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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular responses have been studied in baboons, after total exchange transfusion with hemoglobin solutions having various P50 values. At the end of the exchange transfusion, the hematocrit was 1.5%, the mean hemoglobin concentration was 4.4 g/dl, and the P50 varied between 12 and 26 mm Hg. Cardiac output did not change during the study, although heart rate increased, and stroke volume and MAP decreased. Hemoglobin concentration, per se, does not appear to be the critical stimulus for an increase in cardiac output with hemoglobin solution. In addition, the position of the hemoglobin-oxygen dissociation curve does not appear to influence these hemodynamic responses. The physiological response to anemia in the presence of hemoglobin solution appears different from that observed in the absence of plasma O2 carriers.
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PMID:Cardiac output response to extreme hemodilution with hemoglobin solutions of various P50 values. 11 94

Results from animal experiments have suggested that treatment with recombinant human erythropoietin (rHuEPO) causes changes in renal hemodynamics which are detrimental to renal function. Therefore, the effects of correction of the anemia by rHuEPO on glomerular filtration rate (GFR; inulin clearance) and effective renal plasma flow (ERPF; PAH clearance) were studied in eight pre-dialysis patients. The studies were done before (Hct 0.24 +/- 0.05 liter/liter) and at 89 +/- 19 days after the start of rHuEPO therapy (Hct 0.39 +/- 0.03 liter/liter). To further evaluate the effects of ACE inhibition, 25 mg of captopril was given orally after baseline values had been obtained. Baseline GFR, renal blood flow (RBF) and filtration fraction (FF) did not change during rHuEPO therapy. At low hematocrit (Hct) captopril induced a significant increase in ERPF and RBF, and a decrease in MAP. After correction of the hematocrit the blood pressure lowering effect of captopril remained unchanged. However, captopril no longer induced changes in ERPF and RBF. We conclude that the increase in hematocrit had no adverse effects on GFR. The results suggest that changes in hematocrit may influence the effects of ACE inhibition on efferent vascular resistance. Therefore, the hematocrit should be taken into account when evaluating studies on the effects of ACE inhibition in the progression of chronic renal failure.
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PMID:Evidence for renal vasodilation in pre-dialysis patients during correction of anemia by erythropoietin. 155 11

The results of 8 to 12 weeks of treatment of the anemia of uremia with rHuEPO in patients with chronic renal failure and uremia are: a sustained increased hematocrit; increased RBC mass, and subsequent increased MAP; and increased TPRI. The observed trends of decreased LVEF, and echo Doppler evidence of a trend toward LV systolic and diastolic dysfunction, although not individually statistically significant, represent 3 separate evaluation techniques coupled with hypertension and TPRI increase during administration of rHuEPO to increase the hematocrit and packed red blood cell volume in patients with chronic renal failure and anemia. Increased TPRI and hypertension associated with correction of uremic anemia vasodilation and the increased blood viscosity have been noted in earlier investigations with transfusions. The hypertension and elevated TPRI demonstrated during rHuEPO therapy in patients with progressive chronic renal failure associated with increased hematocrit, and the trends toward systolic and diastolic cardiac dysfunction are noted herein. These changes were associated with the combined increase of packed RBC mass and plasma volume in this study. The natural progressive course of worsening of renal function exhibited by these patients could have limited their ability to regulate plasma volume, making them vulnerable to volume-dependent hypertension and a significant preload adding to potential cardiac dysfunction in addition to the increased TPRI.
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PMID:Cardiovascular hemodynamic effects of correction of anemia of chronic renal failure with recombinant-human erythropoietin. 205 68

We examined the cardiovascular and metabolic response to RBC transfusion in patients with circulatory shock after volume resuscitation. Data were analyzed from 36 transfusions in 32 patients who were undergoing continuous hemodynamic monitoring. Transfusions were administered for moderate to severe anemia, mean Hgb 8.3 g/dl. The diagnosis were sepsis (19/36), cardiogenic shock (14/36), connective tissue disease (2/36), and severe hypocalcemia (1/36). Benefit from transfusion was defined as an improvement in tissue oxygen utilization (increased oxygen consumption [VO2] or decreased lactate), a decrease in myocardial VO2 (MAP x HR), or a decrease in myocardial work (left ventricular work index). Mean transfusion volume was 577 ml over 4.5 h. Hgb and oxygen delivery (DO2) increased by 27% and 28%, respectively, while pulmonary artery wedge pressure and cardiac index were unchanged. No significant change was noted in VO2, or lactate, after augmentation of red cell mass. An increase occurred in myocardial work indices and MAP x HR. No changes were identified when subgroups were analyzed based on diagnosis, pretransfusion Hgb, lactate, or VO2 levels. We conclude that selective increase in DO2 by augmentation of RBC mass and oxygen-carrying capacity did not improve the shock state in these volume-resuscitated patients, regardless of the etiology of the shock.
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PMID:Cardiovascular and metabolic response to red blood cell transfusion in critically ill volume-resuscitated nonsurgical patients. 239 7

Slow progressive improvement of renal anemia from 21 up to 33% hematocrit by rhEPO treatment results in an increase of tissue oxygenation as indicated by a rise of the transcutaneous oxygen pressure. In normotensive patients this was accompanied by an increase in MAP (delta 6 mm Hg) within the normal range and a significant fall of the regional blood flow. These hemodynamic changes are caused by increases of the regional and presumably also of the total peripheral vascular resistance. Most likely the increase in total peripheral vascular resistance represents an autoregulatory event triggered by the rising tissue oxygenation. From the present data it is difficult to estimate to what extent the observed rise in hematocrit affects peripheral vascular resistance also via an increase of blood viscosity.
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PMID:Effect of treatment with recombinant human erythropoietin on peripheral hemodynamics and oxygenation. 329 47

