首页> 美国卫生研究院文献>The Journal of Experimental Medicine >EXPERIMENTAL LOCAL BLADDER EDEMA CAUSING URINE REFLUX INTO URETER AND KIDNEY
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EXPERIMENTAL LOCAL BLADDER EDEMA CAUSING URINE REFLUX INTO URETER AND KIDNEY

机译:实验性局部膀胱水肿导致尿液回流进入输尿管和肾脏

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摘要

Experimental infiltration of the intravesical ureter of the normal bladder in the living, anesthetized animal with magnesium sulfate or physiological salt solution caused a reflux of urine into the ureter in 6 out of 18 guinea pigs (33 per cent); in 22 out of 27 rabbits (81 per cent), and in 14 out of 17 dogs (82 per cent). The vesical pressure necessary to produce this experimental reflux is low and ranges between 2 and 12 mm. of Hg; hydrostatic pressure of the bladder contents often sufficed to drive urine into the kidney pelvis. After an experimental reflux had occurred, increased vesical pressure often failed to raise the level of the regurgitant column in the ureters of rabbit and dog: these higher pressures had rendered an incompetent valve competent. Control pressures ranging between 8 and 40 mm. of Hg without a preceding infiltration, caused no reflux in the great majority of dogs. The amount of infiltrated fluid necessary to produce reflux varied from 0.2 cc. in the guinea pig to 0.5 to 2 cc. in dog. Spontaneous regurgitation, that is regurgitation without a preceding infiltration, was seen in 4 guinea pigs, 4 rabbits and 2 dogs. Antiperistalsis of the ureters, that is a wave of contraction passing from the bladder to the kidney, was never seen in our animals with experimental reflux. Biopsy of the bladder in rabbit and dog showed edema of the ureterovesical valves after infiltration in most of our animals. Hemorrhages into the submucosa in the neighborhood of the ureteral valves were observed in some. The bladders of 3 rabbits, exhibiting spontaneous reflux without infiltration showed pouting, edematous lips of the ureterovesical orifices. The cause of experimental regurgitation is a non-obstructive edema of the vesical valve; this edema renders the valve flap more rigid and therefore incompetent at relatively low intravesical pressures. Higher intravesical pressures may again render the incompetent valve competent. The experimental results are applied to the human subject because the urinary bladder of dog and of man are quite similar in structure and function. Reasons are presented suggesting that the described type of reflux may cause pyelitis and pyelonephritis.
机译:用硫酸镁或生理盐溶液对活体麻醉动物的正常膀胱的膀胱输尿管进行实验性浸润,导致18只豚鼠中的6只出现尿液回流至输尿管(33%); 27只兔子中有22只(81%),17只狗中有14只(82%)。产生该实验性回流所需的囊泡压力低,范围为2至12 mm。汞膀胱内容物的静水压力通常足以将尿液驱入肾盂。在发生实验性反流后,膀胱压力升高常常无法提高兔子和狗输尿管中反流柱的水平:这些较高的压力使瓣膜功能不佳。控制压力在8到40毫米之间。没有事先渗透的汞,在绝大多数狗中都没有引起反流。产生回流所需的渗透流体量为0.2 cc。在豚鼠中为0.5到2 cc。在狗里。在4只豚鼠,4只兔子和2只狗中发现了自发性反流,即没有事先浸润的反流。在我们的实验性反流动物中,从未见过输尿管的抗蠕动,即从膀胱到肾脏的收缩波。在我们的大多数动物中,对兔子和狗进行的膀胱活检表明输尿管后瓣膜水肿。在一些观察到输尿管瓣膜附近粘膜下层有出血。 3只兔的膀胱表现出自发性反流而无浸润,显示输尿管小孔口部呈水肿性水肿。实验性反流的原因是膀胱瓣无阻塞性水肿。这种水肿使瓣膜瓣变硬,因此在相对较低的膀胱内压力下不起作用。较高的膀胱内压力可能再次使功能不全的瓣膜发挥作用。由于狗和人的膀胱在结构和功能上都非常相似,因此该实验结果可用于人类受试者。提出的原因表明所描述的反流类型可能引起肾盂炎和肾盂肾炎。

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