Cerebral circulation after cardiac arrest. Microangiographic and protein tracer studies.

Lin, Shu-Ren; Kormano, Martti

doi:10.1161/01.str.8.2.182

Cited by 27 publications

(8 citation statements)

References 28 publications

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“…Permeability of BBB after VF CA appears to be insult duration-, age- and species-specific. Similar to our study, the BBB was not permeable to small or large tracers either immediately or at 4 h after VF CA in adult dogs [22, 23]. After prolonged periods of hypoxemia without CA, the BBB was not permeable to mannitol, sodium, or antipyrine in newborn piglets [24].…”

Section: Discussionsupporting

confidence: 80%

Blood brain barrier is impermeable to solutes and permeable to water after experimental pediatric cardiac arrest

Tress

Clark

Foley

et al. 2014

Neuroscience Letters

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Pediatric asphyxial cardiac arrest (CA) results in unfavorable neurological outcome in most survivors. Development of neuroprotective therapies is contingent upon understanding the permeability of intravenously delivered medications through the blood brain barrier (BBB). In a model of pediatric CA we sought to characterize BBB permeability to small and large molecular weight substances. Additionally, we measured the percent brain water after CA. Asphyxia of 9 min was induced in 16-18 day-old rats. The rats were resuscitated and the BBB permeability to small (sodium fluorescein and gadoteridol) and large (immunoglobulin G, IgG) molecules was assessed at 1, 4, and 24 h after asphyxial CA or sham surgery. Percent brain water was measured post-CA and in shams using wet-to-dry brain weight. Fluorescence, gadoteridol uptake, or IgG staining at 1, 4 h and over the entire 24 h post-CA did not differ from shams, suggesting absence of BBB permeability to these solutes. Cerebral water content was increased at 3 h post-CA vs. sham. In conclusion, after 9 min of asphyxial CA there is no BBB permeability over 24 h to conventional small or large molecule tracers despite the fact that cerebral water content is increased early post-CA indicating the development of brain edema. Evaluation of novel therapies targeting neuronal death after pediatric CA should include their capacity to cross the BBB.

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Section: Discussionsupporting

confidence: 80%

Blood brain barrier is impermeable to solutes and permeable to water after experimental pediatric cardiac arrest

Tress

Clark

Foley

et al. 2014

Neuroscience Letters

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“…Our previous study had similar results. 26 In the present study, however, 3 animals, in which early measurements of CBF were made, had hyperemia during the first 30 minutes after reperfusion. It is important to recognize differences between the techniques.…”

Section: Discussioncontrasting

confidence: 55%

Effect of dextran on cerebral function and blood after cardiac arrest. An experimental study on the dog.

Lin¹,

O'Connor²,

King³

et al. 1979

Stroke

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SUMMARY EEG activity and regional cerebral blood flow were monitored during S hour survival following cardiac arrest in 32 pentobarbital anesthetized mongrel dogs. The animals were mechanically ventilated and blood gases were maintained at physiologic levels. Regional cerebral blood flow and cardiac output were measured using 15 n microspheres. EEG was recorded from 6 epidural electrodes using bipolar techniques.The animals were divided into 3 groups. The animals in Group I had an arrest of 8-11 minutes and those in Group II and III had an arrest of 12-16 minutes. Group II animals received no treatment. Group III animals were given 1 g/kg of dextran 40 at a concentration of 10% in normal saline following the arrest and maintained with 10 mg/kg/min during the 5 hours of recovery. In Groups I and III there was shorter duration of a flat EEG and 5 hours after the arrest the EEG activity was closer to normal than in Group II. After 5 hours the EEG scores of Group III were significantly greater than Group II (p < 0.03). The cortical grey matter and hippocampus had the greatest reduction of blood flow following cardiac arrest. The mean cortical grey matter blood flow in Group II was less than in Groups I and III at 3 hours. After 5 hours the grey matter blood flow was greater in Group III than in Group II (p < 0.09).The findings of this study are consistent with the hypothesis that after cardiac arrest perfusion abnormalities persist or develop after return of blood pressure and that these can be corrected or prevented with improved functional survival by treatment with dextran 40 after the arrest.Stroke, Vol 10, Nol, 1979 LOW MOLECULAR WEIGHT dextran 40 (Rheomacrodex) has been shown to diminish mortality and to enhance the quality of survival when given to patients following acute stroke." Experimental study also has shown that administration of this hemodiluting agent following cerebral arterial occlusion reduced the circulatory impairment at the microvasculature level. 36 Dextran's effectiveness may be related to its action in reducing blood viscosity and increasing plasma volume; 12 ' 37 to its effect in minimizing aggregation of formed blood elements; 13 or to an antiplatelet aggregation effect. 13 These actions suggest that low molecular weight dextran may be of value in the treatment of the brain injury induced by circulatory arrest, particularly if "no reflow" 1 is an important cause of such injury. MethodsThirty-two nonheparinized mongrel dogs, revived from cardiac arrest and maintained 5 hours during the postarrest period, were analyzed. They were divided into 3 groups. Animals in Group I (n = 8) had an arrest of 8-11 minutes and those in Group II (n = 12) had an arrest of 12-16 minutes. Animals in Group III (n = 12) had an arrest of 12-16 minutes followed by treatment with a high dose of 40,000 molecular weight

