Beal A M
School of Biological Science, University of New South Wales, Kensington, Australia.
J Comp Physiol B. 1991;161(6):611-9. doi: 10.1007/BF00260752.
The effects of carbonic anhydrase inhibitors on secretion by macropodine parotid and mandibular glands were investigated using anaesthetized red kangaroos. In the parotid gland, acetazolamide (500 mumol.l-1) reduced a stable acetylcholine-evoked, half-maximal flow rate of 2.02 +/- 0.034 to 0.27 +/- 0.023 ml.min-1 (87% reduction). Concurrently, salivary bicarbonate concentration and secretion fell (129.4 +/- 1.46 to 80.9 +/- 1.63 mmol.l-1 and 264.8 +/- 7.96 to 22.3 +/- 2.30 mumol.min-1, respectively), phosphate and chloride concentrations rose (14.0 +/- 0.79 to 27.6 +/- 0.85 mmol.l-1 and 5.6 +/- 0.25 to 27.5 +/- 1.32 mmol.l-1, respectively), sodium concentration and osmolality were unaltered, and potassium concentration fell (8.8 +/- 0.33 to 6.4 +/- 0.29 mmol.l-1). High-rate cholinergic stimulation during acetazolamide blockade was unable to increase salivary flow beyond 11 +/- 0.9% of that for equivalent unblocked control stimulation. However, superimposition of isoprenaline infusion on the acetylcholine stimulation caused a three-fold increase in the blocked flow rate. These treatments were accompanied by small increases in salivary phosphate and chloride concentrations but not bicarbonate concentration. Methazolamide infusion caused similar changes in parotid secretion. In the mandibular gland, acetazolamide infusion had no effect on salivary flow rate during either low- or high-level acetylcholine stimulation. Acetazolamide caused no alterations in salivary electrolyte secretion at low flow rates, but curtailed the rise in bicarbonate concentration associated with high-level acetylcholine stimulation. Acetazolamide administration did not affect the increase in salivary flow rate associated with isoprenaline infusion, but did block the concomitant increase in bicarbonate concentration and secretion substantially.(ABSTRACT TRUNCATED AT 250 WORDS)
使用麻醉的红袋鼠研究了碳酸酐酶抑制剂对大袋鼠腮腺和下颌下腺分泌的影响。在腮腺中，乙酰唑胺（500μmol·l-1）将稳定的乙酰胆碱诱发的半最大流速从2.02±0.034降低至0.27±0.023 ml·min-1（降低87%）。同时，唾液碳酸氢盐浓度和分泌量下降（分别从129.4±1.46降至80.9±1.63 mmol·l-1和从264.8±7.96降至22.3±2.30μmol·min-1），磷酸盐和氯化物浓度升高（分别从14.0±0.79升至27.6±0.85 mmol·l-1和从5.6±0.25升至27.5±1.32 mmol·l-1），钠浓度和渗透压未改变，钾浓度下降（从8.8±0.33降至6.4±0.29 mmol·l-1）。在乙酰唑胺阻断期间的高频率胆碱能刺激无法使唾液流速增加超过同等未阻断对照刺激的11±0.9%。然而，在乙酰胆碱刺激上叠加异丙肾上腺素输注导致阻断流速增加了三倍。这些处理伴随着唾液磷酸盐和氯化物浓度的小幅增加，但碳酸氢盐浓度未增加。甲醋唑胺输注导致腮腺分泌出现类似变化。在下颌下腺中，乙酰唑胺输注在低水平或高水平乙酰胆碱刺激期间对唾液流速均无影响。乙酰唑胺在低流速时对唾液电解质分泌无改变，但减少了与高水平乙酰胆碱刺激相关的碳酸氢盐浓度升高。给予乙酰唑胺不影响与异丙肾上腺素输注相关的唾液流速增加，但确实显著阻断了同时出现的碳酸氢盐浓度和分泌量增加。（摘要截短于250字）
