Löfqvist J, Nilsson E
Acta Physiol Scand. 1981 Jan;111(1):59-68. doi: 10.1111/j.1748-1716.1981.tb06705.x.
The influence of acid-base changes (variations of extracellular pH within the range 6.2-8.2 and parallel changes in (HCO3-) and PCO2 at constant external pH) on contractions induced by carbachol and K+ was studied on preparations from taenia coli of the rabbit. Extracellular acidosis increased the concentration of carbachol necessary to evoke a given muscle tension and reduced the maximum response. During a carbachol-induced contraction acidosis reduced and alkalosis enhanced muscle tension. Changes in extracellular pH within the range 6.2-8.2 did not affect the initial, rapid phase of the contraction induced by 145 mmol/l of K+. However, with 40-80 mmol/l of K+ acidosis reduced the phasic response. The tonic contraction following the initial phasic response in 145 mmol/l K+ was enhanced by extracellular acidosis and decreased by alkalosis, whereas at a K+-concentration of 70 mmol/l the amplitude of the tonic contraction was greater at pH 7.4 than at pH 6.2. Propranolol 10(-6) mmol/l did not affect the influence of extracellular pH upon the K+-contracture. An increase of both PCO2 and (HCO-3) at constant extracellular pH did not alter the response of the muscle to carbachol. The tonic contraction during K+-stimulation was diminished by a parallel increase in PCO2 and (HCO-3) and at 47 mmol/l (HCO-3) it was almost abolished. A rise in PCO2 from 5 to 14 kPa without changes in (HCO-3), which caused extracellular pH to drop from 7.4 to 6.3, increased the tonic contraction in the same way as a fall in extracellular pH alone. These results seem to indicate that extracellular acidosis within the pathophysiological range (1) decreases the sensitivity of the polarized smooth muscle membrane to cholinergic stimulation, (2) reduces: the rate of release of stored Ca++, the transmembrane flow of Ca++ into the muscle cell, and the rate of Ca++ inactivation or extrusion during K+-contraction. The reduction of the tonic contracture with increasing PCO2 and (HCO-3) at constant extracellular pH is most likely attributable to the (HCO-3) ion.
在兔结肠带制备物上研究了酸碱变化（细胞外pH在6.2 - 8.2范围内变化以及在恒定外部pH下（HCO₃⁻）和PCO₂的平行变化）对卡巴胆碱和钾离子诱导的收缩的影响。细胞外酸中毒增加了引发给定肌肉张力所需的卡巴胆碱浓度，并降低了最大反应。在卡巴胆碱诱导的收缩过程中，酸中毒降低肌肉张力，碱中毒增强肌肉张力。在6.2 - 8.2范围内的细胞外pH变化不影响由145 mmol/L钾离子诱导的收缩的初始快速阶段。然而，对于40 - 80 mmol/L的钾离子，酸中毒会降低相性反应。在145 mmol/L钾离子作用下，初始相性反应后的紧张性收缩在细胞外酸中毒时增强，在碱中毒时减弱，而在钾离子浓度为70 mmol/L时，pH 7.4时紧张性收缩的幅度大于pH 6.2时。10⁻⁶ mmol/L的普萘洛尔不影响细胞外pH对钾离子挛缩的影响。在恒定细胞外pH下，PCO₂和（HCO₃⁻）两者增加均未改变肌肉对卡巴胆碱的反应。在钾离子刺激期间，紧张性收缩在PCO₂和（HCO₃⁻）平行增加时减弱，在（HCO₃⁻）为47 mmol/L时几乎完全消失。PCO₂从5 kPa升至14 kPa而（HCO₃⁻）无变化（这导致细胞外pH从7.4降至6.3），与单独细胞外pH下降一样增加紧张性收缩。这些结果似乎表明，病理生理范围内的细胞外酸中毒（1）降低极化平滑肌膜对胆碱能刺激的敏感性，（2）降低：储存的Ca²⁺的释放速率、Ca²⁺跨膜流入肌肉细胞的速率以及钾离子收缩期间Ca²⁺失活或外流的速率。在恒定细胞外pH下，随着PCO₂和（HCO₃⁻）增加紧张性挛缩的降低最可能归因于（HCO₃⁻）离子。
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