Acute and chronic cardiovascular adjustments to induced anemia in dogs

Neill, W.A.; Oxendine, JM; Moore, SC

doi:10.1152/ajplegacy.1969.217.3.710

Cited by 21 publications

(2 citation statements)

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“…Investigations of the effects of acute normovolemic anemia induced by blood loss ( i.e ., without concomitant hemolysis) on cardiovascular hemodynamics were started almost 50 years ago by Fowler et al (62), Murray and Rapaport (136), and Neill et al (138). They showed that blood loss in healthy dogs increased heart rate, stroke volume, and cardiac output and decreased mean arterial pressure and systemic vascular resistance.…”

Section: Rbc Dysfunction and Anemiamentioning

confidence: 99%

Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia

Kuhn

Diederich

Keller

et al. 2017

Antioxidants & Redox Signaling

335

250

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Significance: Recent clinical evidence identified anemia to be correlated with severe complications of cardiovascular disease (CVD) such as bleeding, thromboembolic events, stroke, hypertension, arrhythmias, and inflammation, particularly in elderly patients. The underlying mechanisms of these complications are largely unidentified.Recent Advances: Previously, red blood cells (RBCs) were considered exclusively as transporters of oxygen and nutrients to the tissues. More recent experimental evidence indicates that RBCs are important interorgan communication systems with additional functions, including participation in control of systemic nitric oxide metabolism, redox regulation, blood rheology, and viscosity. In this article, we aim to revise and discuss the potential impact of these noncanonical functions of RBCs and their dysfunction in the cardiovascular system and in anemia.Critical Issues: The mechanistic links between changes of RBC functional properties and cardiovascular complications related to anemia have not been untangled so far.Future Directions: To allow a better understanding of the complications associated with anemia in CVD, basic and translational science studies should be focused on identifying the role of noncanonical functions of RBCs in the cardiovascular system and on defining intrinsic and/or systemic dysfunction of RBCs in anemia and its relationship to CVD both in animal models and clinical settings. Antioxid. Redox Signal. 26, 718–742.

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Section: Rbc Dysfunction and Anemiamentioning

confidence: 99%

Red Blood Cell Function and Dysfunction: Redox Regulation, Nitric Oxide Metabolism, Anemia

Kuhn

Diederich

Keller

et al. 2017

Antioxidants & Redox Signaling

335

250

View full text Add to dashboard Cite

show abstract

“…These mechanisms maintain tissue oxygen supply and consumption constant, unless the hemoglobin concentration is reduced to less than one third of the normal value [7]. The two most important adaptive mechanisms are increased oxygen extraction from hemoglobin molecules and an elevation in cardiac output.…”

Section: Physiological Backgroundmentioning

confidence: 99%

Target Hemoglobin in Patients with Renal Failure

Eckardt¹

2001

Nephron

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15 years after recombinant erythropoietin (EPO) has become available for the treatment of renal anemia, the target hemoglobin concentration to be achieved is still controversial. A positive impact of partial correction of renal anemia on quality of life has been conclusively demonstrated. Several more recent studies indicate that further improvement of well-being can be achieved with normalization of hemoglobin levels. In addition, there is increasing evidence that anemia is associated with the progression of left-ventricular hypertrophy and mortality. These findings imply that correction of renal anemia has the potential to improve patient prognosis. However, in patients with advanced cardiac disease, the US normal hematocrit failed to demonstrate a prognostic benefit and instead suggested that the attempt to normalize hemoglobin may be harmful. Nevertheless, in patients with less advanced cardiac disease complete correction of renal anemia may prevent progressive ventricular dilatation. The impact of early anemia correction is currently tested in several trials in predialysis patients. Irrespective of the uncertainities about the upper target range, current US and European guidelines have defined a hemoglobin concentration of 11 g/dl as the lower target range on the basis of both symptomatic and prognostic considerations. In the majority of patients these minimum requirements are not yet achieved. Less then 10% of patients receive EPO prior to the onset of dialysis, the mean hemoglobin level at the start of dialysis is not higher than 9 g/dl and a significant proportion of patients permanently remain below 11 g/dl.

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