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Biomedical subjects

O S Better

Publications and source records attributed to O S Better.

At least 91 records · Page 5Linked to original sources
PubMed1982

Acquired distal renal tubular acidosis in man.

Distal renal tubular acidosis (dRTA) may complicate renal transplantation, liver cirrhosis, and obstructive uropathy. Indeed, its occurrence may be an early clue to an episode of rejection of the graft or to obstructive uropathy. The mechanism in most patients with dRTA is impaired distal secretion of protons. In some patients, however, back leak of protons from tubular lumen to blood may abolish distal tubular ability to maintain urine to blood proton gradients. In patients with obstructive uropathy the spectrum of tubular acidosis is widened by the occurrence of additional defects in tubular secretion of potassium and impairment of hydrogen ion secretion secondary to hypoaldosteronism. Hyperkalemia is also seen in "voltage dependent" states such as following the administration of lithium and amiloride. Hyperkalemia per se is conducive to acidosis by a combination of extrarenal and several intrarenal mechanisms.

Acidosis, Renal Tubular↗
PubMed1982

Pathogenesis of salt retention in dogs with chronic bile-duct ligation.

1. The present study investigates the role of mineralocorticoids in the pathogenesis of salt retention and ascites in dogs with chronic ligation of the common bile duct (CBDL). 2. After CBDL the natriuretic response to an intravenous sodium load [0.9% sodium chloride solution (150 mmol/l): saline; 10% of body weight] was markedly depressed. Urinary sodium excretion was 285 +/- 62 vs 960 +/- 58 mumol/min in the control period before CBDL (P less than 0.001). This antinatriuresis was associated with a significant rise in plasma aldosterone concentration, from 52.5 +/- 5.5 pg/ml before CBDL to 177 +/- 50 pg/ml after CBDL (P less than 0.02). Ascites was present in all salt-retaining CBDL dogs. 3. Bilateral adrenalectomy resulted in disappearance of ascites and in a rise in the natriuretic response to extracellular volume expansion. Urinary sodium excretion was 770 +/- 124 mumol/min, a value significantly higher than in the CBDL dogs with intact adrenals (P less than 0.001). Sodium balance studies in the adrenalectomized CBDL dogs during chronic deoxycorticosterone acetate (DOCA) treatment (25 mg/day) showed that in these animals there was failure to escape from the mineralocorticoid-induced sodium retention. Glomerular filtration rate and renal plasma flow did not change during the studies. 4. The present evidence supports the thesis that sodium retention in the CBDL dog results from a dual mechanism: (a) excess of circulating aldosterone and (b) and extra-adrenal factor which prevents escape from the salt-retaining effect of mineralocorticoids, in the CBDL dogs, thereby perpetuating the antinatriuresis in these animals.

Adrenalectomy↗
PubMed1982

The effect of intrarenal infusion of bile on kidney function in the dog.

1. Obstructive jaundice sensitizes the kidney to anoxic damage. To clarify further this phenomenon the effect of unilateral infusion of bile on kidney function was studied. The contralateral intact kidney served as control. 2. Intrarenal infusion of diluted bile (1:10) resulted in an ipsilateral fourfold increase in mean rate of urinary flow (P less then 0.01), threefold increase in mean fractional excretion of sodium (P less then 0.05) and more than 50% increase in mean rates of potassium excretion (P less then 0.05). Urinary flow rate and electrolyte excretion returned to baseline upon cessation of bile infusion. The mean clearances of inulin and rho-aminohippurate were unchanged during intrarenal bile infusion. 3. Intrarenal infusion of isotonic taurocholate solution (20 mmol/l) mimicked the diuretic, natriuretic and kaliuretic effects of diluted bile, whereas intrarenal infusion of bilirubin did not cause any change in the excretion of electrolytes. 4. It is concluded that increase in circulating bile acids rather than hyperbilirubinaemia may alter kidney function during obstructive jaundice. Acute cholaemia may cause volume depletion by increasing urinary salt loss. This in turn may aggravate the direct nephrotoxicity of circulating bile compounds.

