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Biomedical subjects

K Hruska

Publications and source records attributed to K Hruska.

At least 55 records · Page 3Linked to original sources
PubMed1980

Superovulation in cattle: Effect of goat anti-PMSG serum.

Sixteen heifers were superovulated using 5 000 i.u. PMSG on days 9 to 11 of the oestrous cycle (day 1 of the experiment) followed by two injections of 500 mug Estrumate 48 and 54 hours later. Eight of them were injected with goat anti-PMSG serum 5 hours after the first signs of oestrus were observed. Compared with the control group, the treatment with anti-PMSG serum resulted in a shorter heat period (25.8 vs. 51.3 hours), a higher mean number of ovulations (22.1 vs. 18.0) and a lower number of follicles over 10 mm in diameter (4.1 vs. 22.3). The mean numbers of eggs recovered in the experimental and control groups were 17.8 and 6.9, of which 70.2 and 42.0 per cent, respectively, were viable embryos. The concentrations of progesterone and 17-beta oestradiol in the blood plasma showed no significant differences between the experimental and control animals. A higher oestradiol in the control group on day 9 of the experiment was in keeping with the histological picture of the target organs and with a significantly higher number of follicles at slaughter on days 12 to 14 of the experiment.

Journal Article↗
PubMed1980

Parathyroid hormone metabolism and its potential as a uremic toxin.

Secondary hyperparathyroidism is a universal complication of chronic renal failure. It has been proposed that the markedly elevated levels of immunoreactive parathyroid hormone (i-PTH) in uremia may represent a "uremic toxin" responsible for many of the abnormalities of the uremic state. Plasma i-PTH consists of a mixture of intact hormone, a single-chain polypeptide of 84 amino acids, and smaller molecular weight hormonal fragments from both the carboxy- and amino-terminal portion of the PTH molecule. The hormonal fragments arise from metabolism of intact PTH by peripheral organs as well as from secretion of fragments from the parathyroid glands. The structural requirements for the known biological actions of PTH reside in the amino-terminal portion of the PTH molecule. Carboxy-terminal fragments, biologically inactive at least in terms of adenylate cyclase activation, hypercalcemia, or phosphaturia, depend on the kidney for their removal from plasma, and thus accumulate in the circulation in chronic renal failure. It is unknown at the present time if other biological effects of these carboxy-terminal fragments may contribute to some of the biochemical alterations observed in uremia. The most significant consequence of increased PTH levels in uremia is the development of bone disease characterized by osteitis fibrosa. In addition, it would appear that PTH plays an important role in some of the abnormal electroencephalographic patterns observed in uremia. This may be due to a potential role of PTH in increasing calcium content of brain. Parathyroid hormone also has been implicated as a pathogenetic factor in many other alterations present in uremia, i.e., peripheral neuropathy, carbohydrate intolerance, hyperlipidemia, and other alterations. Unfortunately, outstanding clinical research is lacking in this field and conclusive experimental data are practically nonexistent. Further studies are necessary if one is to accept the concept of PTH being a significant "uremic toxin."

Animals↗
PubMed1980

Effects of parathyroid hormone on glucose production by the liver.

The present studies demonstrate a stimulatory effect of intact parathyroid hormone on hepatic glucose production in vivo. This increased glucose production was accompanied by augmented alanine uptake by the liver. In addition, PTH increased the conversion of 14C-alanine to 14C-glucose. These results suggest that the increased hepatic release of glucose produced by PTH is mediated in part by increased gluconeogenesis. On the other hand, the synthetic 1-34 amino terminal fragment of PTH, which is not extracted by the liver, did not stimulate hepatic glucose production.

Alanine↗
PubMed1980

Branched-chain amino acid nitrogen transfer to alamine in vivo in dogs. Direct isotopic determination with [15N]leucine.

