title: Cerebral small-resistance artery structure and cerebral blood flow in normotensive subjects and hypertensive patients.
abstract: BACKGROUND
  The aim of this study was to prospectively investigate whether the structure of cerebral small-resistance arteries is related to cerebral perfusion parameters as measured with dynamic susceptibility-weighted contrast magnetic resonance imaging (DSC-MRI) in a selected cohort of hypertensive and normotensive patients.
  
  
  METHODS
  Ten hypertensive and 10 normotensive patients were included in the study. All patients underwent neurosurgical intervention for an intracranial tumor and were investigated with DSC-MRI at 1.5 T. Cerebral small-resistance arteries were dissected from a small portion of morphologically normal cerebral tissue and mounted on an isometric myograph for the measurement of the media-to-lumen (M/L) ratio. A quantitative assessment of cerebral blood flow (CBF) and volume (CBV) was performed with a region-of-interest approach. Correlation coefficients were calculated for normally distributed variables. The institutional review board approved the study, and informed consent was obtained from all patients.
  
  
  RESULTS
  Compared with normotensive subjects, hypertensive patients had significantly lower regional CBF (mL/100 g/min) in the cortical grey matter (55.63 ± 1.90 vs 58.37 ± 2.19, p < 0.05), basal ganglia (53.34 ± 4.39 vs 58.22. ± 4.33, p < 0.05), thalami (50.65 ± 3.23 vs 57.56 ± 4.45, p < 0.01), subcortical white matter (19.32 ± 2.54 vs 22.24 ± 1.9, p < 0.05), greater M/L ratio (0.099 ± 0.013 vs 0.085 ± 0.012, p < 0.05), and lower microvessel density (1.66 ± 0.67 vs 2.52 ± 1.28, p < 0.05). A statistically significant negative correlation was observed between M/L ratio of cerebral arteries and CBF in the cortical grey matter (r = -0.516, p < 0.05), basal ganglia (r = -0.521, p < 0.05), thalami (r = -0.527 p < 0.05), and subcortical white matter (r = -0.612, p < 0.01).
  
  
  CONCLUSIONS
  Our results indicate that microvascular structure might play a role in controlling CBF, with possible clinical consequences.
authors.affiliation: Clinica Medica, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy.
authors.forename: Carolina
authors.initials: C
authors.lastname: De Ciuceis
authors.forename: Claudio
authors.initials: C
authors.lastname: Cornali
authors.forename: Enzo
authors.initials: E
authors.lastname: Porteri
authors.forename: Dikran
authors.initials: D
authors.lastname: Mardighian
authors.forename: Chiara
authors.initials: C
authors.lastname: Pinardi
authors.forename: Marco M
authors.initials: MM
authors.lastname: Fontanella
authors.forename: Luigi F
authors.initials: LF
authors.lastname: Rodella
authors.forename: Rita
authors.initials: R
authors.lastname: Rezzani
authors.forename: Damiano
authors.initials: D
authors.lastname: Rizzoni
authors.forename: Gianluca E M
authors.initials: GE
authors.lastname: Boari
authors.forename: Enrico Agabiti
authors.initials: EA
authors.lastname: Rosei
authors.forename: Roberto
authors.initials: R
authors.lastname: Gasparotti
mesh_terms: D000368:Aged; D002536:Cerebral Arteries / Q000033:anatomy & histology* / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012016:Reference Values; D012039:Regional Blood Flow; D014655:Vascular Resistance