title: Phenylephrine-induced hypertension during transient middle cerebral artery occlusion alleviates ischemic brain injury in spontaneously hypertensive rats.
abstract: Arterial hypertension is a major risk factor for ischemic stroke. However, the management of preexisting hypertension is still controversial in the treatment of acute stroke in hypertensive patients. The present study evaluates the influence of preserving hypertension during focal cerebral ischemia on stroke outcome in a rat model of chronic hypertension, the spontaneously hypertensive rats (SHR). Focal cerebral ischemia was induced by transient (1h) occlusion of the middle cerebral artery, during which mean arterial blood pressure was maintained at normotension (110-120mm Hg, group 1, n=6) or hypertension (160-170mm Hg, group 2, n=6) using phenylephrine. T2-, diffusion- and perfusion-weighted MRI were performed serially at five different time points: before and during ischemia, and at 1, 4 and 7 days after ischemia. Lesion volume and brain edema were estimated from apparent diffusion coefficient maps and T2-weighted images. Regional cerebral blood flow (rCBF) was measured within and outside the perfusion deficient lesion and in the corresponding regions of the contralesional hemisphere. Neurological deficits were evaluated after reperfusion. Infarct volume, edema, and neurological deficits were significantly reduced in group 2 vs. group 1. In addition, higher values and rapid restoration of rCBF were observed in group 2, while rCBF in both hemispheres was significantly decreased in group 1. Maintaining preexisting hypertension alleviates ischemic brain injury in SHR by increasing collateral circulation to the ischemic region and allowing rapid restoration of rCBF. The data suggest that maintaining preexisting hypertension is a valuable approach to managing hypertensive patients suffering from acute ischemic stroke.
authors.affiliation: Cerebral Microcirculation Unit, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1065, USA.
authors.forename: Byeong-Teck
authors.initials: BT
authors.lastname: Kang
authors.forename: Renata F
authors.initials: RF
authors.lastname: Leoni
authors.forename: Dong-Eog
authors.initials: DE
authors.lastname: Kim
authors.forename: Afonso C
authors.initials: AC
authors.lastname: Silva
mesh_terms: D000208:Acute Disease; D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology; D001930:Brain Injuries / Q000209:etiology* / Q000628:therapy*; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced*; D020244:Infarction, Middle Cerebral Artery / Q000150:complications*; D008279:Magnetic Resonance Imaging; D008297:Male; D009460:Neurologic Examination; D010656:Phenylephrine / Q000633:toxicity*; D051381:Rats; D011918:Rats, Inbred SHR; D015427:Reperfusion Injury / Q000628:therapy; D018709:Statistics, Nonparametric; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000633:toxicity*
chemical_list: D014662:Vasoconstrictor Agents; D010656:Phenylephrine