BICARBONATE EXCRETION DURING HYPOTHERMIA

1963 ◽  
Vol 41 (1) ◽  
pp. 91-96 ◽  
Author(s):  
G. S. Kanter ◽  
R. H. Lubinski ◽  
I. M. Mielens

The investigation was designed to determine whether the renal loss of bicarbonate contributes significantly to the acidosis of hypothermia. The excretion of bicarbonate during hypothermia was studied in five infused (6% creatinine in saline at 0.4 ml/minute) and five non-infused dogs. All animals were anesthetized and artificial respiration was not used. The rectal temperature was gradually reduced to the 26–27 °C range by approximately 4 hours of exposure to ice packing. After control, clearance periods of 30 minutes' duration were conducted serially and continually through the experiment. There was no significant increase in bicarbonate excretion during hypothermia in the non-infused group. The urinary pH remained at control levels of about 6.2. The fall in arterial pH was not due to urinary bicarbonate loss. The urinary pH in the infused group, which had a higher urine flow, increased to pH 6.7 due to increased excretion of bicarbonate. The urine pH in three animals with highest urine flows in this latter group approached plasma levels. The excretion rate of bicarbonate in the infused group, however, was similarly insufficient to account for the decrease in arterial pH. The hypothermic kidney is quite effective in reabsorbing bicarbonate.

1963 ◽  
Vol 41 (1) ◽  
pp. 91-96 ◽  
Author(s):  
G. S. Kanter ◽  
R. H. Lubinski ◽  
I. M. Mielens

The investigation was designed to determine whether the renal loss of bicarbonate contributes significantly to the acidosis of hypothermia. The excretion of bicarbonate during hypothermia was studied in five infused (6% creatinine in saline at 0.4 ml/minute) and five non-infused dogs. All animals were anesthetized and artificial respiration was not used. The rectal temperature was gradually reduced to the 26–27 °C range by approximately 4 hours of exposure to ice packing. After control, clearance periods of 30 minutes' duration were conducted serially and continually through the experiment. There was no significant increase in bicarbonate excretion during hypothermia in the non-infused group. The urinary pH remained at control levels of about 6.2. The fall in arterial pH was not due to urinary bicarbonate loss. The urinary pH in the infused group, which had a higher urine flow, increased to pH 6.7 due to increased excretion of bicarbonate. The urine pH in three animals with highest urine flows in this latter group approached plasma levels. The excretion rate of bicarbonate in the infused group, however, was similarly insufficient to account for the decrease in arterial pH. The hypothermic kidney is quite effective in reabsorbing bicarbonate.


1986 ◽  
Vol 70 (2) ◽  
pp. 141-145 ◽  
Author(s):  
J. Haylor ◽  
C. J. Lote ◽  
A. Thewles

1. The influence of oral water loading on the excretion rate of prostaglandin (PG) E was investigated in healthy human subjects in a control study where the urine was acidic (pH 5.7) and after oral sodium bicarbonate, which made the urine mildly alkaline (pH 7.2). PGE was immediately extracted from urine and measured by a radioimmunoassay technique. 2. After sodium bicarbonate (5 g) the urinary PGE excretion rate was some three-fold higher (P < 0.01) than in the control study, in the absence of any significant difference in the urine flow (approximately 80 ml/h). 3. In the control study (urine pH 5.7) the urinary PGE excretion rate increased significantly (P < 0.01) as the urine flow rose in response to the oral fluid load. However, after sodium bicarbonate, PGE excretion did not alter after the fluid load despite a 10-fold increase in urine flow. 4. Since after bicarbonate administration PGE excretion is independent of urine flow, mildly alkaline urine may represent a condition under which renal PGE synthesis can be effectively assessed from measurements of urinary PGE excretion, in the presence of changes in urine flow. 5. In addition, the results are compatible with the hypothesis that, in man, PGE may be passively reabsorbed in the distal nephron, and a reduction in this reabsorption could contribute to or be responsible for the dependency of the excretion rate of PGE on urine flow.


