Custom-tailored hemodilution with albumin and crystalloids in acute ischemic stroke.

Goslinga, H.; Eijzenbach, V.; Heuvelmans, J.H.A.; Vries, Erhard van der; Melis, V. M. J.; Schmid‐Schönbein, H.; Bezemer, P.D.

doi:10.1161/01.str.23.2.181

Cited by 93 publications

(63 citation statements)

References 36 publications

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“…911 In addition, hypervolemia should be therapeutic for dehydration/hypovolemic conditions which have been implicated as exacerbating ischemia in a subpopulation of stroke patients. 42 And finally, is the issue of decreased oxygen content when using non-oxygen binding fluids for hemodilution. Such fluids place inherent limits on oxygen transport, and therefore the effectiveness and magnitude of therapy.…”

Section: Discussionmentioning

confidence: 99%

Focal Cerebral Ischemia in Rats: Effect of Hemodilution with α-α Cross-Linked Hemoglobin on Brain Injury and Edema

Cole

Schell

Drummond

et al. 1993

Can. j. neurol. sci.

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ABSTRACT:The effect of hemodilution, with a-oc cross-linked hemoglobin (DCLHb), on brain injury and edema was assessed after temporary middle cerebral artery occlusion in rats. Injury was analyzed with 2,3,5-triphenyltetrazolium chloride (TTC) stain and edema by microgravimety. Part A: DCLHb was given to maintain one of the following hematocrits (Hct) and normotension: 1) 45/Hct, 2) 30/Hct, 3) 16/Hct, or 4) 9/Hct. Brain injury (% of ischemic hemisphere, mean ± SD) was less in the 30/Hct group (31 ± 4 ) versus the 45/Hct group (42 ± 5); and in the 16/Hct (20 ± 3) and 9/Hct (19 ± 4) groups versus the 45/Hct and 30/Hct groups. Edema was less in the hemodiluted groups versus the 45/Hct group. Part B: DCLHb was given to maintain one of the following hematocrits and hyper (HTN) -or normotension (Norm): 1) 45/Norm, 2) 30/Norm, 3) 30/HTN, 4) 16/Norm, or 5) 16/HTN. In hematocrit matched groups hypertension decreased brain injury (30/HTN -24 ± 2 < 30/Norm -34 ± 4; and 16/HTN -17 ± 3 < 16/Norm -24 ± 4). Edema was not effected by hypertension. These results suggest that hemodilution with DCLHb decreases focal ischemic injury, and is most effective when given in a manner that induces hypertension.

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Section: Discussionmentioning

confidence: 99%

Focal Cerebral Ischemia in Rats: Effect of Hemodilution with α-α Cross-Linked Hemoglobin on Brain Injury and Edema

Cole

Schell

Drummond

et al. 1993

Can. j. neurol. sci.

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“…Mortality at 6 months was similar in the two groups, and there was no improvement with treatment even in the subgroups with ischemic stroke < 6 h and highest hematocrit. In another trial, the Amsterdam Stroke Study (Goslinga et al, 1992), 300 patients were studied. Normovolemic hemodilution was induced with 20% albumin plus crystalloids, targeting a pulmonary capillary wedge pressure of 12 mmHg and hematocrit of 32%.…”

