Cerebral Circulation and Metabolism in Sickle Cell and Other Chronic Anemias, With Observations on the Effects of Oxygen Inhalation 1

Heyman, Albert; Jl, Patterson; Tw, Duke

doi:10.1172/jci102668

Cited by 78 publications

(13 citation statements)

References 11 publications

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“…[22][23][24] The present study throws doubt on this suggestion, which was based on the finding of low cerebral blood flow in patients with polycythaemia who have high whole blood viscosity22 25 26 and conversely high cerebral blood flow in anaemic patients with low whole blood viscosity.4 27 The present results similarly do not support the suggestion that the generalised increase in cerebral blood flow produced by therapeutic haemodilution is due mainly to a reduction in visCoSity. 28 29 The mean whole blood viscosities in this study after plasma exchange were equivalent to the viscosity of blood with normal plasma viscosity and a haemoglobin concentration of approximately 10 g/dl and were therefore below those normally achieved by therapeutic haemodilution and similar to those found in mild anaemia.…”

Section: Discussioncontrasting

confidence: 69%

Effect of plasma exchange on blood viscosity and cerebral blood flow.

Brown¹,

Marshall²

1982

BMJ

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The effects of plasma exchange using a low viscosity plasma substitute on blood viscosity and cerebral blood flow were investigated in eight subjects with normal cerebral vasculature. Plasma exchange resulted in significant reductions in plasma viscosity, whole blood viscosity, globulin and fibrinogen concentration without affecting packed cell volume. The reduction in whole blood viscosity was more pronounced at low shear rates suggesting an additional effect on red cell aggregation. Despite the fall in viscosity there was no significant change in cerebral blood flow. The results support the metabolic theory of autoregulation. Although changes in blood viscosity appear not to alter the level of cerebral blood flow under these circumstances, plasma exchange could still be of benefit in the management of acute cerebrovascular disease.

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Section: Discussioncontrasting

confidence: 69%

Effect of plasma exchange on blood viscosity and cerebral blood flow.

Brown¹,

Marshall²

1982

BMJ

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“…Calculations based on our data indicate that the oxygen transport to the tissues (cardiac index times total systemic arterial oxygen content) increased by 5% during oxygen breathing, despite a reduction in cardiac index of 14%. It is probable that the benefits of oxygen breathing will be greatest when anemia is severe; the extra amount of oxygen that can be put into solution by breathing 100% oxygen approximately equals the oxygen carried by 1 g of hemoglobin, or oxygen administration can increase the total oxygen content Cifculation, Volume XL, October 1969 of systemic arterial blood by 25 to 35% when the hemoglobin level is below 4 g/100 ml blood. The benefits of oxygen administration are also likely to be greater in Denver (altitude 5,300 feet) than at sea level, since at this altitude during air breathing, hemoglobin is less saturated with oxygen than at sea level.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Responses to Oxygen Breathing in Children with Severe Anemia

Cropp

1969

Circulation

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Hemodynamic responses to 100% oxygen inhalation were examined in seven anemic children (hemoglobin 1.9 to 3.8 g/100 ml blood; hematocrit 9 to 14%). During air breathing mean values for cardiac index were 7.71 L/min/m2, for heart rate 129/min, for stroke index 61.7 ml/m2, and for systemic vascular resistance 11.5 R.U. Oxygen administration significantly decreased mean values of cardiac index to 6.61 L/min/m2, of heart rate to 119/min and of stroke index to 56.6 ml/m2, and increased mean systemic vascular resistance to 14.2 R.U. Oxygen breathing raised systemic oxygen content 23% and oxygen transport 5%, despite decreases in cardiac ouput. Since oxygen breathing did not change the hematocrit (and thus viscosity), the increase in vascular resistance indicates active vasoconstriction. It is postulated that in anemia tissue hypoxia causes vasodilation of systemic resistance vessels. When anemia is not severe, baroreceptor reflexes prevent significant reductions in blood pressure and systemic vascular resistance by compensatory, neurogenic vasoconstriction. When anemia becomes severe and vasodilation extreme, blood pressure is maintained by an increase in cardiac output. Cardiac output is elevated by decreased vagal inhibition and increased myocardial contractility, which cause tachycardia and increased stroke volumes respectively.

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“…In addition, Edgerton et al [37] established a significant reduction of spontaneous physical activity in rats with less than 11 g% hemoglobin. This phenomenon, which seems particularly noteworthy because it may mask the reduced exercise tolerance in anemic subjects, might be due either to the lower endurance limits of anemic muscle [37], to the curtailment of cerebral oxygen consumption by anemia [50], or to both of these factors.…”

Section: General Circulation and Oxygen Transportmentioning

confidence: 99%

Section: Exercise Tolerancementioning

confidence: 99%

“…A constant oxygen extraction in vol% low ers endcapillary and cerebral venous oxygen saturation and tension and triggers an in crease of flow [50]. Despite this increase, which commences at hematocrit levels around 30% in man [96,101], the oxygen consumption of the brain is significantly de pressed in patients with < 10 g% hemo globin [50], The distribution of cerebral blood flow becomes abnormal even above this level [101]. Anemia and the well-known cerebral vasoconstriction under hyperventi lation are additive factors in reducing oxy gen consumption [89], and the cerebral ef fects of anemia and hypotension potentiate CO, l/m!n [118].…”

Section: Exercise Tolerancementioning

confidence: 99%

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Hemodilution - New Clothes for an Anemic Emperor

Lundsgaard-Hansen¹

1979

Vox Sanguinis

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This review deals with the rationale for the use of hemodilution in patients not subjected to open heart surgery. The claim for an optimum of circulatory oxygen transport at 30% hematocrit has been disproved; hemodilution thus simply means acute normovolemic anemia. Accordingly, it generates a cardiovascular strain and particularly jeopardizes cerebral and myocardial oxygen supply. Potentially serious clinical side effects have been reported. Hemodilution should therefore not be carried beyond the lower normal range for the hemoglobin or hematocrit level, i.e. 12-12.5 g% or 35-36%.

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Cerebral Circulation and Metabolism in Sickle Cell and Other Chronic Anemias, With Observations on the Effects of Oxygen Inhalation 1

Cited by 78 publications

References 11 publications

Effect of plasma exchange on blood viscosity and cerebral blood flow.

Effect of plasma exchange on blood viscosity and cerebral blood flow.

Hemodynamic Responses to Oxygen Breathing in Children with Severe Anemia

Hemodilution - New Clothes for an Anemic Emperor

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