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“…The "no-reflow" phenomenon, i.e., an initial failure of brain microvascular reperfusion, fre quently detected following periods of complete global ischemia Ginsberg and Myers, 1972;Wade et aI., 1975;Fischer et aI., 1977;Lin and Kormano, 1977) is not a common finding following periods of severe incomplete ischemia (Pulsinelli et aI., 1982b;Kagstrom et aI., 1983b). Potential mechanisms responsible for overt "no-re flow" include increased blood viscosity following extended periods of erythrocyte stasis (Merrill, 1969;Hallenbeck, 1977;Fischer et aI., 1979), the physical compression of vascular lumina by peri vascular glial swelling (Chiang et aI., 1968;Little et aI., 1976), or inadequate perfusion pressure (Ljung gren et aI., 1974).…”

Section: Discussionmentioning

confidence: 99%

Histopathological and Hemodynamic Consequences of Complete versus Incomplete Ischemia in the Rat

Dietrich

Busto

Yoshida

et al. 1987

J Cereb Blood Flow Metab

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The primary objective of this study was to compare the histopathological consequences of complete versus incomplete ischemia under experimental conditions that limit lactate accumulation. Fasted rats underwent 1 h of either complete or incomplete ischemia by a procedure combining bilateral common carotid artery occlusion, halothane-induced systemic hypotension, and CSF pressure elevation. Histopathological outcome was evaluated 4 h later and was graded on a 4-point scale. Incomplete ischemia resulted in ischemic neuronal damage within selectively vulnerable brain regions. In contrast, complete ischemia, in addition to diffuse neuronal damage, resulted in focal sites of parenchymal necrosis with vascular stasis. Perfusion defects were detected by carbon black infusion within cortical and subcortical regions following only 25 min of complete, but not incomplete, ischemia. Ultrastructural abnormalities at the same duration of complete ischemia included a high frequency of endothelial microvilli and compressed lumina with severe perivascular astrocytic swelling. When recirculation was instituted for 1 h following 1 h of complete ischemia, regions of nonperfusion were detected autoradiographically. Thus, when the degree of lactic acidosis is controlled, prolonged periods of complete ischemia result in a more severe pathological outcome compared to incomplete ischemia. Focally impaired postischemic cerebral perfusion appears to be an important factor in infarct formation under the present experimental conditions.

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Cerebral circulation after cardiac arrest. Microangiographic and protein tracer studies.

Cited by 27 publications

References 28 publications

Blood brain barrier is impermeable to solutes and permeable to water after experimental pediatric cardiac arrest

Blood brain barrier is impermeable to solutes and permeable to water after experimental pediatric cardiac arrest

Effect of dextran on cerebral function and blood after cardiac arrest. An experimental study on the dog.

Histopathological and Hemodynamic Consequences of Complete versus Incomplete Ischemia in the Rat

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