To investigate the contribution of branched-chain amino acids as a nitrogen source for alanine in vivo, dogs were infused with l-[(15)N]leucine, l-[U-(14)C]leucine, l-[2,3,3,3-(2)H(4)]alanine, and d-[6,6-(2)H(2)]-glucose. (14)C and (15)N isotopic equilibrium in plasma leucine, and deuterium enrichment in arterial and femoral plasma glucose and alanine were achieved within 3 h of initiation of the respective isotope infusion in all animals. The average flux of leucine determined by [(15)N]leucine was 5.4 mumol.kg(-1).min(-1), whereas using [(14)C]leucine it was 3.7 mumol.kg(-1).min(-1). Turnover rates for alanine and glucose were 11.0 and 17.2 mumol.kg(-1).min(-1), respectively.[(15)N]alanine was detected as early as 30 min, but nitrogen isotopic equilibrium in alanine was not achieved until 6 h. The absolute rate of leucine nitrogen transfer to alanine was 1.92 mumol.kg(-1).min(-1), which represented 41-73% (mean 53%) of leucine's nitrogen and 15-20% (mean 18%) of alanine's nitrogen. Fractional extraction of alanine and leucine by the dog hindlimb was 35 and 24%, respectively. Average net alanine balance was -6.7 mumol.leg(-1).min(-1), reflecting a release rate (17.4 mumol.kg(-1).min(-1)) that exceeded the rate of uptake (10.8 mumol.leg(-1).min(-1)). Of the leucine taken up by the hindlimb, 34% transferred its nitrogen to alanine and 8% was oxidized to CO(2). Since the latter value reflects transamination as well as irreversible catabolism, the nitrogen derived from the oxidation of leucine by the hindlimb could account for only 25% of the observed (15)N incorporation into alanine. The significantly faster flux of leucine nitrogen when compared with leucine carbon suggests significant recycling of the leucine alpha-ketoacid. These studies demonstrate that leucine is a major donor of nitrogen to circulating alanine in vivo.

Alanine↗
PubMed1979

[Effect of chorionic gonadotropin administration on the concentration of testosterone in the blood of boars].

In intact boars, intravenous administration of 100 to 6000 I. U. chorionic gonadotropin elicited a pronounced rise in the plasma level of testosterone, depending on the time interval from the administration of chorionic gonadotropin and on the size of the administered dose. In the blood of castrated boars such an application of choronic gonadotropin did not influence the concentration of testosterone. It was inferred that the rise in the levels of blood testosterone in boars after administration of chorionic gonadotropin was specific for testicular incretion and indicated the endocrine reserve of the testes. There is a discussion concerning the importance of the functional testing of the incretion capacity of testes for differential diagnosis different forms o incretion hypogonadism.

Animals↗
PubMed1978

[Variation of the serum testosterone level in boars during 24 hours and during a period of several days].

Seven sexually mature boars were studied in two-hour intervals for 8 to 32 hours, as to the variation of testosterone levels in the blood plasma. Blood samples were obtained by means of a cannula inserted in the v. cava cranialis. The hormone level under study showed marked fluctuation. The coefficient of variation of testosterone concentration ranged from 12.7% to 35.2% in the individual animals and for the whole part of the study it was 33.0%. It appeared impossible to derive seriously any regular periodicity of testosterone concentration in boar blood in the 24-hour period from the analysis of the variation of the levels of the hormone in individual animals during the period under study. Further, the study revealed a marked fluctuation of testosterone levels in the blood plasma of twelve sexually mature boars in the course of several days' study. The coefficient of variation of testosterone concentration in individual animals ranged from 18.1% to 106.5%, reaching 77.0% for the whole part of study. The analysis of variance showed statistically significant differences of hormonal levels in individual boars in which the fluctuation of testosterone was studied in the 8- to 32-hour period as well as in several days' period. This proved the role of the animals' individuality in determining the concentration of testosterone in their blood. The discussion concerns the importance of these findings for the evaluation of the role of basal testosterone levels in the blood in classifying the incretion function of the gonads and in the diagnosis of incretion hypogonadism of boars.

Age Factors↗
PubMed1978

[Effect of bilateral orchidectomy on serum testosterone levels in boars].

