Prothrombolytic action of normobaric oxygen given alone or in combination with recombinant tissue-plasminogen activator in a rat model of thromboembolic stroke

2012 ◽  
Vol 112 (12) ◽  
pp. 2068-2076 ◽  
Author(s):  
H. N. David ◽  
B. Haelewyn ◽  
M. Degoulet ◽  
D. G. Colomb ◽  
J. J. Risso ◽  
...  

The potential benefit of 100 vol% normobaric oxygen (NBO) for the treatment of acute ischemic stroke patients is still a matter of debate. To advance this critical question, we studied the effects of intraischemic normobaric oxygen alone or in combination with recombinant tissue-plasminogen activator (rtPA) on cerebral blood flow and ischemic brain damage and swelling in a clinically relevant rat model of thromboembolic stroke. We show that NBO provides neuroprotection by achieving cerebral blood flow restoration equivalent to 0.9 mg/kg rtPA through probable direct interaction and facilitation of the fibrinolytic properties of endogenous tPA. In contrast, combined NBO and rtPA has no neuroprotective effect on ischemic brain damage despite producing cerebral blood flow restoration. These results 1) by providing a new mechanism of action of NBO highlight together with previous findings the way by which intraischemic NBO shows beneficial action; 2) suggest that NBO could be an efficient primary care therapeutic intervention for patients eligible for rtPA therapy; 3) indicate that NBO could be an interesting alternative for patients not eligible for rtPA therapy; and 4) caution the use of NBO in combination with rtPA in acute stroke patients.

Neurosurgery ◽  
1984 ◽  
Vol 15 (4) ◽  
pp. 535-539 ◽  
Author(s):  
James H. Wood ◽  
Konstantinos S. Polyzoidis ◽  
David B. Kee ◽  
Antonio R. Prats ◽  
Gordon L. Gibby ◽  
...  

Abstract Experimental hemodilutional therapy has been shown to raise collateral perfusion to acutely ischemic brain regions distal to occluded internal carotid (ICA) and middle cerebral (MCA) arteries and to reduce infarct size. Superficial temporal (STA)-MCA anastomosis surgically establishes additional regional collateralization, and this bypass angiographically enlarges over time. Despite bypass patency verification by Doppler recording made at the edge of the craniectomy, the microsurgical STA-MCA anastomosis in 11 stroke patients did not produce early changes in cerebral perfusion parameters in the MCA territory of either hemisphere as determined by 133xenon inhalation. Therefore, hemodilution was initiated in an effort to increase cerebral perfusion during this marginal period when the STA was beginning to dilate progressively. Incremental venesections with equal intravenous volume replacement with 5% human serum albumin caused a significant lowering of the hematocrit from 40 ± 1 to 33 ± 1%. This isovolemic hemodilutional therapy resulted in significant mean regional cerebral blood flow (rCBF) elevations of 23 ± 5% (SE) in the bypassed MCA territory and of 25 ± 6% in the opposite MCA region. The mean gray flow (F1) in the involved and homologous MCA regions significantly increased 27 ± 8% and 30 ± 11%, respectively. Similarly, the initial slope index (ISI2) significantly rose by 17 ± 5% in the bypassed MCA territory and by 18 ± 6% in the homologous region. These data objectively support the premise that reductions in hematocrit without intravascular volume expansion augment cerebral blood flow, probably by reducing blood viscosity. Moreover, inovolemic hemodilution, the effect of which lasts several weeks, may be useful adjunct therapy for the postoperative care of patients with marginal cerebral circulation who undergo cerebral revascularization.


2021 ◽  
Vol 5 (1) ◽  
pp. 2514183X2110071
Author(s):  
Mohamad El Amki ◽  
Susanne Wegener

Current treatment for acute ischemic stroke aims at recanalizing the occluded blood vessel to reperfuse ischemic brain tissue. Clot removal can be achieved pharmacologically with a thrombolytic drug, such as recombinant tissue plasminogen activator, or with mechanical thrombectomy. However, reopening the occluded vessel does not guarantee full tissue reperfusion, which has been referred to as reperfusion failure. When it occurs, reperfusion failure significantly attenuates the beneficial effect of recanalization therapy and severely affects functional recovery of stroke patients. The mechanisms of reperfusion failure are somewhat complex and not fully understood. Briefly, after stroke, capillaries show stalls, constriction and luminal narrowing, being crowded with neutrophils, and fibrin–platelet deposits. Furthermore, after recanalization in stroke patients, a primary clot can break, dislodge, and occlude distal arterial branches further downstream. In this review, we highlight a rodent model that allows studying the pathophysiological mechanisms underlying reperfusion failure after stroke. We also describe the vascular and intravascular changes involved in reperfusion, which may provide relevant therapeutic targets for improving treatment of stroke patients.


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