Caflisch C R, DuBose T D
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77550.
Am J Physiol. 1990 Jan;258(1 Pt 1):E143-50. doi: 10.1152/ajpendo.1990.258.1.E143.
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 mmHg), 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.(ABSTRACT TRUNCATED AT 250 WORDS)