In 74 chronic glomerulonephritis (CGN) and 13 hemodialysis patients (HD) blood volume and hemodynamic indices were examined. Significant correlation was observed between MPA and PV in CGN. High PV in high S-Cr group is considered to be correlated with anemia. Salt restriction reduced MAP without the change in BV in the impaired kidney function group in CGN. Volume depletion in HD shifted TPRI to lower level in the group with significant MAP reduction. The results indicate that sodium rather than water will play an important role in this type of hypertension.
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PMID:Hypertension in chronic glomerulonephritis. 675 Jan 90

Anemia, through a hyperkinetic state, is an important contributor to myocardial function impairment. To determine the cardiovascular effects of recombinant human erythropoietin (rHuEPO) therapy, 10 chronic peritoneal dialysis (CPD)-treated anemic children were studied before and during 18 months of treatment. The following parameters were recorded: hemoglobin (Hb) [percent of target level (TL) = x-2 standard deviations of normal Hb values for age and sex], heart rate (HR, beats/minute), mean arterial pressure (MAP, mmHg), end-diastolic left ventricular diameter (EDLVD, mm/sm BSA), shortening fraction (SF, percent), and interventricular septal thickness (IVS, mm/sm BSA). Student's t-test for paired data showed (vs time before treatment, T0) a progressive increase in Hb, a progressive decrease in HR, and a progressive increase in MAP. EDLVD progressively decreased, while SF and IVS remained unchanged throughout the study. Regression analysis showed a close correlation between anemia correction and decrease of HR (p < 0.01), while no correlation was found between Hb and EDLVD or SF, IVS, or MAP. Our data indicate that anemia correction in these patients is mainly associated with a decrease in hyperkinetic state (HR reduction with SF unvaried), while left ventricular function and dimensions remain normal, despite an increase in MAP.
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PMID:Cardiovascular function in a chronic peritoneal dialysis pediatric population on recombinant human erythropoietin treatment. 839 85

We report a case of transfusion-associated graft-versus-host disease (GVHD). A 79-year-old woman with Hodgkin's disease, respiratory failure and severe anemia who had been treated with two courses of chemotherapy was transfused with red cell concentrate (MAP-CRC) and fresh frozen plasma (FFP) in the ICU. On the 7-9th days after transfusion, she developed a diffuse erythematous rash mainly on the chest, high fever, liver dysfunction and thrombocytopenia. Despite treatment with immunoglobulin products and methylprednisolone, her condition deteriorated rapidly, and she died of multiple organ failure on the 7th day after appearance of rash. Skin biopsy demonstrated typical features of acute GVHD, suggesting that MAP-CRC-associated GVHD had occurred.
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PMID:[A case of graft-versus-host disease following red cell concentrate (MAP-CRC) transfusion]. 852 63

Ten normotensive hemodialysis patients with severe anemia participated in the study. Human recombinant erythropoietin (rHuEpo) was administered i.v. 3 times a week in doses of 50 U/kg of body weight. During 12 weeks of observation, the mean hematocrit value increased from 19%, before start of therapy, to 32%. Simultaneous monitoring of serum plasma noradrenaline (NA) concentration showed an elevation from 202 to 281 pg/ml. An increase of NA concentration after a cold pressure stimulating test (CP) was not statistically significant after as compared to before treatment, but became statistically significant after 12 weeks of rHuEpo therapy (281 pg/ml before to 441 pg/ml after CP test, p < 0.01). The mean arterial blood pressure increased from 92 - 109 mmHg after 12 weeks of rHuEpo therapy (p < 0.001). We have demonstrated significantly increased NA blood concentrations after 12 weeks of rHuEPO therapy in normotensive patients, which correlated with increased MAP. This may suggest that the observed increase of noradrenaline concentration as a vasoactive substance after the CP test may contribute to hypertension during rHuEPO therapy.
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PMID:Effect of recombinant human erythropoietin on adrenergic activity in normotensive hemodialysis patients. 1152 86

The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway is an essential cascade for mediating normal functions of different cytokines in the development of the hematopoietic and immune systems. Chronic exposure to arsenic has been found to cause immunotoxicity and has been associated with the suppression of hematopoiesis (anemia and leukopenia). Here, we report the novel finding of arsenic-mediated inactivation of the JAK-STAT signaling pathway by its direct interaction with JAK tyrosine kinase. Pretreatment with sodium arsenite strongly inhibited IL-6-inducible STAT3 tyrosine phosphorylation in HepG2 cells and did not affect its serine phosphorylation. As a result, sodium arsenite completely abolished STAT activity-dependent expression of suppressors of cytokine signaling (SOCS). Both cellular and subcelluar experiments showed that the inhibition of JAK-STAT signaling resulted from JAK tyrosine kinase's direct interaction with arsenite, and that arsenic's suppression of JAK tyrosine kinase activity also occurred in the interferon gamma (IFNgamma) pathway. The ligand-independent inhibition by arsenic indicates that JAK was the direct target of arsenic action. Other inflammatory stimulants, stress agents, and metal cadmium failed to induce similar effects on the tyrosine phosphorylation of STAT3 as arsenic does. Our experiments also revealed that arsenic inactivation of the JAK-STAT pathway occurred independent of arsenic activation of MAP kinases. Taken together, our findings indicate that arsenic directly inhibits JAK tyrosine kinase activity and suggest that this direct interference in the JAK-STAT pathway may play a role in arsenic-associated pathogenesis.
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PMID:Arsenic inhibition of the JAK-STAT pathway. 1511 95


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