Thomas P J, Fry C H
Institute of Urology and Nephrology, University College London, United Kingdom.
J Urol. 1996 Feb;155(2):726-31.
The effect of cellular hypoxia on the phasic isometric contraction of isolated preparations of human detrusor muscle was measured and the influence of the accumulation of extracellular H+ and K+ on the inotropic effects ascertained.
Strips of human detrusor smooth muscle were field stimulated and superfused with an HCO3-/CO2 medium. Cellular hypoxia was generated by superfusion with 1) a low PO2 (approximately 5 kPa) solution; 2) 5 mM. Na azide; or 3) 10 mM. 2-deoxyglucose and omission of glucose and Na pyruvate. Extracellular pH or [K+] was simultaneously measured with ion-selective microelectrodes placed in the muscle strip.
Interventions produced a reversible contractile decay in the steady state, but the decay was preceded by a transient increase of force in most preparations. A small rise of the extracellular [K+] was also measured, but the effect was significantly smaller with 2-deoxyglucose. Extracellular acidosis was recorded with low PO2 and Na azide, but was absent with 2-deoxyglucose. The extracellular acidosis was usually preceded by a transient extracellular alkalosis.
Part of the contractile changes under these conditions could result from an extracellular acidosis generated via glycolysis; the accumulation of extracellular K+ was insufficient to exert inotropic effects.
测定细胞缺氧对人逼尿肌离体标本等长收缩相的影响,并确定细胞外H⁺和K⁺的蓄积对变力作用的影响。
用人逼尿肌平滑肌条进行场刺激,并用HCO₃⁻/CO₂培养基进行灌流。通过以下方法造成细胞缺氧:1)用低PO₂(约5 kPa)溶液灌流;2)5 mM叠氮化钠;或3)10 mM 2-脱氧葡萄糖并去除葡萄糖和丙酮酸钠。用置于肌条中的离子选择性微电极同时测量细胞外pH或[K⁺]。
干预措施在稳态下导致可逆的收缩性衰减,但在大多数标本中,衰减之前力会短暂增加。还测量到细胞外[K⁺]略有升高,但2-脱氧葡萄糖的这种作用明显较小。低PO₂和叠氮化钠导致细胞外酸中毒,但2-脱氧葡萄糖则不会。细胞外酸中毒通常之前会出现短暂的细胞外碱中毒。
这些条件下部分收缩变化可能是由糖酵解产生的细胞外酸中毒引起的;细胞外K⁺的蓄积不足以发挥变力作用。