Section: Hemodilutionmentioning

confidence: 99%

Neuroprotection for ischemic stroke: Past, present and future

2008

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Neuroprotection for ischemic stroke refers to strategies, applied singly or in combination, that antagonize the injurious biochemical and molecular events that eventuate in irreversible ischemic injury. There has been a recent explosion of interest in this field, with over 1000 experimental papers and over 400 clinical articles appearing within the past 6 years. These studies, in turn, are the outgrowth of three decades of investigative work to define the multiple mechanisms and mediators of ischemic brain injury, which constitute potential targets of neuroprotection. Rigorously conducted experimental studies in animal models of brain ischemia provide incontrovertible proof-of-principle that high-grade protection of the ischemic brain is an achievable goal. Nonetheless, many agents have been brought to clinical trial without a sufficiently compelling evidence-based pre-clinical foundation. At this writing, around 160 clinical trials of neuroprotection for ischemic stroke have been initiated. Of the approximately 120 completed trials, two-thirds were smaller early-phase safetyfeasibility studies. The remaining one-third were typically larger (>200 subjects) phase II or III trials, but, disappointingly, only fewer than one-half of these administered neuroprotective therapy within the 4-6 hour therapeutic window within which efficacious neuroprotection is considered to be achievable. This fact alone helps to account for the abundance of "failed" trials.This review presents a close survey of the most extensively evaluated neuroprotective agents and classes and considers both the strengths and weakness of the pre-clinical evidence as well as the results and shortcomings of the clinical trials themselves. Among the agent-classes considered are calcium channel blockers; glutamate antagonists; GABA agonists; antioxidants/radical scavengers; phospholipid precursor; nitric oxide signal-transduction down-regulator; leukocyte inhibitors; hemodilution; and a miscellany of other agents. Among promising ongoing efforts, therapeutic hypothermia, high-dose human albumin therapy, and hyperacute magnesium therapy are considered in detail. The potential of combination therapies is highlighted. Issues of clinical-trial funding, the need for improved translational strategies and clinical-trial design, and "thinking outside the box" are emphasized. Part I: Neuroprotection -from Past to the PresentNeuroprotection for ischemic brain injury has emerged only recently as a topic of serious biomedical inquiry. A MEDLINE survey (PubMed, 2007) reveals virtually no publications on this topic until the early 1990's but a remarkable surge in publications over the past 10 years Correspondence and reprint requests to:

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“…Several large trials, including the Scandinavian Stroke Study, 126 the Italian Acute Stroke Study, 72 the Amsterdam Stroke Study, 55 the Italian Acute Stroke Study-Hemodilution (IASS-H) trial, 9 and the Multicenter Austrian Hemodilution Trial, 1 all failed to show benefits in a variety of primary outcomes.…”

Section: Hemodilution As Treatment For Strokementioning

confidence: 99%

Neuroprotective strategies and the underlying molecular basis of cerebrovascular stroke

Karsy¹,

Brock²,

Guan³

et al. 2017

FOC

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Stroke is a leading cause of disability in the US. Although there has been significant progress in the area of medical and surgical thrombolytic technologies, neuroprotective agents to prevent secondary cerebral injury and to minimize disability remain limited. Only limited success has been reported in preclinical and clinical trials evaluating a variety of compounds. In this review, the authors discuss the most up-to-date information regarding the underlying molecular biology of stroke as well as strategies that aim to mitigate this complex signaling cascade. Results of historical research trials involving N-methyl-d-aspartate and α-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor antagonists, clomethiazole, antioxidants, citicoline, nitric oxide, and immune regulators have laid the groundwork for current progress. In addition, more recent studies involving therapeutic hypothermia, magnesium, albumin, glyburide, uric acid, and a variety of other treatments have provided more options. The use of neuroprotective agents in combination or with existing thrombolytic treatments may be one of many exciting areas of further development. Although past trials of neuroprotective agents in ischemic stroke have been limited, significant insights into mechanisms of stroke, animal models, and trial design have incrementally improved approaches for future therapies.

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Custom-tailored hemodilution with albumin and crystalloids in acute ischemic stroke.

Cited by 93 publications

References 36 publications

Focal Cerebral Ischemia in Rats: Effect of Hemodilution with α-α Cross-Linked Hemoglobin on Brain Injury and Edema

Focal Cerebral Ischemia in Rats: Effect of Hemodilution with α-α Cross-Linked Hemoglobin on Brain Injury and Edema

Neuroprotection for ischemic stroke: Past, present and future

Neuroprotective strategies and the underlying molecular basis of cerebrovascular stroke

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