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Biomedical subjects

O S Better

Publications and source records attributed to O S Better.

At least 73 records · Page 4Linked to original sources
PubMed1986

Oral calcium carbonate as phosphate-binder in infants and children with chronic renal failure.

In view of the known toxicity of aluminum, we studied the effects of CaCO3 as an alternative phosphate binder in 12 chronic renal failure (CRF) children during 152 patient-months. Mean (+/- SD) serum creatinine concentration rose during that period from 3.7 +/- 1.8 to 5.1 +/- 3.0 mg/dl. 8 patients received CaCO3 from the start, and 4 were switched from A1(OH)3 after 2 months of interruption. In addition to CaCO3 (0.1-0.3 mg/kg BW) all patients received NaHCO3, and all but two received 1 alpha-hydroxyvitamin D3 [1 alpha(OH)D3] or dihydrotachysterol (DHT). Urine and blood variables were checked every 4-6 weeks and medication dosages were adjusted accordingly, aiming to keep serum Ca at 10.4-10.8 mg/dl, serum Pi at 3.5-5.5 mg/dl, and serum HCO-3 above 18 mEq/l. Bone X-rays were obtained every 6-9 months. With treatment, mean serum Ca increased from 8.9 +/- 0.7 to 10.3 +/- 0.4 mg/dl (p less than 0.01), serum Pi decreased from 6.3 +/- 0.9 to 4.2 +/- 0.5 mg/dl (p less than 0.01), and the mean Ca X P product decreased slightly and insignificantly. Mean serum alkaline phosphatase levels decreased significantly from 486 +/- 251 to 168 +/- 28 IU (p less than 0.01). Bone X-rays at the end of the study showed either healing of renal osteodystrophy or its prevention. Only one episode of mild hypercalcemia (serum Ca 11.7 mg/dl) was observed in 1 patient, but his Ca X P product remained low.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1985

Modification of pulmonary metabolism of noradrenaline in experimental obstructive jaundice.

The pulmonary metabolism of noradrenaline (NA) was measured in lungs removed from 3 day sham-operated rats and from rats whose bile ducts had been ligated 3 days earlier (BDL). The pulmonary metabolism of NA as measured by a single clearance of the radio-labelled 14C-amine was significantly increased in lungs excised from BDL rats as compared to that measured in the sham-operated rats. The change in metabolism was associated with an alteration in the pulmonary uptake of NA and not with the activities of the enzymes monoamine oxidase types A and B and catechol-O-methyl transferase. Moreover, it was not correlated with rises in the bilirubin or cholesterol concentrations in the serum of the BDL rats and occurred independent of any changes in pulmonary pressure. In a second series of experiments, the evolution of this abnormality over the period of one to six days postoperative was investigated. In the sham-operated rats, there was no significant change in the pulmonary metabolism of NA even by the sixth day. In contrast, there were time-dependent increases from one to six days in these metabolic processes in BDL rats with the highest values being at six days. In contrast, the serum concentrations of bilirubin and cholesterol and activities of the enzymes, alanine transaminase and alkaline phosphatase all rose to their maximum by the fourth day and thereafter declined. Although serum albumin levels fell significantly in BDL rats they were not significantly different from sham-controls. Thus, change in pulmonary metabolism of NA with obstructive jaundice increases with time from one to six days and it not related to the blood chemical changes of biliary obstruction or hepatic synthetic function.

Alanine Transaminase↗
PubMed1985

Serum bilirubin constituents in different experimental models of conjugated hyperbilirubinemia.