1963 ◽  
Vol 204 (5) ◽  
pp. 953-956 ◽  
Author(s):  
G. S. Kanter

The ability of the hypothermic kidney to handle massive exogenous bicarbonate loads was studied in five dogs given 2.6% NaHCO3 plus 0.75% creatinine and 0.1% PAH intravenously at the rate of 4.0 ml/min. The renal hemodynamic pattern was typical of hypothermia with decreasing GFR, RPF, and blood pressure and increasing renal resistance. Urine pH rose to 7.95 while arterial pH, corrected to body temperature, reached a maximum of 7.56 and then slowly declined to 7.51 at 27 C. In spite of the fall in GFR, the urine flow, under the influence of the hyperosmotic load, increased progressively throughout the exposure. Although the bicarbonate load presented to the tubules remained near control levels throughout most of the exposure, the absolute reabsorption of bicarbonate fell from a normothermia value of 1.5 mEq/min to 0.9 mEq/min at 27 C. In terms of mEq of bicarbonate reabsorbed/100 ml of glomerular filtrate, bicarbonate reabsorption increased from 2.1 mEq/min at 38 C to 2.7 mEq/min at 27 C. On the basis of the progressive increase in the clearance ratio for bicarbonate, from a normothermia value of .15 to .34 at 27 C, it is concluded that a depressing effect of cold on the tubular transport of bicarbonate had occurred.


1958 ◽  
Vol 193 (1) ◽  
pp. 108-122 ◽  
Author(s):  
William A. Brodsky ◽  
John F. Miley ◽  
John T. Kaim ◽  
Nareshchandra P. Shah

Hydropenic, anesthetized dogs were given loading infusions of 0.5 m lactic acid and beta-hydroxybutyric acid with and without mannitol. In some experiments blood was collected from the femoral artery, and urine from the bladder. In other experiments, blood was collected from the renal vein, and urine from the renal pelvis. In serum, pH and CO2 content fell to values as low as 6.7 and 4 mm/l., respectively. Urine flow reached maximal levels of 1.5–2.5 cc/min. after lactic acid alone, and 4.0–6.0 cc/min. after mannitol plus lactic acid. The pattern of osmotic activity versus urine flow was characteristic of a nonspecific type of osmotic diuresis. Titratable acid excretion increased to levels of 9–72 µm/min. Loading solute contributed to the bulk of the observed titratable acid even though its pKa was 1–2 u below the usual urinary pH. In urine, pH and CO2 content were reduced to levels of 4.76 and 0.64 mm/l., respectively. Calculated value of CO2 tension of urine was greater than that of plasma in 106 observations; was less than that of plasma in 33 observations; and was equal to that of plasma in 25 observations. Tonometric measurements were made on standard solutions and on samples of urine and plasma of two dogs during lactic acid acidosis. Tonometrically determined values of pCO2 agreed (to within 1 mm of Hg) with calculated values of pCO2.


1982 ◽  
Vol 243 (1) ◽  
pp. F60-F66
Author(s):  
S. Long

In hydrated toads reabsorption of 92% of filtered bicarbonate produces a urine of pH at 22 degrees C. Average blood-to-urine pH gradient is 0.8-0.9 U under these conditions but may reach 3-4 U. Net acid excretion rate in hydrated animals is approximately 30 mu eq . h-1 . kg-1. Flow-independent acid excretion is a negative nonlinear function of urinary pH and passes from positive to negative values in the range of normal urinary pH due to rapid rise in [HCO3-] and slower decline in [NH4+]. [H2PO4-] accounts for only 10-20% of buffer-bound acid excreted. Sulfate loading in Cl-restricted toads is without effect on blood pH but produces significant reduction in blood [Cl-]/[Na+] and in urinary pH, and increased urinary [K+] and net acid secretion rates relative to controls. These renal responses are diminished or absent during sulfate loading in Cl-rich toads. In both groups [Cl-] shows significant positive correlation with pH in sulfate-containing urines. These results are discussed in the context of the nonhomeostatic model of urinary acidification developed in mammals.


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.


