An Appliance to Direct Urine Flow following Penile Amputation

1991 ◽  
Vol 68 (3) ◽  
pp. 328-329 ◽  
Author(s):  
C. L. GARBUTT ◽  
A.-M. GARDNER ◽  
N. E. DUDLEY
Keyword(s):  
1959 ◽  
Vol XXXII (I) ◽  
pp. 134-141 ◽  
Author(s):  
Niels A. Thorn

ABSTRACT Arginine-, lysine- and leucine-vasopressin, injected i. v. into hydrated rats or dogs caused different patterns of response in that urine osmolality fell much more slowly after the maximum increase following arginine-vasopressin, than after the other two preparations. Using 3 different parameters for antidiuretic response, arginine-vasopressin was somewhat more potent than leucine-vasopressin in both rats and dogs, considerably more potent than lysine-vasopressin in rats, and much more so in dogs.


Author(s):  
Jaimin R. Patel

Bladder outlet obstruction (BOO) produces compression or resistance upon the bladder outflow channel at any location from the bladder neck to urethral meatus. It may be induced by specific functional and anatomic causes. Functional obstruction may be caused by detrusor-sphincter dyssynergia (DSD) and anatomic obstruction most commonly from benign prostatic enlargement (BPH) or urethral stricture. Obstructive symptoms include hesitancy, sensation of incomplete bladder emptying, diminished urinary stream. The combination of PVR, urinary flow measures, and symptom appraisal has been generally accepted as the initial screening and evaluation paradigm for BOO. In, Ayurveda, BOO is similar to Mutraghata means obstruction in the urine flow. Uttarbasti is the prime treatment of Mutraghata. Present case is diagnosed as a functional bladder outlet obstruction (BOO) on the basis of symptoms, normal reports of USG and ascending urethrogram and diminished flow of urine in Uroflowmetry. Total 7 Uttarbasti with 50ml Sahcharadi Tailam was given along with Rasayana and Mutraghatahara medicine. Patient has complete relief in his obstructive urine complains and has normal urine flow without taking Tab. AFDURA after 7 years. And also improvement appear in Uroflowmetry.


1976 ◽  
Vol 85 (5) ◽  
pp. 617 ◽  
Author(s):  
D. G. OREOPOULOS
Keyword(s):  

1956 ◽  
Vol 4 (1) ◽  
pp. 85-90 ◽  
Author(s):  
JAMES P. HENRY ◽  
OTTO H. GAUER ◽  
J. L. REEVES
Keyword(s):  

1986 ◽  
Vol 32 (3) ◽  
pp. 529-532 ◽  
Author(s):  
K Jung ◽  
G Schulze ◽  
C Reinholdt

Abstract We studied how much of the lysosomal enzyme N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) and of the brush-border enzymes alanine aminopeptidase (EC 3.4.11.2), alkaline phosphatase (EC 3.1.3.1), and gamma-glutamyltransferase (EC 2.3.2.2) was excreted in urine over 8 h after a high intake of fluid (22 mL per kilogram of body weight). The hourly excretion of all four enzymes increased with the increasing urine flow rate. The excretion rate of the brush-border enzymes was more markedly influenced than that of N-acetyl-beta-D-glucosaminidase. By relating the enzyme excretion to urinary creatinine we could reduce the variability of brush-border enzyme output and could completely compensate for the effect of diuresis on the excretion of N-acetyl-beta-D-glucosaminidase.


1999 ◽  
Vol 45 (10) ◽  
pp. 1879-1880 ◽  
Author(s):  
Andreas Lun ◽  
Reinhard Ziebig ◽  
Hannes Hammer ◽  
Uwe Otting ◽  
Guido Filler ◽  
...  

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Toru Kawada ◽  
Takuya Nishikawa ◽  
Satoru Suehara ◽  
Satoshi Sawada ◽  
Tetsuo Tanaka ◽  
...  

AbstractPrimary acute sympathetic activation (PASA) causes a subsequent arterial pressure (AP) elevation. In this case, an antidiuretic effect via the renal innervation and pressure diuresis can act antagonistically on the kidneys. We examined the effect of PASA on urine output in spontaneously hypertensive rats (SHR) 4–7 days after unilateral renal denervation (RDN) (n = 9). The slope of the plot of urine flow versus AP was positive (0.120 ± 0.031 μL min−1 kg−1 mmHg−1) on the intact side, but it was less than 1/3 of the slope observed previously in normotensive Wistar–Kyoto rats (WKY). RDN did not normalize the slope of urine flow versus AP (0.179 ± 0.025 μL min−1 kg−1 mmHg−1, P = 0.098 versus the intact side). The urine flow at the operating point of the AP tended to be greater on the denervated than the intact side (29.0 ± 1.8 vs. 25.3 ± 1.9 μL min−1 kg−1, P = 0.055). The percent increase (17.2 ± 7.2%) was not different from that observed previously in WKY. Although high-resting sympathetic nerve activity is prerequisite for maintaining hypertension in SHR, the effect of sympathetic innervation on the urine output function was not greater than that in WKY.


1972 ◽  
Vol 15 (4) ◽  
pp. 338-346 ◽  
Author(s):  
Herbert S. Diamond ◽  
Robert Lazarus ◽  
David Kaplan ◽  
David Halberstam

2000 ◽  
Vol 279 (4) ◽  
pp. R1268-R1276 ◽  
Author(s):  
Paul P. Leyssac ◽  
Niels-Henrik Holstein-Rathlou ◽  
Ole Skøtt

Inconsistencies in previous reports regarding changes in early distal NaCl concentration (EDNaCl) and renin secretion during osmotic diuresis motivated our reinvestigation. After intravenous infusion of 10% mannitol, EDNaCl fell from 42.6 to 34.2 mM. Proximal tubular pressure increased by 12.6 mmHg. Urine flow increased 10-fold, and sodium excretion increased by 177%. Plasma renin concentration (PRC) increased by 58%. Renal blood flow and glomerular filtration rate decreased, however end-proximal flow remained unchanged. After a similar volume of hypotonic glucose (152 mM), EDNaClincreased by 3.6 mM, ( P < 0.01) without changes in renal hemodynamics, urine flow, sodium excretion rate, or PRC. Infusion of 300 μmol NaCl in a smaller volume caused EDNaCl to increase by 6.4 mM without significant changes in PRC. Urine flow and sodium excretion increased significantly. There was a significant inverse relationship between superficial nephron EDNaCl and PRC. We conclude that EDNa decreases during osmotic diuresis, suggesting that the increase in PRC was mediated by the macula densa. The results suggest that the natriuresis during osmotic diuresis is a result of impaired sodium reabsorption in distal tubules and collecting ducts.


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