Search PubMed⌕ Search

Biomedical subjects

J Caro

Publications and source records attributed to J Caro.

119 records · Page 7Linked to original sources
PubMed1981

Erythropoietin production in fasted rats. Effects of thyroid hormones and glucose supplementation.

The effect of T3 replacement and glucose supplementation on erythropoietin production was investigated in fasted hypoxic rats. It was found that 48 hr of fasting significantly reduced the circulating levels of thyroid hormones and the production of renal and extrarenal erythropoietin in response to hypoxia. These effects of fasting were completely abolished when the animals had free access to 25% glucose solution as drinking water, despite their lack of protein intake. Replacement doses of T3 (0.5 micrograms/100 gm per day) restored erythropoietin production in the fasted animals but also increased the response of the fed controls. To avoid the effect of endogenous T3, the experiments were repeated in thyroidectomized rats. Erythropoietin production in athyroid rats was found to be markedly decreased, with values equivalent to those found in normal fasted animals, and were not affected by fasting or glucose supplementation. Replacement doses of T3 increased erythropoietin production in all three groups, but the fasted animals needed five times as much T3 to obtain a response similar to that observed in the fed group. Glucose supplementation enhanced the effect of T3 in the fasted animals but did not completely restore it. These results indicate that caloric deprivation is primarily responsible for the decreased erythropoietin production induced by fasting and that this effect is probably mediated by both a decreased level of T3 and a decreased responsiveness to it.

Acid-Base Equilibrium↗
PubMed1980

Spontaneous increase in erythropoietin and hematocrit value associated with transient liver enzyme abnormalities in an anephric patient undergoing hemodialysis.

An anephric patient undergoing hemodialysis experienced an increase in his hematocrit value (19 +/- 1 per cent to 31 +/- 1 per cent) as a result of increased erythropoiesis (reticulocyte count 1.8 per cent to 7.4 per cent). This increase occurred in concert with an elevation of the patient's liver enzyme levels and was maintained for four months. The hematocrit value returned to its base line only after the liver function tests showed improvement. During the period when the hematocrit value was increasing, the circulating level of erythropoietin was elavated to 71.0 mU/ml--a level higher than that seen in either anephric or nephric patients undergoing dialysis. When the hematocrit value and liver enzyme levels had returned to their base line values, the erythropoietin level was 4.3 mU/ml--a level in the range seen in anephric patients undergoing dialysis. The observations in this patient suggest that under certain circumstances, the liver can produce erythropoietin in the anephric patient; and, more importantly, that the bone marrow of at least some uremic patients is capable of responding to the endogenous erythropoietin.

Bone Marrow↗
PubMed1980

Renal and extrarenal erythropoietin production in anaemic rats.

Rats were rendered anaemic by a single bleeding or by a single injection of phenylhydrazine. At various times after the onset of anaemia they were nephrectomized and challenged with a 6 h exposure to hypoxia. The erythropoietin titre observed at the end of this hypoxic period was corrected for renal erythropoietin induced by the anaemia alone, and the resulting extrarenal component was compared to total erythropoietin production of nephric rats in response to anaemia plus 6 h hypoxia. Extrarenal erythropoietin production was found to increase from 10.3% in normal rats to 12.5% in moderately anaemic rats to 15.1% in rats with severe bleeding anaemia. In phenylhydrazine-treated rats this extrarenal component was found to be 18.3% possibly due to stimulation of extrarenal erythropoietin by haemolysed red cells. Chronic phenylhydrazine administration resulted in splenomegaly and Kupffer cell hyperactivity but not in any further stimulation of extrarenal erythropoietin production.

Anemia↗
PubMed1980

The biogenesis of erythropoietin.

Aerobic living demands a constant supply of oxygen at the cellular mitochondrial level. Numerous interlocking feedback mechanisms insure the constancy of this supply by adapting the supply lines to changes in the intra and extracellular milieu. Among these mechanisms is the feedback circuit which, triggered by an intracellular decrease in oxygen supply, initiates the production of a polypeptide hormone, erythropoietin, which in turn augments the production of an oxygen carrier, the hemoglobin-containing red cell. The biogenesis of this hormone is an important biologic process which is being studied intensively and slowly unravelled.

