Since August 1965, 166 hemodialyses have been performed on 36 patients with renal failure at the Department of Urology, Osaka University Hospital.
Dialyser is Kolff-Twin-Coil type (Junken) and dialysate constituents are as follows: Na 126mEq/L, K 2.6mEq/L, Ca 3.6mEq/L, HCO₃ 24mEq/L, Glucose 2g/dl.
BUN, creatinine, potassium and inorganic phosphate decreased effectively after 6-hour-dialysis.
In 91-hemodialysis-series performed on 9 patients treated over 1 month duration, nausea, vomiting and general fatigue occurred in high incidence and convulsion and coma were also met in some cases.
To study the biochemical changes of body fluids caused by hemodialysis, thoracic duct drainage and hemodialysis were performed on the dogs, which were nephrectomised bilaterally 48 hrs. prior to the procedure.
Serum and lymph were collected serially during 3-hour-dialysis and cerebrospinal fluid was obtained by the suboccipital puncture at the end of dialysis.
On these samples, urea-nitrogen, creatinine, sodium, potassium, chloride and osmolarity were studied.
Biochemical changes of thoracic duct lymph during hemodialysis were very similar to those of serum.
Concentration of urea-nitrogen in cerebrospinal fluid was lower than that of serum before hemodialysis, but was higher at the end of dialysis.
However, osmotic gradient was not found between serum and cerebrospinal fluid.
Following clinical study on the changes of blood glucose level and serum osmolarity, induced transient hyperglycemia during hemodialysis might compensate the osmotic gradient between serum and cerebrospinal fluid.
Considering the relatively higher incidence of dialysis-related neurological symptoms, hyperosmolarity caused by the hyperglycemia must play an important role of the origin for so-called “disequilibrium syndrome”, when high-glucose concentration is applied in the rinsing fluid.

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Fibrinolytic enzyme system in fresh urine and acid treated urine was examined on fibrin plates, where various kinds of solvents of fibrinogen and thrombin was used.
Acid treated urine was made as follows, the pH of fresh urine was adjusted to 2 with 1N HCl, and neutralized with 1N NaOH, after standing for 30 minutes.
1) As the solvent of fibrinogen-and thrombin-solution, borate saline buffer was most suitable for making fibrin plates to estimate fibrinolytic activity of urine, and veronal buffer was available when the activity of urine sample was weak. Physiologic saline was in use, when the activity was estimated within 18 hours.
2) It is known that there are urokinase, uropepsin, trypsin inhibitor and thromboplastin-like substances, as substances related with fibrinolysin in urine.
Nevertheless, fresh urine (non treated urine) was available in the examination of fibrinolytic activity in urine clinically.
3) As the control enzyme, 10u/ml of UK was available in order to determine the fibrinolytic activity in urine on fibrin plates. The activity of UK did not decrease after keeping for 21 days in 20°C.
When the lysed area was determined after incubation for 18 hours, 100u/ml trypsin, a rather stable enzyme, was available for the purpose.
4) By the acidification of urine, even after neutralization, the fibrinolytic activity of urine was extremely decreased. In the process of acid treatment, pepsinogen in urine might be converted to pepsin and then the enzyme might destroy UK. Despite of the destruction of UK, the lysed area produced by acid treated urine plus UK or acid treated urine plus trypsin was always larger than that produced by the same units of UK or trypsir separately.
This result suggests that there exists a pre-enzyme which is stable by acidification.
5) The lysed area produced by fresh urine plus trypsin was smaller than that produced by only fresh urine. This implies that there exists the inhibitor of fibrinolysi in urine.
But on the contrary, acid treated urine plus trypsin showed stronger fibrinolytic activity than that of only trypsin or acid treated urine.
This suggests the possibility that there is a pre-enzyme which will be activated by trypsin in urine.