Bilateral orchidectomy caused a marked decrease in the concentration of testosterone in the bood plasma of boars already in the early post-castration stage of three hours after the operation. In the period from 3 to 207 days after castration, the pre-operation levels of plasma testosterone decrease by 84.4%, on an average. Adreno-cortical compensation of the concentration of the hormone did not occur in the post-castration period. The conclusion is that the levels of testosterone in the blood of boars are mostly of testicular origin and can be considered as the main criterion of the incretion function of the testes. The discussion concerns the practical importance of the determination of testosterone levels in the blood of boars for clinical evaluation of the hormonal function of the testes and for diagnostics of incretion hypogonodism.

Animals↗
PubMed1977

Phosphate control and 25-hydroxycholecalciferol administration in preventing experimental renal osteodystrophy in the dog.

Previous studies from this laboratory demonstrated that secondary hyperparathyroidism in dogs with chronic renal disease may occur, at least in part, as a consequence of the need for progressive adaptation in renal phosphorus (P) excretion that occurs as glomerular filtration rate falls. However, the studies were of relatively short duration. Moreover, no information emerged regarding a potential role of calcium malabsorption in the pathogenesis of secondary hyperparathyroidism. The short duration of the protocol did not lend itself to the study of the effect of P control or the administration of vitamin D in the pathogenesis of renal osteodystrophy. In the present studies, 14 dogs with experimental chronic renal disease were studied serially for a period of 2 yr. Each animal was studied first with two normal kidneys on an intake of P of 1,200 mg/day. Then, renal insufficiency was produced by 5/6 nephrectomy. The dogs then were divided into three groups. In group I, 1,200 mg/day P intake was administered for the full 2 yr. In group II, P intake was reduced from the initial 1,200 mg/day, in proportion to the measured fall in glomerular filtration rate, in an effort to obviate the renal adaptation in P excretion. In group III, "proportional reduction" of P intake also was employed; but in addition, 20 mug of 25(OH)D(3) were administered orally three times a week. In group I, parathyroid hormone (PTH) levels rose throughout the 2-yr period reaching a final concentration of 557+/-70 U (normal 10-60). In group II, values for PTH remained normal throughout the 1st yr, increased modestly between the 12th and the 18th mo, but then did not rise after the 18th mo. In group III, no elevation of PTH levels was observed at any time; however, these animals were hypercalcemic. Histomorphologic analyses of the ribs of these dogs were performed serially throughout the 2-yr period. A linear relationship was obtained between the osteoclastic resorption surface and the concentration of circulating immunoreactive PTH. The osteoid volume was greater in group I animals when compared to those in group II. None of the morphologic abnormalities associated with renal osteodystrophy were observed in the animals in the third group.

Animals↗
PubMed1977

Ischemic bowel disease following bilateral nephrectomy or renal transplant.

In a 2 year period five patients developed pathologically proved ischemic bowel disease (IBD) following either renal transplantation or bilateral nephrectomy in preparations for transplantation. This entity accounted for 42% of all major gastrointestinal complications in this transplant unit. Three patients presented with abdominal pain and ileus, and two patients developed massive lower gastrointestinal hemorrhage. All five patients had nonocclusive ischemic disease because obstruction of a major intestinal vessel could not be documented in any case. Each patient was treated with bowel resection and three of the five patients survived. Although sepsis, shock, and large doses of immunosuppressive drugs have been implicated in predisposing such patients to IBD, these factors were not uniformly present in our cases. Blood volume redistribution with transient episodes of hypotension, especially during postoperative hemodialysis, may be significant. IBD in uremic patients can occur in the presence or absence of renal transplantation and may be the cause of massive intestinal hemorrhage in these individuals.

Adult↗
PubMed1977

Hyperphosphatemia.

Serum phosphorus concentrations are maintained within narrow limits in humans. In the extracellular fluid most of the phosphorus is present in the inorganic form and at the level of the glomerulus greater than 90% of PO4 is ultrafilterable. The kidney plays a key role in PO4 homeostasis. Micropuncture experiments have demonstrated that 60 to 70% of the filtered PO4 is reabsorbed in the proximal tubule; however, there is evidence that a significant amount of PO4 is reabsorbed in the distal tubule. Phosphate secretion probably plays a minor role in the overall renal regulation of phosphate. In normal individuals the amount of PO4 ingested plays a key role in the amount that ultimately will be excreted in the urine. The reabsorption of PO4 along the nephron is regulated by a series of factors of which parathyroid hormone is the most important one. Hyperphosphatemia is seen frequently in clinical medicine and by far, the most common cause is a decrease in urinary PO4 excretion secondary to renal failure. From the practical point of view, the most effective way to treat hyperphosphatemia is to decrease PO4 absorption in the GI tract by the use of PO4 binders.

