Transient appearance of "no-reflow" phenomenon in Mongolian gerbils.

Ito, Umeo; Ohno, Kikuo; Yamaguchi, Takekane; Tomita, Hiroki; Inaba, Yutaka; Kashima, Masaaki

doi:10.1161/01.str.11.5.517

Cited by 49 publications

(21 citation statements)

References 25 publications

(7 reference statements)

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“…Physiological values, MCA vascular diameter, and neurological function after sham surgery were similar in the transgenic and wild-type groups, indicating similar phenotypic baselines on which the effects of SAH were superimposed. Similarities of basilar (12) 15 (15) 12 (12) 39 (39) Wild-type SAH 7 (7-9) 7 (6-11) 10 (9-12) 23 (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) EC-SOD SAH 7 (6-8) 8 (8-11) 10 (9-11) 26 (23)(24)(25)(26)(27)(28)(29)(30) Values are median (IQR). *Range: 9ϭcomplete loss of function; 39ϭno deficit.…”

Section: Discussionmentioning

confidence: 99%

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Attenuation of Cerebral Vasospasm After Subarachnoid Hemorrhage in Mice Overexpressing Extracellular Superoxide Dismutase

McGirt

Parra

Sheng

et al. 2002

Stroke

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Section: Discussionmentioning

confidence: 99%

“…10,26 Furthermore, perfusion fixation has become standard in the histological measurement of lumen diameters in rat and rabbit SAH models. 27,28 …”

Section: Cerebral Vascular Perfusionmentioning

confidence: 99%

Attenuation of Cerebral Vasospasm After Subarachnoid Hemorrhage in Mice Overexpressing Extracellular Superoxide Dismutase

McGirt

Parra

Sheng

et al. 2002

Stroke

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“…Our findings are in line with those of several other studies that also reported transient no-reflow or impaired reflow after brief periods of cerebral ischemia. 21 - 26 Other studies did not show impairment of reperfusion, 27 -29 but these studies may have overlooked transient recirculation deficits because blood flow was measured intermittently.…”

Section: Discussionmentioning

confidence: 99%

Laser doppler flowmetry in CA1 sector of hippocampus and cortex after transient forebrain ischemia in gerbils.

Kuroiwa

Bonnekoh

Hossmann

1992

Stroke

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Background and Purpose: Local differences in the hemodynamic response to transient ischemia could be involved in the development of selective vulnerability. These differences were studied in vulnerable and nonvulnerable regions of the brain.Methods: Five gerbils were subjected to 10 minutes of bilateral forebrain ischemia, and cerebral blood flow was measured continuously in the frontal cortex and CA1 sector of the hippocampus using laser Doppler flowmetry. Carotid artery pressure was recorded simultaneously with a pressure transducer.Results: After induction of ischemia, blood flow in the cortex and CA1 sector decreased to 11.8% and 18.0% of the baseline value, respectively. After release of the vascular occlusion, blood flow in the cortex returned to the preischemic level at 7.5 minutes (recovery time), reached the hyperemic peak (123.8%) at 12.4 minutes (peak latency), and again decreased to the preischemic level at 27.2 minutes. In the CA1 sector, blood flow returned to the preischemic level at 2.1 minutes, reached the hyperemic peak (122.2%) at 5.7 minutes, and decreased again to the preischemic level at 21.3 minutes. In both the cortex and CA1 sector, recovery time and peak latency correlated inversely with the amount of residual blood flow during ischemia. Histologically, cortical neurons were not injured but only 14.6% of CA1 neurons survived 1 week after ischemia.Conclusions: CA1 neurons were selectively injured despite the milder percentage decrease of blood flow during ischemia and the more prompt recovery of flow after ischemia. These findings stress the importance of intrinsic rather than hemodynamic factors in the pathogenesis of selective vulnerability of CA1 neurons after transient bilateral forebrain ischemia. (Stroke 1992;23:1349-1354

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“…The existence of this phenomenon was confirmed in a variety of animal models of brain ischemia. [3][4][5][6] It was also shown in a variety of other organs, including skin, 7,8 skeletal muscle, 9 and the kidney. 10 -12 Kloner et al 13 sought to find out whether the no-reflow phenomenon would be observed in ischemic canine hearts and whether it was related to microvascular damage.…”

Section: Historical Perspectivementioning

confidence: 99%