The object of the study was to explain the differences in bilirubin level in various experimental jaundice models. The Bil constituents in conjugated hyperbilirubinemic dog models were identified. Total Bil was measured using the Jendrassik and Grof method and direct spectrophotometry. Conjugated and unconjugated Bil were measured using the Weber-Schalm extraction method. Bilirubin covalently bound to albumin was measured indirectly from the total Bil and the non-CBBA fraction. The non-CBBA was estimated either as the sum of the CB and UCB concentrations determined by the W-S method or as the nonprecipitated fraction after deproteinization with ammonium sulfate-saturated ethanol when using DS. The TB, CB, UCB, and CBBA levels were compared in two hyperbilirubinemic dog models: chronic bile duct ligation (CBDL) and internal choledochocaval anastomosis (CDCA). The mean TB in internal CDCA (16.5 +/- 3.67 mg%) was significantly higher than in CBDL (3.4 +/- 1.75 mg%). Most of the serum Bil in these two models was conjugated, 13.4 +/- 2.24 and 3.2 +/- 1.7 mg%, respectively. No CBBA was found in the CBDL or in the partially obstructed internal-CDCA dogs. The TB in an external-CDCA model was essentially similar to the internal-CDCA model. The indirect Bil level in the external-CDCA model was six to seven times higher than the UCB level, and the CBBA level varied between 30 and 80% of the TB. Up to 50% CBBA was found also in patients with intra- or extrahepatic cholestasis. The findings indicate that, unlike the commonly assumed hypothesis, the serum TB level in the CDCA models, which was higher than in the CBCL one, is not due to high UCB levels. Rather, hyperbilirubinemia in the external-CDCA model is due to increased levels of CBBA or, perhaps, to variations in the amount and/or composition of CB entering the blood and cleared by the kidney.

Animals↗
PubMed1985

Obstructive jaundice blunts myocardial contractile response to isoprenaline in the dog: a clue to the susceptibility of jaundiced patients to shock?

Patients with obstructive jaundice are susceptible to postoperative shock. To clarify the mechanism of this phenomenon, we compared the contractile response to isoprenaline of isolated ventricular preparations from three groups of dogs: (a) dogs with chronic bile-duct ligation (CBDL), (b) dogs with choledochocaval anastomosis (CDCA) and (c) sham-operated dogs (SO). Isolated ventricular muscles from CBDL and CDCA dogs showed a depressed contractile response to isoprenaline as compared with SO dogs. Mechanical performance was spared in the CBDL and CDCA dogs. There were no differences in the contractile responses of SO and CBDL dogs, either to ouabain or to changes in the rates of stimulation (force-frequency relationships). These data demonstrate that, in the dog, obstructive jaundice and/or cholaemia are associated with blunted contractile response to beta-adrenoreceptor stimulation in the face of intact basic mechanical performance. Similar inotropic refractoriness to beta-adrenoreceptor stimulation could contribute to the susceptibility to postoperative shock in patients with obstructive jaundice.

Alanine Transaminase↗
PubMed1985

Reversible acute interstitial nephritis associated with indomethacin.

Nonsteroidal, anti-inflammatory drugs have been implicated in causing acute renal failure of several distinct patterns. We report a case of reversible acute renal failure associated with indomethacin therapy. Renal function recovered upon cessation of indomethacin treatment. Renal biopsy disclosed the presence of tubulointerstitial nephritis which was thought to have been responsible for the acute renal failure in this patient. Following presentation of this unusual side effect within the wide spectrum of renal and electrolyte disorders related to nonsteroidal, anti-inflammatory agents, we recommend that kidney function indices should be frequently tested in patients receiving indomethacin.

Acute Kidney Injury↗
PubMed1985

Reversible suppression of the vascular contractile response in rats with obstructive jaundice.

Both patients and experimental animals with obstructive jaundice manifest vascular instability, with animals showing a blunted vascular response to norepinephrine (NE). We sought an intrinsic abnormality of vascular smooth muscle by studying the contractile response of isolated, helically cut aortic strips and intact portal veins to cumulative doses of NE in rats with bile duct ligation (BDL) at different times compared with sham-operated (SO) rats as controls. At 3 days after surgery, the mean cumulative maximal contractile response (Rmax) of the aortic strip of BDL rats (94.3 +/- 9.0 mg/mg tissue) was significantly lower than that of SO controls (145.3 +/- 11.5 mg/mg tissue) (P less than 0.005), associated with a tendency toward decreased sensitivity (half-maximal dose [ED50]) (18.2 +/- 6.75 nmol/L vs. 6.7 +/- 0.6 nmol/L). By 6 days, there was no difference between the two groups. Similarly, by 3 days the mean Rmax for portal vein contraction in BDL rats (694 +/- 72 mg) was significantly lower than that for SO rats (1000 +/- 143 mg). In contrast, mean ED50 of the portal veins of BDL rats (327 +/- 65 nmol/L) was significantly less than that of SO rats (881 +/- 216 nmol/L), indicating greater sensitivity. At 1 and 6 days after surgery there was no significant difference between the two groups. These alterations in the vascular contractile response coincided with the maximum increases in serum bilirubin and liver enzyme levels. In conclusion, this study indicates that the circulatory abnormalities associated with obstructive jaundice are associated, at least in part, with suppression of the vascular contractile response caused by some abnormality of the vascular musculature.

