Permanent Occlusion (permanent + occlusion)

Distribution by Scientific Domains


Selected Abstracts


Liposome-Encapsulated Hemoglobin Alleviates Brain Edema After Permanent Occlusion of the Middle Cerebral Artery in Rats

ARTIFICIAL ORGANS, Issue 2 2009
Akira T. Kawaguchi
Abstract Liposome-encapsulated hemoglobin (LEH) was proven to be protective in cerebral ischemia/reperfusion injury. The present study evaluated LEH in a rat model of permanent middle cerebral artery (MCA) occlusion to clarify its effect during ischemia and reperfusion. Five minutes after thread occlusion of the MCA, rats were infused with 10 mL/kg of LEH (LEH, n = 13), and compared with normal controls (n = 11). Additional animals received the same MCA occlusion with no treatment (CT, n = 11), saline (saline, n = 10), empty liposome solution (EL, n = 13), or washed red blood cells (RBC, n = 7). Severity of brain edema was determined 24 h later by signal strength in T2-weighted magnetic resonance imaging of the cortex, striatum, hippocampus, and pyriform lobe. The results showed that brain edema/infarction observed in any vehicle-infused control was significantly more severe than in LEH-treated rats. There was a tendency toward aggravated edema in rats receiving ELs. LEH infusion at a dose of 10 mL/kg significantly reduced edema formation as compared to other treatments in a wide area of the brain 24 h after permanent occlusion of the MCA. Low oncotic pressure of EL and LEH solution (vehicle solution) appeared to cause nonsignificant aggravation of edema and reduced protective effects of LEH. [source]


Human neural stem cell transplantation attenuates apoptosis and improves neurological functions after cerebral ischemia in rats

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2009
P. ZHANG
Background: Neuroprotection is a major therapeutic approach for ischemic brain injury. We investigated the neuroprotective effects induced by transplantation of human embryonic neural stem cells (NSCs) into the cortical penumbra 24 h after focal cerebral ischemia. Methods: NSCs were prepared from human embryonic brains obtained at 8 weeks of gestation. Focal cerebral ischemia was induced in adult rats by permanent occlusion of the middle cerebral artery. Animals were randomly divided into two groups: NSCs-grafted group and medium-grafted group (control). Infarct size was assessed 28 days after transplantation by hematoxylin and eosin staining. Neurological severity scores were evaluated before ischemia and at 1, 7, 14, and 28 days after transplantation. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and immunohistochemical analysis of Bcl-2 and Bax were performed at 7, 14, and 28 days after transplantation. Results: Physiological parameters of the two groups were comparable, but not significantly different. NSC transplantation significantly improved neurological function (P<0.05) but did not reduce the infarct size significantly (P>0.05). Compared with the control, NSC transplantation significantly reduced the number of TUNEL- and Bax-positive cells in the penumbra at 7 days. Interestingly, the number of Bcl-2-positive cells in the penumbra after NSC transplantation was significantly higher than that after medium transplantation (P<0.05). Conclusions: The results indicate that NSC transplantation has anti-apoptotic activity and can improve the neurological function; these effects are mediated by the up-regulation of Bcl-2 expression in the penumbra. [source]


Occlusion of the Middle Cerebral Artery: a New Method of Focal Cerebral Ischemia in Rats

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 2005
E. Cam
The study in Wistar rats attempted to improve the occlusion technique of the middle cerebral artery (MCA) as a precise method for initiating stroke. In a first part it was necessary to study the exact anatomy of blood vessels of the brain in seven rats of 170-410 g body weight by corrosion cast. The lengths and diameters of defined locations of the blood vessels were measured. The temporary as well as the permanent methods were refined or replaced. The first one was completed in main training the physiological blood flow after temporary occlusion, while the permanent occlusion was performed by positioning a silicone cap in the MCA. A filament guide was introduced from the common carotid artery (CCA) via internal carotid artery (ICA) to guide the silicon cap at the branch of the MCA. Histological sections of the brain of rats showed 24 h after the permanent occlusion a reproducible infarct in the brain. This area corresponded very well with the supply of the MCA. The new occlusion method with a silicon cap was compared with the occlusion methods of CCA route and external carotid artery (ECA) route. The total infarct volume was significantly larger in the CCA route and ECA route groups than in the silicon cap group (means: CCA route 261 mm3; ECA route 191 mm3 vs. 128 mm3 silicon cap group; P < 0,05). It could be demonstrated that the new silicon cap occlusion technique imitates the pathological situation of a cerebral infarct in man. Moreover it is less invasive for the animals and more precise and reproducible regarding the infarcted area in comparison to the other occlusion methods. Based on anatomical measurements of the blood vessels the described silicon cap method can be recommended for rats of a body weight between 340,370 g. [source]


Liposome-Encapsulated Hemoglobin Alleviates Brain Edema After Permanent Occlusion of the Middle Cerebral Artery in Rats

ARTIFICIAL ORGANS, Issue 2 2009
Akira T. Kawaguchi
Abstract Liposome-encapsulated hemoglobin (LEH) was proven to be protective in cerebral ischemia/reperfusion injury. The present study evaluated LEH in a rat model of permanent middle cerebral artery (MCA) occlusion to clarify its effect during ischemia and reperfusion. Five minutes after thread occlusion of the MCA, rats were infused with 10 mL/kg of LEH (LEH, n = 13), and compared with normal controls (n = 11). Additional animals received the same MCA occlusion with no treatment (CT, n = 11), saline (saline, n = 10), empty liposome solution (EL, n = 13), or washed red blood cells (RBC, n = 7). Severity of brain edema was determined 24 h later by signal strength in T2-weighted magnetic resonance imaging of the cortex, striatum, hippocampus, and pyriform lobe. The results showed that brain edema/infarction observed in any vehicle-infused control was significantly more severe than in LEH-treated rats. There was a tendency toward aggravated edema in rats receiving ELs. LEH infusion at a dose of 10 mL/kg significantly reduced edema formation as compared to other treatments in a wide area of the brain 24 h after permanent occlusion of the MCA. Low oncotic pressure of EL and LEH solution (vehicle solution) appeared to cause nonsignificant aggravation of edema and reduced protective effects of LEH. [source]