor acetazolamide (20 or 50 mg/kg). Values for in situ pH during control conditions in seminiferous tubules (ST; 6.96 .+-. 0.01), proximal caput (PCP; 6.62 .+-. 0.01), middle caput (MCP; 6.59 .+-. 0.01), middle corpus (MCR; 7.10 .+-. 0.02), and proximal cauda epididymidis (PCD; 6.85 .+-. 0.01) were significantly more acidic than in testicular artery (TA; 7.36 .+-. 0.01) or systemic arterial blood (SAB; 7.40 .+-. 0.01) and did not change significantly after acetazolamide. In situ partial pressure of CO2 (PCO2) in TA (52.2 .+-. 0.6 mmHg), ST (52.3 .+-. 0.4 mm Hg), PCP (52.9 .+-. 0.4 mmHg), MCP (53.0 .+-. 0.7 mmHg), MCR (53.4 .+-. 0.4 mmHg), and PCD (52.4 .+-. 0.4 mmHg), were indistinguishable from each other, but all values were significantly higher than SAB PCO2 (39.2 .+-. 0.5 mmHg). Acetazolamide increased in situ PCO2 significantly in all structures except the MCR. The total CO2 concentration in normal ST fluid (10.7 .+-. 0.5 mM) was significantly higher than in "primary" fluid (6.9 .+-. 0.3 mM), and both values were well below TA (26.9 .+-. 1.3 mM) or SAB (24.6 .+-. 0.4 mM) total CO2 concentrations. In the epididymis, total CO2 concentrations were indistinguishable and not different from the value in primary fluid. In conclusion, the apparent lack of effect of acetazolamide on luminal acidification is compatible with the absence of the enzyme in Sertoli cells and suggests, in contrast to previous studies, that acidification in the epididymis is not dependent on carbonic anhydrase.