Alanine Transaminase↗
PubMed1984

Bile salts, hypotension and obstructive jaundice.

We have examined the effects of bile duct ligation on vascular and extravascular smooth muscle responsiveness to noradrenaline and tyramine using isolated rat hindlimb perfusion, and portal vein and vas deferens preparations. Bile duct ligation reduced the contractile responses to noradrenaline of vascular and extravascular smooth muscle. Exposure of smooth muscle to some bile salts caused a reduction in contractility. This effect was dependent upon bile salt type and concentration. These studies in vitro suggest that the reduced total peripheral resistance and hypotension seen in obstructive jaundice cannot be explained by a spasmolytic effect of some of the bile salts on smooth muscle.

Animals↗
PubMed1984

Jaundice, the circulation and the kidney.

(Fig. 1) Cholemia per se (i.e. independent of parenchymal liver damage) causes a profound disturbance of systemic hemodynamics. This includes decrease in total peripheral vascular resistance, and possible impairment of left ventricular performance. These, in turn, lead to a decrease in effective blood volume, a tendency to hemorrhagic shock and prerenal failure. Early in the course of cholemia , the natriuretic effects of bile salts in the circulation may aggravate the hypovolemia. In marked contrast to the decrease in total peripheral vascular resistance, the regional vascular beds of the kidney and the brain constrict during cholemia . The combined effect of cholemia may thus lead to redistribution of cardiac output away from the kidney and the brain. When parenchymal liver damage complicates obstructive jaundice, the tendency to arterial hypotension is aggravated. The overall interrelationship between jaundice and circulatory homeostasis is depicted in figure 1.

Animals↗
PubMed1984

High dose of L-carnitine increases platelet aggregation and plasma triglyceride levels in uremic patients on hemodialysis.

Uremic patients undergoing chronic hemodialysis demonstrate a secondary systemic carnitine deficiency. We studied the effect of carnitine replacement with high doses (L-carnitine, 3 g/day) similar to those used in the treatment of primary systemic carnitine deficiency. 10 uremic patients on hemodialysis were randomly selected into a control group (4 patients) treated by placebo and a treatment group (6 patients) treated by L-carnitine. Plasma lipoprotein concentration and composition as well as platelet aggregation were studied before and after treatment. Following carnitine administration, a paradoxical rise in plasma triglyceride concentration from 180 +/- 66 to 219 +/- 88 mg% (p less than 0.05) was noted. No other significant changes in lipoprotein concentration and composition or in plasma apoprotein A-I and B concentration were observed. Carnitine treatment caused a significant rise in platelet aggregation induced by epinephrine, ADP, and thrombin. These findings suggest a harmful effect of L-carnitine replacement therapy when given in high doses, causing aggravation of uremic hypertriglyceridemia and increased platelet aggregation in patients predisposed to thromboembolic phenomena.

Adult↗
PubMed1984

Renal tubular handling of potassium in patients with medullary sponge kidney. A model of renal papillectomy in humans.

Renal tubular function, with special emphasis on potassium excretion, was studied in three patients with medullary sponge kidney (MSK). Urinary acidification and concentration abilities were impaired, while glomerular filtration rates remained normal. After short-term intravenous (IV) potassium chloride loading, maximal excretion of potassium was lower in the patients with MSK than in the normal controls. The kaliuretic response to IV sodium sulfate and acetazolamide infusion was maintained. The capacity of the kidney to sustain potassium balance under conditions of either long-term potassium loading or depletion was preserved. We have concluded that the medullary and papillary segments of the human collecting duct, have an important role in the handling of short-term potassium loading. The integrity of these segments, however, is not essential for adaptation to prolonged potassium surfeit or dietary depletion.

Acetazolamide↗
PubMed1984

Prevention of acute renal failure in traumatic rhabdomyolysis.

