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Biomedical subjects

A Hoppe

Publications and source records attributed to A Hoppe.

At least 55 records · Page 3Linked to original sources
PubMed1988

Serum proline and blood lactate levels in alcoholic patients without hepatic failure: relationship with alcohol ingestion and histological activity.

It has not yet been established whether serum proline and blood lactate levels are increased in alcoholic liver disease. We measured serum proline and blood lactate in controls and in patients with different stages of alcoholic liver disease in the absence of hepatic failure. Samplings were done in both abstinent and drinking alcoholics. Compared to controls, there was a striking increase in serum proline levels in 52 abstinent alcoholics with little or no hepatic fibrosis by histological assessment (0.10 +/- 0.01 vs. 0.155 +/- 0.008; p less than 0.005). Blood lactate levels were within the normal range and did not correlate with serum proline levels. On the other hand, serum proline and blood lactate levels were independent of hepatic necrosis and inflammation scores. In addition, in 10 patients with blood alcohol concentrations between 0.3 mg/ml and 7.8 mg/ml, serum lactate and proline were significantly elevated (2.42 +/- 0.29 mg/ml and 0.275 +/- 0.0026 mg/ml, respectively; p less than 0.005). These results show that there is an association between serum proline levels and the abstinence period in alcoholic patients. They further suggest that in alcoholic patients neither serum proline nor blood lactate concentrations are reliable markers for liver histological activity (necrosis and inflammation) or fibrosis.

Adult↗
PubMed1988

Beta-receptors in resistance to phosphaturic effect of PTH in respiratory alkalosis.

Respiratory alkalosis results in a resistance to the phosphaturic effect of parathyroid hormone (PTH) and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). The present studies evaluated the role of the beta-adrenergic system in that resistance phenomenon. In clearance experiments on acutely thyroparathyroidectomized male Wistar rats, respiratory alkalosis blunted the PTH-mediated increase in absolute and fractional excretion of phosphate (FEPi). Propranolol infusion restored the phosphaturic response to PTH:FEPi, 0.8 +/- 0.3 vs. 8.1 +/- 2.5% (P less than 0.005). Similarly, the increase of FEPi during cAMP infusion was also diminished by respiratory alkalosis: FEPi, 15.5 +/- 2.2 vs. 5.5 +/- 1.1% (P less than 0.005). This hypophosphaturic effect of respiratory alkalosis in the presence of cAMP was not observed in rats infused with propranolol compared with the period of normal ventilation: FEPi, 21.1 +/- 1.7 vs. 15.3 +/- 1.6 (P less than 0.02). Also, during the infusion of the highly selective beta 2-adrenoceptor antagonist, ICI 118,551, cAMP was phosphaturic in respiratory alkalosis compared with FEPi in the absence of the antagonist: FEPi, 13.0 +/- 2.5 vs. 5.5 +/- 1.1% (P less than 0.02). Finally, the infusion of the beta 2-agonist, fenoterol, to the normally ventilated rats significantly decreased FEPi in cAMP-infused rats in comparison to the absence of the agonist: FEPi, 4.0 +/- 0.7 vs. 22.1 +/- 2.6% (P less than 0.001). We conclude that the resistance to the phosphaturic effect of PTH and cAMP in respiratory alkalosis is mediated by beta-adrenoceptors.

Alkalosis↗
PubMed1988

Treatment of clinically normal and cystinuric dogs with 2-mercaptopropionylglycine.

In a pharmacokinetic and tolerance study, 2 healthy Beagles were given 13.2 to 39.5 mg of 2-mercaptopropionylglycine (2-MPG)/kg of body weight orally once daily in increasing doses for 3 weeks. A third dog was given 10 mg of 2-MPG/kg of body weight, IV. The drug was well tolerated. After these initial studies, 15 cystinuric dogs were treated with 2-MPG orally once daily for 5 to 45 months and with sodium bicarbonate for urine alkalinization and fluid diuresis. Pharmacokinetic studies were done in 7 dogs on the third day of oral treatment with 2-MPG. After oral administration of 15.6 to 31.3 of 2-MPG/kg of body weight, maximal serum/plasma concentrations were from 28.6 to 76.3/mumol/L after 1 to 3 hours in 6 cystinuric dogs. The mean urinary excretion was 22% (range, 0.3 to 58.9%) of the dose. Ten of 15 cystinuric dogs had no re-formation of uroliths. Of 4 dogs with uroliths at the beginning of treatment, 3 had total urolith dissolution on continuous treatment. During treatment, further growth of the uroliths was inhibited in one dog, and in another dog with re-formed uroliths, they dissolved. We concluded that 2-MPG is well tolerated and promising for treatment of cystinuric dogs, but the pharmacokinetic studies should be expanded to include different dosage regimens, and results of long-term treatment should be evaluated. Our recommendations for treatment of dogs with cystine uroliths include surgical intervention if the dog has urethral obstruction or has dysuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

High-performance liquid chromatography of 2-mercaptopropionylglycine and its metabolite 2-mercaptopropionic acid in plasma and urine after treatment with thiopronine.