Animals↗
PubMed1979

Plasma erythropoietin in polycythemia.

Erythropoietin titers of plasma cannot be used to differentiate polycythemia vera from secondary polycythemia since the limit of sensitivity of our current bioassay technics is 50 mU, considerably higher than levels found in normal subjects and in patients with polycythemia. However, erythropoietin is relatively heat stable, and since abundant plasma is available from therapeutic phlebotomies it is possible to prepare and assay highly concentrated, erythropoietin-containing extracts. In 35 normal subjects, erythropoietin levels ranged from less than 5 mU/ml (the limit of sensitivity) to 18 mU/ml with a mean of 7.8 mU/ml. In 21 patients with proved polycythemia vera, the levels were less than 5 mU/ml in all. In 41 patients with suspected secondary polycythemia or polycythemia of unknown origin, the levels ranged from less than 5 to 3,000 mU/ml. Three of the 11 patients with levels less than 5mU/ml were subsequently shown to have polycythemia vera. These results suggest that this refinement of the routine bioassay for erythropoietin may be of clinical importance in the differential diagnosis of polycythemia.

Erythropoietin↗
PubMed1979

Are the native kidneys responsible for erythrocytosis in renal allorecipients?

The development of erythrocytosis following renal transplantation has been reported to be caused by a number of factors. These include acute and chronic rejection, hydronephrosis and renal artery stenosis. In this study, seven patients were noted to have erythrocytosis with hematocrits ranging between 53.5 and 66%. Serum erythropoietin levels were elevated and ranged between 11 and 60 mU/ml with a mean of 31.9 mU/ml in six of seven patients. Selective catheterization of veins of native and transplanted kidneys in three patients revealed mean serum levels of 40.9 and 13.0 mU/ml, respectively. This suggests that excess erythropoietin is being produced from the diseased native kidneys. Bilateral nephrectomy in one patient cured erythrocytosis and dropped systemic levels of erythropoietin (EP) to 6.1 mU/ml. In four of the remaining five patients, hematocrits came down spontaneously to within normal over a 1- to 3-year period. Consequently, it appears that in a number of transplant patients the retained diseased kidneys, having lost all excretory and concentrating function, may remain capable of functioning as endocrine erythropoietin-producing organs.

Erythropoietin↗
PubMed1979

Erythropoietin levels in uremic nephric and anephric patients.

Erythropoietin titers were measured in anemic nephric and anephric patients undergoing chronic hemodialysis by utilizing a plasma concentration technique. In eight out of 11 anephric patients studied, decreased but detectable levels of erythropoietin were found, suggesting that extrarenal erythropoietin plays a role in the regulation of red cell production in anephric patients. In 14 nephric uremic patients, erythropoietin production was found to be more variable, with one group of eight patients having erythropoietin levels in the range for normal nonanemic individuals (3.9 to 15 mU/ml), and a second group of six patients with erythropoietin higher than normal (greater than 15 mU/ml). Both groups were found to be equally anemic, indicating that in the second group the bone marrow is less responsive to erythropoietin. The severity of secondary hyperparathyroidism was found to be higher in this second group, suggesting a role of PTH in the bone marrow unresponsiveness. A good correlation between biological and immunological erythropoietin activities was found in the plasma from normal subjects and uremic nephric and anephric patients.

Animals↗
PubMedDate not supplied

Plasma erythropoietin in health and disease.

Erythropoietin is a hormone produced by the kidneys and by certain extrarenal tissues and released into the circulation in response to tissue hypoxia. Its study has provided new information about oxygen transport and bone marrow stem cell function and its determination in plasma can give valuable diagnostic clues as to the etiology and pathogenesis of anemias and polycythemias. The various methods used for such measurements are discussed, and it is recommended that the in vivo bioassay in polycythemic mice be utilized until a workable radioimmune assay has been perfected. The results with the use of this in vivo bioassay to measure plasma erythropoietin in patients with uncomplicated anemia, aplastic anemia, anemia of renal disease, anemia of chronic inflammatory or neoplastic disorder polycythemia vera, and secondary polycythemia are charted and their diagnostic significance discussed.

Anemia↗