Acromegaly↗
PubMed1976

Selective uptake of intact parathyroid hormone by the liver: differences between hepatic and renal uptake.

Hepatic and renal extraction of immunoreactive parathyroid hormone (i-PTH) was studied in awake dogs with explanted kidneys and chronic indwelling hepatic vein catheters. After a single injection of bovine PTH 1-84 (b-PTH 1-84), hepatic arteriovenous (A-V) differences for immunoreactive PTH (i-PTH) was 39% at 2 min after injection but decreased to 0% by 25 min, despite high levels of i-PTH in the arterial circulation. Gel filtration of arterila and hepatic venous samples obtained when hepatic A-V differences for i-PTH were demonstrable revealed hepatic uptake of the intact hormone and addition of a smaller COOH-terminal fragment, eluting just after the intact hormone, to the hepatic venous blood. Gel filtration of samples obtained 20-30 min after injection of b-PTH was demonstrable) revealed no detectable intact hormone in the circulation. Levels of COOH-terminal fragments of the hormone at the time were identical in arterial and hepatic venous samples. In additional experiemtns no hepatic A-V difference was observed after the injection of the synthetic bovine PTH 1-34 (syn b-PTH 1-34). By comparison there was a demonstrable A-V difference of 20% across the kidney for both intact PTH and COOH-terminal fragments that persisted until i-PTH disappeared from the circulation. The kidney also demonstrated an A-V difference of 22% after injection of syn b-PTH 1-34. These studies demonstrate selective extraction of intact PTH but not of its fragments by the liver. The kidney, on the other hand, extracted the intact hormone and both COOH and NH2 terminal fragments. The studies demonstrate that the kidney was the only organ of those examined that detectably removed the fragments of PTH from the circulation.

Animals↗
PubMed1976

[Concentration of testosterone in the blood of sexually immature boars after stimulation with chorionic gonadotropin].

Levels of testosterone concentration in blood increased significantly in sexually immature boars after application of chorionic gonadotropin. Existence of considerable function reserve and readines of the incretion component of gonads were proved in sexually immature boars. The paper discusses a possibility of utilizing this phenonmenon in diagnostics of disorders of the incretion testicular function in individuals of the animal species under study in their pre-puberal age.

Animals↗
PubMed1975

Effect of 25-hydroxycholecalciferol on calcium absorption in chronic renal disease.

Calcium absorption was measured in eight uremic patients before and after eight days of treatment with 100 or 500 mug of 25-hydroxycholecalciferol (25(OH)D3) per day. Fractional calcium absorption was estimated by administering 47Ca i.v. and orally on separate days and counting forearm radioactivity four hours later. Calcium absorption in four patients with residual renal function rose from 16.3 +/- 2.5 to 40.8 +/- 5.5% after treatment. In order to determine if the increased calcium absorption was mediated by an increase in the production of 1,25-dihydroxycholecalciferol (1,25(OH)2D3) by virtue of increased substrate delivery to the 25-hydroxycholecalciferol-1-hydroxylase system present in the residual renal tissue, identical studies were performed in four anephric patients. Calcium absorption in these patients averaged 15.7 +/- 2.2% during the control period and rose to 46.0 +/- 11.1% after treatment. Increments in serum calcium after treatment were similar in both groups of patients; the mean concentration rose from 9.6 +/- 0.3 to 11.0 +/- 0.6 mg/100 ml. The results indicate that 25(OH)D3 can improve calcium absorption in the absence of renal tissue suggesting that its conversion to 1,25(OH)2D3 may not be necessary for its effect on the gastrointestinal tract in the uremic patient.

Absorption↗