Mustafa S M, Thulesius O
Department of Pharmacology and Toxicology, Faculty of Medicine, Kuwait University, Safat.
Urology. 1999 Mar;53(3):653-7. doi: 10.1016/s0090-4295(98)00568-8.
Detrusor muscle contraction and uninhibited micturition after intravesical instillation of ice water is interpreted as a sign of upper motor neuron lesions. The basic mechanism of cooling-induced contraction (CIC) at the level of smooth muscle, however, has not been satisfactorily explained. We therefore designed model experiments with cooling of rat detrusor muscle.
We recorded isometric tension from strips of rat urinary detrusor muscle in organ baths during stepwise cooling. CIC was tested before and after addition of various standard agents interfering with known neurogenic (autonomic blockers, tetrodotoxin, capsaicin) and myogenic mechanisms of contraction (calcium channel blockers).
Stepwise cooling (37 degrees to 5 degrees C) of detrusor muscle induced reproducible graded contractions, inversely proportional to temperature. CIC was not dependent on a neural mechanism (not blocked by tetrodotoxin or capsaicin) or the release of neurotransmitters but was linked to translocation of calcium. It was reduced by calcium channel blockers and Ca(2+)-free solution. Blockage of the Ca(2+)-adenosine triphosphatase pump, which inhibits the extrusion of calcium, also plays a significant role in the process and enhances CIC.
Cooling of detrusor muscle preparations induces a graded myogenic contraction inversely proportional to the temperature. The mechanism is not dependent on local nervous control but is related to calcium translocation.
膀胱内灌注冰水后逼尿肌收缩和无抑制性排尿被解释为上运动神经元损伤的迹象。然而，平滑肌水平上冷却诱导收缩（CIC）的基本机制尚未得到令人满意的解释。因此，我们设计了大鼠逼尿肌冷却的模型实验。
在逐步冷却过程中，我们记录了器官浴中大鼠膀胱逼尿肌条带的等长张力。在添加各种干扰已知神经源性（自主阻滞剂、河豚毒素、辣椒素）和肌源性收缩机制（钙通道阻滞剂）的标准试剂之前和之后测试CIC。
逼尿肌的逐步冷却（37摄氏度至5摄氏度）诱导了可重复的分级收缩，与温度成反比。CIC不依赖于神经机制（不受河豚毒素或辣椒素阻断）或神经递质的释放，而是与钙的转运有关。它被钙通道阻滞剂和无钙溶液降低。抑制钙外排的钙-三磷酸腺苷酶泵的阻断在该过程中也起重要作用并增强CIC。
逼尿肌制剂的冷却诱导与温度成反比的分级肌源性收缩。其机制不依赖于局部神经控制，而是与钙转运有关。