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Experimental observations.
Adult dogs, anesthetized with sodium isomital, were used in all experiments.
Experiment I.
The partial resection of ureteral orifice was performed and immediately the cystogram were obtained at several pressure levels. Only one cystogram revealed a vesicoureteral reflux. (V. U. R.)
Experiment II.
Nylon ureteral catheter of about 1.5cm lengths was inserted into the intravesical ureter to break down the physiological function of the ureterovesical junction. (U. V. J.) Then immediatly a cystogram was obtained. No reflux was demonstrated.
Experiment III.
A Nylon ureteral catheter was inserted into the lower ureter. The contrast agent was gradually poured into the ureter through the catheter elevating slowly the other tip of the catheter connected with the small bottle containing the contrast agent. Then cystograms were obtained, and ureteral pressure (resistance against the reflux) was observed.
Experiment IV.
As Experiment III, the ureter was incised 5cm above the tip of the inserted catheter. For the purpose of interrupting the urinary flows, the upper part of the ureter was ligated. Intraureteral pressure never showed the zero point.
Experiment V.
The partial cystectomies were performed as nearly as possible at the right ureteral orifices. In dogs that V. U. R. were demonstrated to be in good health 2, 3 and 6 months after operation, specimens of ureterovesical junction and bladder wall were removed and histologically studied. V. U. R. was seen at the ureter near the resected bladder wall without remerkable changes at V. U. J..
Experiment VI.
The partial resection of ureteral orifice was performed and the ureter was incised 5 cm from ureteral orifice. The upper part of the ureter was ligated, then the bladder was closed and indigocarmine solution was poured into the bladder through an urethral catheter. The efflux of liquid (indigocarmine solution) from the incised orifice of the ureter was observed only after the death of the animal.
Clinical observations
V. U. R. after partial cystectomy was frequently observed without remerkable changes at U. V. J. and at the upper urinary tract. V. U. R. after ureterocystoneostomy was not observed in spite of the remarkable anatomical changes of the upper urinary tract having a low intraureteral pressure.
V. U. R. following contracted bladder, neurogenic bladder, diverticulum of bladder, complete duplication of ureters, megacystis syndrom, cystitis and radiation therapy was discussed.
V. U. R. after transurethral ureteral meatotomy or transvesical resection of the submucosal ureteral wall and V. U. R. of residualureter after nephrectomy and other operations were observed in a few cases having some special changes.
From the results of the recordings of the intraureteral pressure by means of a strain gauge in 2 channels, it has been observed that the intraureteral pressure of the ureter showing a reflux is usually low.
Based on these findings, the following conclusions were drawn: It is believed that, the action of the bladder wall has been observed to play an important role in the mechanism of preventing the reflux, in addition to the action of U. V. J., the pressure of the intraureteral urinary flow and the action of the ureteral wall.