Following the collapse of a building, seven subjects (aged 18 to 41 years) were released from under the rubble within one to 28 hours. All seven suffered from extensive crush injuries with evidence of severe rhabdomyolysis and were treated by the induction of an alkaline solute diuresis immediately on their extrication from the debris. The leakage of muscle constitutents was estimated by quantifying the net total body potassium losses, which averaged 395 mEq (SD, +/- 198) over the first 60 hours of therapy. In the past, injuries of similar severity have been associated with a high incidence of acute renal failure and a high mortality rate, yet none of our patients had azotemia or renal failure. We attribute this success to the unprecedented early institution of appropriate therapy.

Acid-Base Equilibrium↗
PubMed1984

Volume regulation in man during neck-out immersion in a medium with high specific gravity (Dead Sea water).

The effect of immersion for 4 h on arterial blood pressure and the rate or urinary sodium excretion was studied in five subjects both in fresh water and in Dead Sea water (specific gravity 1.19) at 34 C. Following 100 min of immersion, mean systolic and diastolic blood pressure decreased (P less than 0.01) in subjects immersed in fresh water, and increased (P less than 0.05) in those immersed in Dead Sea water. While immersion in fresh water led to hypotension, it was associated with an increased natriuresis. In contrast, the hypertensive response to immersion in Dead Sea water was not associated with an increased natriuresis. It is concluded that under the unique conditions of this experiment, urinary excretion of sodium becomes independent of systemic arterial blood pressure, and is presumably governed by neurohumoral influences originating in the baroreceptors of the low pressure system.

Adult↗
PubMed1983

Accumulation of lipoprotein remnants in patients with chronic renal failure.

The composition and concentration of remnant lipoprotein particles accumulating in the plasma of patients with chronic renal failure (CRF) was determined. Ten patients on chronic hemodialysis were compared with 8 controls. The patients' very low density lipoproteins (VLDL) were abnormal and contained more of the dense VLDL subfraction (VLDL3). The concentration of intermediate density lipoproteins (IDL) was increased 3-fold in CRF plasma, whereas the amount of low density lipoprotein (LDL) was decreased by 25%. On electrophoresis of plasma lipoproteins the beta-band from the patients' samples demonstrated increased anodal mobility, indicating an abnormality in composition of the patients' LDL. These abnormalities were present regardless of whether patients were hyperlipidemic or not. These findings suggest defective conversion of VLDL to LDL in CRF, allowing for the accumulation of lipoprotein particles usually absent from plasma. The latter may account for the accelerated atherosclerosis reported in patients with CRF.

Adult↗
PubMed1983

Investigation of tubular handling of bicarbonate in man. A new approach utilizing stable carbon isotope fractionation.

Two alternative mechanisms have been proposed for tubular reabsorption of bicarbonate: (a) H+ secretion and CO2 reabsorption and (b) direct reabsorption of HCO-3. In an attempt to differentiate between the two mechanisms, the present study utilized the natural abundance of stable carbon isotopes (13C, 12C) in the urinary total CO2. This novel methodology used mass spectrometric analysis of 13C/12C ratios in urinary total CO2 under normal conditions and during acetazolamide treatment. Blood and respiratory CO2 were analyzed to yield reference values. The results demonstrate that alkaline urine is preferentially enriched with 13C relative to the blood. It is suggested that this fractionation results from reaction out of isotopic equilibrium in which HCO-3 converts to CO2 during the reabsorption process in the distal nephron. The presence of carbonic anhydrase in the proximal nephron results in rapid isotopic exchange between CO2 and HCO-3 and keeps them in isotopic equilibrium. The ratio of urinary 13C/12C increases strikingly after acetazolamide administration and consequent inhibition of carbonic anhydrase in the proximal tubule. Although it is possible that in the latter case high HCO-3 generates the CO2 (ampholyte effect), the isotope fractionation indicates that CO2 rather than HCO-3 is reabsorbed. In contrast, at low urinary pH and total CO2 values, the carbon isotope composition approaches that of blood CO2. This indicates rapid CO2 exchange between urine and blood, through luminal membrane highly permeable to CO2. These results could be anticipated by a mathematical model constructed to plot 13C concentration of urinary total CO2. It is concluded that the mechanism of HCO-3 reclamation in man (and, by inference, in other mammals as well) works by conversion of HCO-3 to CO2 and reabsorption of CO2.

Absorption↗