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Article type: Research Article
Authors: Lapi, Dominga | Mastantuono, Teresa | Sapio, Daniela | Paterni, Marco | Colantuoni, Antonio
Affiliations: Department of Clinical Medicine and Surgery, “Federico II” University Medical School, Naples, Italy | CNR Institute of Clinical Physiology, Pisa, Italy
Note: [] Corresponding author: Dominga Lapi, PhD, Department of Clinical Medicine and Surgery “Federico II” University Medical School Via S. Pansini, 5 80121 Naples, Italy. Tel.: +39 0817463212; Fax: +39 0815453045; E-mail: [email protected]
Abstract: This study was aimed to assess the in vivo geometric and functional characteristics of lean Zucker (ZL) and obese Zucker rat (ZO) pial microvascular networks and to evaluate the vascular responses to cerebral hypoperfusion-reperfusion. Rat pial microcirculation was observed by fluorescence microscopy through a closed cranial window. Bilateral common carotid artery occlusion (BCCAO) lasted 30 min and reperfusion 60 min. Arterioles were classified according to Strahler's ordering scheme. Arteriolar diameter was determined by computer assisted-method as well as permeability increase, leukocyte adhesion and perfused capillary length. Neuronal damage was evaluated by TTC staining. ZO rats did not show order 5 vessels; ZO pial arterioles showed high asymmetry in the largest vessels and reduced number of branchings compared with those detected in ZL and Wistar rats. BCCAO and reperfusion caused more severe microvascular damages in ZO compared with ZL and Wistar rats. Vascular responses to acetylcholine and papaverine in ZO rats were significantly reduced compared with Wistar and ZL rats under baseline condition and at the end of reperfusion. Moreover, ZO rats showed more pronounced lesion in the cortex and striatum. Obesity and hyperglycemia could increase vascular remodeling in cerebral networks, with elevated risk of adverse outcome after brain hypoperfusion-reperfusion.
Keywords: Zucker rats, hyperglycemia, bilateral common carotid artery occlusion-reperfusion, pial microcirculation geometric remodeling, vascular and neuronal damage
DOI: 10.3233/CH-131763
Journal: Clinical Hemorheology and Microcirculation, vol. 54, no. 4, pp. 415-429, 2013
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