Ischemic brain rescue by transvenous perfusion in baboons with venous sinus occlusion.

Frazee, John G.; Jordan, Sheldon E.; Dion, J E; Kar, Snehendu B.; Viñuela, Fernando; Rand, Robert W.; Corday, Eliot

doi:10.1161/01.str.21.1.87

Cited by 5 publications

(1 citation statement)

References 19 publications

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“…For example, transvenous retroperfusion, where oxygenated blood is mechanically delivered under pressure through the venous system where it can reach the ischemic penumbra, has shown promise in baboon models of stroke. 69 Phase I trials have been completed. Beside restoring nutritive flow to the ischemic brain, transvenous retroperfusion could be a more effective vehicle of drug delivery.…”

Section: Human Neuroprotection Trialsmentioning

confidence: 99%

Neuroprotection and the Ischemic Cascade

Felberg¹,

Burgin²,

Grotta³

2000

CNS spectr.

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Brain ischemia is a process of delayed neuronal cell death, not an instantaneous event. The concept of neuroprotection is based on this principle. Diminished cerebral blood flow initiates a series of events (the “ischemic cascade”) that lead to cell destruction. This ischemic cascade is akin to a spreading epidemic starting from a hypothesized core of ischemia and radiating outward. If intervention occurs early, the process may be halted.Interventions have been directed toward salvaging the ischemic penumbra. Hypothermia decreases the size of the ischemic insult in both anecdotal clinical and laboratory reports. In addition, a wide variety of agents have been shown to reduce infant volume in animal models. Pharmacologic interventions that involve thrombolysis, calcium channel blockade, and cell membrane receptor antagonism have been studied and have been found to be beneficial in animal cortical stroke models. Human trials of neuroprotective therapies have been disappointing. Other than thrombolytics, no agents, have shown an unequivocal benefit. The future of neuroprotection will require a logical extension of what has been learned in the laboratory and previous human trials. A sensible approach to the use of multiple-agent cocktails used in combination with thrombolytics is likely to offer the highest chance for benefit.

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Section: Human Neuroprotection Trialsmentioning

confidence: 99%

Neuroprotection and the Ischemic Cascade

Felberg¹,

Burgin²,

Grotta³

2000

CNS spectr.

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Neuroendovascular rescue: Interventional treatment of acute ischemic stroke

Gomez

Orr²,

Soto³

2002

Curr Treat Options Cardio Med

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Stroke continues to be a major health problem for our society. Despite the proven effectiveness of intravenous tissue plasminogen activator (t-PA) for the treatment of acute ischemic stroke, only a minority of patients qualify for this type of therapy. Furthermore, the existing literature has demonstrated that t-PA is not as effective in the treatment of occlusion of large cerebral arteries. The benefit-to-risk assessment of this subpopulation of stroke patients makes them the best candidates for neuroendovascular rescue. This term refers to the intra-arterial application of techniques designed to promote arterial recanalization, and includes intra-arterial thrombolysis and antithrombotic agents, direct mechanical disruption, angioplasty, stenting, embolectomy, and vasoactive pharmacologic intervention. The timing and choice of these procedures, as well as the care of the patient prior to, during, and after the intervention, requires a highly focused and expert approach.

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