12 research outputs found
Thrombospondin-1 in Early Flow-Related Remodeling of Mesenteric Arteries from Young Normotensive and Spontaneously Hypertensive Rats
We tested the hypotheses that TSP-1 participates in the initiation of remodeling of small muscular arteries in response to altered blood flow and that the N-terminal domain of TSP-1 (hepI) can reverse the pathological inward remodeling of resistance arteries from SHR
Structural alterations in the microcirculation predict subsequent changes of the renalfunction in hypertensive patients.
Structural alterations of subcutaneous resistance-sized arteries predict long term outcome or renal function.
Cerebral Small Resistance Artery Structure and Cerebral Blood Flow in Normotensive Subjects andHypertensive Patients Investigated with Perfusion MRImaging
PURPOSE
It has been demonstrated previously that, in essential hypertensive patients, subcutaneous small resistance artery structural
alterations, as indicated by an increased media to lumen
ratio (M/L), may predict coronary and forearm flow reserve.
In essential hypertension also human cerebral small arteries
present a clear increase in M/L. The purpose of the study is
to investigate the relationship between cerebral blood flow
(CBF) and cerebral small resistance artery structure.
MATERIALS & METHODS
Ten subjects were included in the present study, five hypertensive
patients and five normotensive control subjects. All
subjects underwent a neurosurgical intervention. A small
portion of morphologically normal cerebral tissue was
excised and rapidly put in chilled physiologic saline solution.
Cerebral small resistance arteries were dissected and
mounted on an isometric myograph, and the M/L was measured.
Before neurosurgical intervention patients underwent
dynamic susceptibility-weighted contrast (DSC)-enhanced
MR imaging (MRI) with a single-shot gradient-echo EPI
sequence (TR/TE 1.4 sec/30 msec, slice thickness, 5 mm;
field of view, 230 mm; acquisition matrix, 128x128) and
bolus injection of Gd-DTPA at a rate of 4 ml/sec. Maps of
regional cerebral blood flow (CBF), regional cerebral blood
volume (CBV) and of the mean transit time (MTT) were calculated
with the commercial software NordicICE (version
2.3.9, NordicImagingLab AS, Bergen, Norway). Cerebral blood volume and CBF maps were corrected for contrast
agent leakage. Round-shaped ROIs were manually placed in
the lenticular nucleus, thalami, fronto-temporo-occipital
gray matter, frontal and temporal white matter and the mean
values of CBF (ml/100g/min) and CBV (ml/100g) were
determined in both intact and affected hemispheres.
RESULTS
Cerebral blood flow values were reduced in different areas
of the brain in hypertensive patients compared with normotensive
subjects. However, these differences reached statistical
significance only in the thalamus. No difference
between groups was observed for CBV (Table 1). A statistically
significant inverse correlation was observed between
M/L of cerebral arteries and CBF in the cortical gray matter
(r=-0.65, p<0.05), lenticular nucleus (r=-0.74, p<0.01), thalamus
(r=-0.71, p<0.01 and subcortical white matter (r=-0.60,
p<0.05), while correlation with CBV in the different areas
were not statistically significant. Microvessel density in the
brain was not significantly correlated with CBF or CBV in
any area.
Table 1. Regional CBF and CBV as evaluated by MRI in the
study population.
Normotensive Hypertensive
subjects (n=5) patients (n=5)
CBF cortical gray matter (m;l/1--g/min) 72.9±5.19 66.4±6.74
CBF lenticular nucleus (ml/100g/min) 72.8±5.58 64.8±7.95
CBF thalamus (ml/100g/min) 73.1±6.33 59.2±9.55*
CBF subcortical white matter (ml/100g/min) 22.9±3.29 21.9±4.1
CBV cortical gray matter (ml/100g) 5.48±0.42 5.93±0.58
CBV lenticular nucleus (ml/100g) 5.12±0.82 5.53±0.87
CBV thalamus (ml/100g) 4.99±0.79 5.53±0.3
CBV subcortical white matter (ml/100g) 1.69±0.21 1.81±0.11
*=p<0.05 vs normotensive subjects
CONCLUSION
The present study has shown a direct relationship between
cerebral blood flow and cerebral small resistance artery
structure. Our results indicate that microvascular structure
might play a major role in controlling CBF, and this might
help to explain the relevant role of structural alterations of
small resistance arteries in predicting cerebrovascular
events