猫脑对乙酰唑胺和高碳酸血症的pH值反应。
Brain pH responses to acetazolamide and hypercapnia in cats.
作者信息
Kohshi K, Kinoshita Y, Fukata K
机构信息
Department of Neurosurgery, School of Medicine, University of Occupational and Environmental Health, Fukuoka.
出版信息
Neurol Med Chir (Tokyo). 1997 Apr;37(4):313-8; discussion 318-9. doi: 10.2176/nmc.37.313.
The involvement of increased brain tissue CO2 tension in acetazolamide-induced brain acidosis was investigated by comparing the brain pH response to acetazolamide with that to hypercapnia. CO2 and pH sensors were placed bilaterally into cerebral white matter to 15 mm depth in cats. Group 1 cats (n = 9) breathed spontaneously, and in situ brain tissue PCO2, and pH (PbCO2 and pHb) were measured after intravenous acetazolamide administration (20 mg/kg). Group 2 cats (n = 9) were paralyzed and ventilated mechanically, and the changes of pHb were investigated by adjusting the ventilation to maintain the same Pbco2 values as in the acetazolamide-treated group. PbCO2 changes were not significantly different between the two groups. However, pHb responses were quite different: the fall in pHb was progressive in Group 1 but transient in Group 2. Brain acidosis after acetazolamide administration is not due to the rise in brain tissue CO2 tension.
通过比较乙酰唑胺和高碳酸血症对脑pH的反应，研究了脑组织二氧化碳分压升高在乙酰唑胺诱导的脑酸中毒中的作用。将二氧化碳和pH传感器双侧置于猫脑白质中15毫米深处。第1组猫（n = 9）自主呼吸，静脉注射乙酰唑胺（20毫克/千克）后测量原位脑组织PCO2和pH（PbCO2和pHb）。第2组猫（n = 9）进行麻痹并机械通气，通过调整通气以维持与乙酰唑胺治疗组相同的Pbco2值来研究pHb的变化。两组之间PbCO2变化无显著差异。然而，pHb反应却大不相同：第1组中pHb的下降是渐进性的，而第2组中是短暂性的。乙酰唑胺给药后脑酸中毒并非由于脑组织二氧化碳分压升高所致。
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