Observations During Hypervolemic Hemodilution of Patients With Acute Focal Cerebral Ischemia

Wood, James H.

doi:10.1001/jama.1982.03330220043034

Cited by 77 publications

(15 citation statements)

References 46 publications

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“…16 The in vitro viscosity measurements do not take into account, however, an important denominator of blood viscosity in vivo, i.e., erythrocyte deformability. Although it has been shown that mannitol reduced blood viscosity probably at least in part by enhancing erythrocyte deformability,' 7 it is not known how much this effect contributes to the in vivo viscosity decrease. Similarly, it is unknown whether the "rebound" increase of blood viscosity at 75 minutes postmannitol is accompanied by a decrease in erythrocyte deformability, which would result in a larger blood viscosity increase in vivo than we have measured in vitro.…”

Section: Discussionmentioning

confidence: 99%

Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.

Muizelaar¹,

Wei²,

Kontos³

et al. 1986

Stroke

133

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SUMMARY There is still considerable controversy regarding the influence of blood viscosity upon CBF. We have measured CBF with microspheres in 23 cats. Autoregulation was disturbed in the left caudate nucleus by microsurgical occlusion of the left middle cerebral artery. Induced hypertension or hypotension was used and i.v. mannitol (1 g/kg) administered. In all cats blood viscosity decreased an average of 16% at 15 minutes and, in 16 cats, increased 10% at 75 minutes post-mannitol. CBF in the right caudate was 79 ± 6 ml/lOOg/min, in the left 38 ± 6 (p < 0.001). Only minor changes of CBF occurred in areas with presumed normal autoregulation, including the right caudate, in conjunction with pressure or viscosity changes. In the left caudate CBF decreased 21% with hypotension and 18% with higher viscosity, more than on the right (p < 0.01 and p < 0.2, respectively). CBF increased in the left caudate 56% with hypertension and 47% with lower viscosity, again much more than on the right ( p < 0.001 and p < 0.01, respectively). In the other area which is (nearly) exclusively supplied by the middle cerebral artery of the cat, i.e., the ectosylvian cortex, results were similar to those in the caudate nucleus. These results show that viscosity changes must result in compensatory readjustments of vessel diameter, but that these adjustments do not occur where autoregulation to pressure changes is known to be defective. The adjustments to viscosity changes might be called blood viscosity autoregulation of CBF. We hypothesize that pressure autoregulation and blood viscosity autoregulation share the same mechanism. Stroke Vol 17, No 1, 1986 THERE IS STILL CONSIDERABLE CONTROVER-SY regarding the influence of blood viscosity upon cerebral blood flow (CBF).1 One factor in this controversy is the report of some authors that changes in blood viscosity lead to changes in CBF, 2 -3 or that CBF is inversely correlated with blood viscosity, 2 -4 while others have been unable to find any relation between the two; 5 6 it has also been reported that decreasing blood viscosity leads to a large increase in CBF in ischemic brain, but to a lesser increase in nonischemic brain, if at all.7 -8 Another factor leading to uncertainty is that it remains unknown whether or not blood viscosity as measured in vitro, even at different shear rates, correlates well with viscosity as it prevails in vivo. 9In an earlier paper we found a very good correlation between changes in blood viscosity, brought about by the intravenous administration of mannitol, and changes in pial arteriolar diameter observed through a cranial window in the cat. 10 With decreased viscosity vasoconstriction occurred; with increased viscosity the pial arterioles dilated. We assumed that these vessel diameter responses were autoregulatory in nature, similar to responses to blood pressure alterations. In those experiments, however, CBF was not measured, blood pressure changes were not induced and only normal cats with normal CO 2 responsitivity and, presumably, normal autoregulati...

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Section: Discussionmentioning

confidence: 99%

Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.

Muizelaar¹,

Wei²,

Kontos³

et al. 1986

Stroke

133

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“…Whilst tissue oxygen delivery is also related to the haematocrit, reducing viscosity by a reduction in haematocrit has little effect on oxygen delivery until haematocrit falls below 33%. A number of trials have examined the use of venesection accompanied by plasma replacement with dextran 40 or hydroxyethyl starch, within the period after acute stroke (Gilroy et al, 1969;Gottstein, 1981;Kaste et al, 1976;Mast & Marx, 1991;Matthews et al, 1976;Popa et al, 1989;Spudis et al, 1973;Wood & Fleischer, 1982). Initial trials were inconclusive but two large trials have since proved negative.…”

Section: Haemodynamic and Vascular Mechanismsmentioning

confidence: 99%

Therapeutic interventions in acute stroke.

Lees

1992

Brit J Clinical Pharma

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1. Potential therapies for ischaemic stroke include agents to reduce oedema, to improve cerebral perfusion, to reduce excitotoxic damage, to minimise free‐radical induced injury and to reduce complications such as deep venous thrombosis. 2. Of the anti‐oedema drugs, steroids are ineffective and possibly dangerous; intravenous glycerol is unproven. 3. Haemodilution to reduce whole blood viscosity and improve perfusion is ineffective. Thrombolytic drugs have not been adequately tested but several randomised multicentre trials are now commencing. Early treatment and CT scanning are essential. 4. Anticoagulants and antiplatelet drugs may have wide applicability but have not been tested in the acute phase of stroke. A multi‐centre trial will address this issue. 5. Neuronal cytoprotection offers exciting prospects for acute stroke treatment. Antagonists of glutamate at the NMDA receptor, calcium and sodium channel blocking agents and free radical scavenging drugs have potent effects experimentally. Several agents are now reaching clinical trials. The calcium antagonist nimodipine has been disappointing in large scale trials but some studies were flawed by late treatment. 6. Successful treatment of acute stroke is likely to combine several approaches. 7. Therapeutic trials in stroke must include CT scanning, early treatment and a multicentre approach to achieve large numbers of patients.

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“…58 Both short-term and long-term 52 -55 results will be necessary to adequately evaluate any difference between treated and untreated groups.…”

Section: -59mentioning

confidence: 99%

Hemorheology of the cerebral circulation in stroke.

Wood¹,

Kee²

1985

Stroke

157

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Observations During Hypervolemic Hemodilution of Patients With Acute Focal Cerebral Ischemia

Cited by 77 publications

References 46 publications

Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.

Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.

Therapeutic interventions in acute stroke.

Hemorheology of the cerebral circulation in stroke.

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