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“Neurogenic Bladder” includes all dysfunctions and diseases of the urinary bladder due to organic disorders arising in the central, peripheral or intrinsic nervous system of the bladder.
Up to the present, the cystometrogram was thought to reveal directly such causal nervous disorders of this disease as well as the activity of the residual innervation. However, recent studies in our department offered a new concept for the clinical evaluation of the cystometrogram as it represent the physiological and histological properties of the vesical wall itself involving the activity of the intramural ganglions. Therefore, the author had tried to examine the physiological nature of the normal dog bladder as well as that of the experimental neurogenic bladder with the observation on “Basal Rhythm” (B. R.), in order to clarify the difference between these two conditions.
B. R. is a small but rather regular contraction of the vesical wall which is found during isometric cystometryo The standard dimensions of it in a normal dog are as follows: amplitude: 0.5-6.0cmH₂O, duration: 10-20sec., frequency: 1 time/5-6min. to continuous. It becomes gradually prominent as the bladder is filling, and at last it is fused to produce micturition contraction.
While, the mode of B. R. is altered showing a regular pattern after the systematic section of the nerve innervating the urinary bladder, as follows:
(1) Brain: resection of the frontal cerebral cortex, disappeared; total resection of the cerebrum, reappeared; rostal supracollicular decerebration, activated; caudal infracollicular decerebration, disappeared.
(2) The spinal cord: section of the 7th cervical and/or the 4th thoracic cord, almost no effect; section of the 6th lumbar cord, slightly reduced.
(3) Sacral nerve: section of the ventral root, reduced; section of the dorsal root, reduced; section of the ventral-and-dorsal root, reduced; resection of the spinal ganglion, activated
(4) Peripheral nerve: section of the hypogastric nerve, markedly activated; section of the pelvic nerve, activated; section of the pudendal nerve, no effect.
(5) Miscellaneous: extirpated bladder, activated and regular; ice-cooled bladder (4 hours and 24 hours), disappeared; pharmacological stimulation of the bladder, specific responses corresponding to the kind of the drug.
Next, B. R. of the experimental neurogenic bladder in the dog was examined one month after selective sections of the ventral, the dorsal, the ventral-and-dorsal root of the sacral nerve, resection of the spinal ganglion of the same nerve, and section of the hypogastric or the pelvic nerve, respectively. Neither characteristic difference of the mode of B. R. between these neurogenic bladders nor that in the normal bladder could be found. However, it was clearly found that there were characteristic differences between the alteration pattern of the mode of B. R. after systematic section of the residual innervation between normal and these abnormal bladders.
The marked findings in this differing from that of normals were as follows:
(1) Section of the 7th cervical cord: reduced or disappeared in all cases except the ventral rootresected bladder.
(2) Section of the 6th lumbar cord: specific reactions corresponding to the kind of prior nerve section.
(3) Section of the hypogastric nerve: reduced or disappeared in all cases except the spinal ganglionresected bladder. This was the most significant result of the neurogenic bladders compared to that of the normals.
(4) Section of the pelvic nerve: no effect in ventral root-resected or dorsal root-resected bladders; reduced in the spinal ganglion-resected bladder.
With the results obtained above, it was clarified that:
(1) The mode of B. R. in the normal bladder was affected by the amount of intravesical content as well as the activity of the nervous innervation from the central to the peripheral.
(2) The mode of B. R. in the

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It was possible to record the renal impedance plethysmogram (RIP) by our method using needle electrodes inserted into the kidney. Many variable factors influenced upon the pattern and the amplitude of the RIP and it was often difficult to obtain the same recording even in the same kidney under similar condition. Therefore the quantitative evaluation was questionable.
However, relatively stable recording could be obtained for 5-10 minutes, and in this stable period it was possible to observe the change of RIP induced by various loads which affected the intrarenal hemodynamics.
1) Following the intravenous (i. v.) administration of adrenaline the amplitude of RIP begun to decrease in 10 to 15 seconds and became almost zero 2 minutes after, but returned to the previous amplitude several minutes after.
2) Following the i. v. administration of papaverin, the amplitude of RIP begun to increase in 10 to 15 seconds, and reached its maximum several minutes after, and returned to the previous amplitude about 10 minutes after.
3) Gradual decrease of the RIP amplitude was induced by the progressive compression of the renal artery, and it decreased remarkably when the blood flow reached to the level less than 50% of the original value measured by electromagnetic flowmeter. When the renal blood flow decreased to the level less than 20%, the RIP faded away. When the compression was released, RIP returned to almost the previous state.
4) By the uniform compression of the renal vein the RIP amplitude changed indefinitly increased, remained unchanged, or decreased; that is, definite reaction pattern could not be observed.
5) By acute elevation of intrapelvic pressure of the autotransplanted kidney to femoral site the amplitude of RIP decreased and returned to previous level after lowering the intrapelvic pressure.
6) Diminished amplitude of RIP produced by the elevated intrapelvic pressure was increased by the i. v. administration of papaverin.

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1) In 22 adult dogs with a normal urinary bladder or inflammatory one, we performed a series of rexperiments for the purpose of discovering whether Sulfamethizole solution would pass into the urinary bladder wall. Results showed that in 4 out of 12 dogs with the normal bladder the drug passed into the bladder wall and that in all of the 10 dogs with inflammatory bladder the drug passed into the wall and the concentration of the drug in the bladder tissue was predominantly high.
2) It has been demonstrated that the therapeutic drug excreted in the urine was reabsorbed from the urinary bladder wall and this fact may accelerate the antibacterial effect on the chemotherapy of the cystitis.

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