title: A photothrombotic ring stroke model in rats with sustained hypoperfusion followed by late spontaneous reperfusion in the region at risk.
abstract: In clinical thromboembolic stroke, spontaneous late recanalization is a common feature, but one which has been very sparsely studied experimentally. This study aimed at enabling the study of spontaneous reperfusion and exploring its consequences by modifying a recently developed photothrombotic-stroke model that focuses on the region-at-risk located within an ischemic ring-locus. The exposed crania of male Wistar rats (280-340 g) were subjected to a ring-shaped (5.0 mm outer diameter and 0.35 mm thick) laser-irradiation beam (514.5 nm; 0.89 W/cm2) for 2 min simultaneously with intravenous erythrosin B (17 mg/kg) infusion for 30 s. Transcardial carbon-black perfusion experiments revealed a ring-shaped cortical perfusion deficit at 4 h post-irradiation, which progressively increased at 10, 24, and 48 h, at which time the whole region-at-risk was pale with single distal branches of the middle cerebral artery being extensively narrowed, but not occluded. At 72 h, spontaneous reperfusion was observed in the region-at risk, which was even more pronounced at 7 and 28 days. Cortical cerebral blood flow (cCBF), measured by laser-Doppler flowmetry, was distinctly reduced at 2 min post-irradiation and further decreased slightly during 4 h of recording to ca. 24% of baseline values at the ring locus and 40% in the region-at-risk. In the region-at-risk, cCBF flow values were 23-30% of the baseline at 2448 h post-irradiation, followed by a relative cCBF increase to 71 and 77% at 72 and 96 h post-irradiation. Brain water content in the ischemic part of the cortex increased steadily from 4 to 48 h post-irradiation; at 72 h, it leveled off and returned to control values at 7 days. In conclusion, by employing a laser beam in the shape of a thin ring, critically sustained cCBF reduction was followed by late, consistent spontaneous reperfusion in the region-at-risk in this novel photochemically induced stroke-in-evolution model.
authors: Umeå Stroke Center, Department of Medicine, University of Umeå, Sweden.
authors: W
authors: W
authors: Gu
authors: W
authors: W
authors: Jiang
authors: P
authors: P
authors: Wester
mesh_terms: D000818:Animals; D001834:Body Water / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000098:blood supply; D002561:Cerebrovascular Disorders / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D003326:Coronary Circulation / Q000502:physiology* / Q000528:radiation effects; D004195:Disease Models, Animal; D002542:Intracranial Embolism and Thrombosis / Q000150:complications* / Q000209:etiology*; D007834:Lasers; D008297:Male; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012075:Remission, Spontaneous; D012964:Sodium / Q000378:metabolism
chemical_list: D012964:Sodium; D011188:Potassium