2-Mercaptopropionic acid has been identified as a normal metabolite of 2-mercaptopropionylglycine (thiopronine) when this drug was given to humans and dogs. A high-performance liquid chromatographic method was developed to resolve the derivatives of these two thiols and thus enable simultaneous determination of the two compounds in plasma and urine.

Amino Acids, Sulfur↗
PubMed1982

Effect of respiratory alkalosis on renal phosphate excretion.

Respiratory alkalosis induced hypophosphatemia and hypophosphaturia in intact animals. The present studies evaluated the effect of respiratory alkalosis on tissue phosphate distribution and renal phosphate transport in the presence and absence of parathyroid hormone (PTH). Respiratory alkalosis decreased plasma phosphate concentration and increased phosphate concentrations in muscle and liver. It decreased fractional phosphate excretion (FEPi) from 6.1 +/- 1.4 to 0.6 +/- 0.2%. In thyroparathyroidectomized (TPTX) rats infused with 20 mM phosphate, respiratory alkalosis decreased FEPi from 15.0 +/- 0.9 to 5.5 +/- 0.1%. PTH or dibutyryl cAMP administration produced a phosphaturia that was blunted by respiratory alkalosis. The phosphaturic response to PTH was also blunted in hypocapnic rats in which alkalosis was prevented by infusion of HCl. We conclude that respiratory alkalosis increases phosphate uptake by muscle, which largely accounts for the hypophosphatemia. The kidney response with increased phosphate reabsorption independent of plasma and kidney phosphate concentrations and with refractoriness to the phosphaturic effect of PTH. This refractoriness to the phosphaturic effect of PTH is due to decreased PCO2 rather than to the concomitant extracellular alkalosis.

Alkalosis, Respiratory↗
PubMed1980

Effect of NH4Cl on phosphaturic response to PTH in the hamster: dissociation from acidemia.

Previous studies indicate that the hamster fasted for 16 h fails to demonstrate a significant phosphaturic response to parathyroid hormone (PTH). However, when hamsters were infused with ammonium chloride, a phosphaturic response to PTH was observed. The present studies evaluate the respective roles of acidemia and the ammonium ion in this response. As in previous studies, fasted thyroparathyroidectomized (TPTX) hamsters infused with PTH showed no significant increase in the fractional excretion of phosphate (FE rho), from 19 +/- 2 to 22 +/- 1%. Neither respiratory acidosis (hypercapnia) nor metabolic acidosis (HCl infusion) enhanced the phosphaturic effect of PTH, FE rho 21 +/- 4 to 20 +/- 6 and 15 +/- 2 to 16 +/- 3%, respectively. Both ammonium chloride and ammonium bicarbonate infusions enhanced the phosphaturic response; FE rho increased from 15 +/- 5 to 27 +/- 5% (P < 0.02) and 17 +/- 3 to 25 +/- 3% (P < 0.05), respectively. We conclude that the enhancement of the phosphaturic effect of PTH in the fasted hamster by ammonium chloride infusions can be dissociated from acidemia.

Acidosis↗
PubMed1976

Additive inhibition of renal bicarbonate reabsorption by maleate plus acetazolamide.

The effects of two potent inhibitors of renal bicarbonate reabsorption--maleate and acetazolamide--were investigated in the rat using clearance techniques. Acetazolamide given in high dose (50 mg/kg body wt) inhibited fractional bicarbonate reabsorption by ca. 30%, maleate (2.58 nmol/kg body wt) by 25%, and maleate plus acetazolamide by 54-72%. GFR was depressed, and urine volume was increased by both drugs in an additive manner. Maleate was equally effective as inhibitor of HCO3- reabsorption in the presence and absence of carbonic anhydrase activity. It is suggested that the site of action of both drugs is predominantly proximal, but they act on different steps in the transcellular HCO3- transport. A hypothetical mechanism of maleate action is presented, which takes into account the changes in passive HCO3- flux through the basolateral membrane.

Acetazolamide↗