PEDIATRICS ◽  
1990 ◽  
Vol 85 (6) ◽  
pp. 1114-1117
Author(s):  
STEPHEN B. SULKES ◽  
ELISE W. VAN DER JAGT

Despite prevention efforts, pool immersion accidents continue to occur all too frequently. In this article we describe a new danger associated with an advance in swimming pool technology, the "solar pool blanket." CASE REPORTS Patient 1 A 30-month-old boy with infantile autism was noted to be missing by his parents, who, after an initial look at their above-ground pool, found him submerged under the intact pool blanket, pulseless and breathless 5 minutes later. Cardiopulmonary resuscitation was performed, and he was transported to a local hospital, where he arrived comatose with decerebrate posturing. His rectal temperature was 33.7°C and his arterial pH was 7.0. Diazepam, phenobarbital, and mannitol were administered and he was intubated and hyperventilated.


1995 ◽  
Vol 268 (1) ◽  
pp. E1-E5 ◽  
Author(s):  
A. Quinones Galvan ◽  
A. Natali ◽  
S. Baldi ◽  
S. Frascerra ◽  
G. Sanna ◽  
...  

Although hyperuricemia is a frequent finding in insulin-resistant states, insulin's effect on renal uric acid (UA) handling is not known. In 20 healthy volunteers, diastolic blood pressure, body weight, and fasting plasma insulin were positively (and age was negatively) related to fasting plasma UA concentrations, together accounting for 53% of their variability. During an insulin clamp, urine flow was lower than during fasting conditions (1.01 +/- 0.12 vs. 1.56 +/- 0.32 ml/min, P = 0.04), whereas creatinine clearance was unchanged (129 +/- 7 and 131 +/- 9 ml/min, P = not significant). Hyperinsulinemia did not alter serum UA concentrations (303 +/- 13 vs. 304 +/- 12 microM) but caused a significant decrease in urinary UA excretion [whether expressed as absolute excretion rate (1.66 +/- 0.21 vs. 2.12 +/- 0.23 mumol/min, P = 0.03), clearance rate (5.6 +/- 0.8 vs. 7.3 +/- 0.8 ml/min, P = 0.03), or fractional excretion (4.48 +/- 0.80 ml/min vs. 6.06 +/- 0.64%, P < 0.03)]. Hyperinsulinemia was also associated with a 30% (P < 0.001) fall in urine Na excretion. Fractional UA excretion was related to Na fractional excretion under basal conditions (r = 0.59, P < 0.01) and during the insulin period (r = 0.53, P < 0.02). Furthermore, the insulin-induced changes in fractional UA and Na excretion correlated with one another (r = 0.66, P < 0.001). Physiological hyperinsulinemia acutely reduces urinary UA and Na excretion in a coupled fashion.


2018 ◽  
Vol 368 (2) ◽  
pp. 157-168 ◽  
Author(s):  
Takanobu Matsuzaki ◽  
Daniel Scotcher ◽  
Adam S. Darwich ◽  
Aleksandra Galetin ◽  
Amin Rostami-Hodjegan

1990 ◽  
Vol 78 (2) ◽  
pp. 181-184 ◽  
Author(s):  
J. Haylor ◽  
C. J. Lote

1. The influence of urine pH on the urinary excretion of prostaglandin (PG) F2α and the PGE2/PGF2α ratio has been examined in the conscious rat. 2. The basal urinary PGF2α excretion rate of 3.9 pmol/h (n = 23) did not vary with urine pH. In marked contrast, PGE2 excretion increased as the urine became more alkaline. The PGE2/PGF2α ratio therefore progressively increased from 1.5 to 22 as the pH of the urine changed from pH 5.8 to pH 7.8. 3. The independence of PGF2α excretion from urine pH: (a) excludes cyclo-oxygenase as a potential site of action for the pH-dependence of urinary PGE2 excretion; (b) suggests that the urinary PGE2/PGF2α ratio measured in alkaline urine may be a more accurate reflection of the kidneys, ability to synthesize these two prostaglandins in vivo; (c) suggests that control of urine pH is required before the urinary PGE2/PGF2α ratio can be employed as an index of PGE2 9-ketoreductase (EC 1.1.1.189) activity in vivo.


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