Animals↗
PubMed1982

Effect of isolated cholaemia on systemic haemodynamics and kidney function in conscious dogs.

1. Systemic haemodynamics and kidney function were studied in the same dogs before and 14 days after choledochocaval anastomosis. 2. All dogs became deeply jaundiced whereas parenchymal liver function remained unchanged as assessed biochemically. 3. After choledochocaval anastomosis there was a decrease in mean arterial pressure (118 +/- 18 to 98 +/- 13 mmHg, P less than 0.005), and total peripheral resistance (4073.8 +/- 620.0 to 3327.6 +/- 244.9 kPa 1-1 s kg, P less than 0.01), whereas mean cardiac index and plasma volume corrected for body weight did not change. 4. Despite their disturbed systemic haemodynamics the cholaemic dogs and normal mean glomerular filtration rate and renal plasma flow. Maximal ability to concentrate and dilute the urine was, however, impaired during cholaemia. 5. It is concluded that cholaemia per se causes peripheral vasodilatation, hypotension and renal tubular dysfunction. Similar phenomena in jaundiced patients may contribute to their susceptibility to postoperative shock and acute renal failure.

Animals↗
PubMed1982

Tubular handling of sodium following immersion to the neck and salt-induced volume expansion.

We wished to compare the natriuretic and diuretic effect of extracellular volume expansion (ECVE) with 0.9% NaCl to that obtained with up-to-the-neck immersion (NI) in healthy volunteers. Clearance techniques during maximal antidiuretic hormone suppression were utilized to pinpoint the sites of tubular NaCl reabsorption. Mean glomerular filtration rate (GFR) did not differ significantly between ECVE and NI; mean rate of sodium excretion during ECVE was significantly greater than during NI, whereas mean water clearance for a given rate of distal delivery was higher with NI than with ECVE. Our findings suggest that ECVE is associated with greater natriuresis than NI, despite the equality of filtered sodium loads and of distal deliveries under both these procedures.

Adult↗
PubMed1981

Factors affecting sperm motility. VII. Sperm viability as affected by change of pH and osmolarity of semen and urine specimens.

The effects of pH and osmolarity of semen and urine specimens on motility and velocity of human spermatozoa were studied objectively with the aid of the multiple exposure photography (MEP) method. The pH of fresh ejaculates ranged from 7.2 to 8.2 and specimens were slightly hyperosmotic ranging between 300 to 380 mOsm/kg. Gradually changing the pH and osmolarity to either side of normal values led to progressive loss of sperm motility. However, sperm velocity was slightly increased by mild alkalinization and hyperosmolarity. Spermatozoa that became immobilized by acidification regained their motility shortly after pH was restored to normal values. In the majority of instances spermatozoa lost their motility when mixed with fresh urine specimens. Neutralization of urinary pH could not protect them from this effect unless urine osmolarity was also isotonically adjusted. It is suggested that patients with retrograde ejaculation should adequately increase their fluid intake before recovery of sperm from their bladder for artificial insemination.

Humans↗
PubMed1981

Blunted pressor response to angiotensin and sympathomimetic amines in bile-duct ligated dogs.

1. The pressor and heart rate response to angiotensin II, noradrenaline, isoprenaline, tyramine and beta-phenylethylamine were examined before and after bile-duct ligation in conscious trained dogs. 2. The pressor response to angiotensin II was markedly suppressed after bile-duct ligation, although responses to noradrenaline and the indirectly acting sympathomimetic amines were only slightly reduced. 3. Bradycardia, in response to the pressor drugs, and tachycardia, in response to isoprenaline, were unchanged after bile-duct ligation. 4. Refractoriness to the pressor action of angiotensin after chronic bile-duct ligation in the present study is similar to that reported previously by others in patients with liver cirrhosis. 5. No evidence was found in the bile-duct ligated dog to support a role of false neurotransmitters as mediators of the circulatory disturbances associated with liver injury.

Angiotensin II↗