Brain Blood Flow and Mean Transit Time as Related to Aging

Gerontology ◽  
1980 ◽  
Vol 26 (2) ◽  
pp. 104-107 ◽  
Author(s):  
M. Fujishima ◽  
T. Omae
Stroke ◽  
1974 ◽  
Vol 5 (5) ◽  
pp. 630-639 ◽  
Author(s):  
ROBERT L. GRUBB ◽  
MARCUS E. RAICHLE ◽  
JOHN O. EICHLING ◽  
MICHEL M. TER-POGOSSIAN

1992 ◽  
Vol 262 (6) ◽  
pp. H1908-H1914 ◽  
Author(s):  
M. Ferrari ◽  
D. A. Wilson ◽  
D. F. Hanley ◽  
R. J. Traystman

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.


Stroke ◽  
1974 ◽  
Vol 5 (6) ◽  
pp. 719-724 ◽  
Author(s):  
YOSHIHIRO KURIYAMA ◽  
TAKASHI AOYAMA ◽  
KUNIHIKO TADA ◽  
SHOTARO YONEDA ◽  
TADAATSU NUKADA ◽  
...  

1956 ◽  
Vol 184 (3) ◽  
pp. 593-598 ◽  
Author(s):  
Ralph W. Brauer ◽  
G. F. Leong ◽  
R. F. McElroy ◽  
R. J. Holloway

P32-labeled chromic phosphate colloid disappears from the circulation of the isolated rat liver preparation according to a single exponential term of time. A small nonextracted contaminant, less than 3% of the total activity is also detected. At comparable blood flow rates the colloid is extracted about as completely by the isolated liver preparation as by the liver in situ in the intact animal. The efficiency with which chromic phosphate colloid is removed from perfusate passing through the isolated rat liver decreases with increasing perfusion rate. If whole blood is used as a perfusate, the efficiency of colloid extraction is almost twice as high as it is if rat blood plasma is employed, even if adequate oxygenation of the tissue is assured by high oxygen partial pressures in the latter series. A theoretical treatment of these results is given in terms of first order reaction kinetics. Agreement of experimental results with this theory at perfusion rates greater than 2 cc/gm/min. indicates that the rate of chromic phosphate colloid extraction is a function of plasma concentration of the colloid, and that the extraction efficiency for a given perfusate varies as a function of the mean transit time of perfusate through the liver. Deviations from the predictions of the theory occur at low perfusion rates, and are discussed in the light of the above concepts. A decrease of the ratio of transit time to perfusion rate under these conditions suggests a decrease in the number of channels open to blood flow at low perfusion pressures.


2018 ◽  
Vol 129 (6) ◽  
pp. 1464-1474 ◽  
Author(s):  
Ethan A. Winkler ◽  
Harjus Birk ◽  
Jan-Karl Burkhardt ◽  
Xiaolin Chen ◽  
John K. Yue ◽  
...  

OBJECTIVEBrain arteriovenous malformations (bAVMs) are rupture-prone tangles of blood vessels with direct shunting of blood flow between arterial and venous circulations. The molecular and/or cellular mechanisms contributing to bAVM pathogenesis and/or destabilization in sporadic lesions have remained elusive. Initial insights into AVM formation have been gained through models of genetic AVM syndromes. And while many studies have focused on endothelial cells, the contributions of other vascular cell types have yet to be systematically studied. Pericytes are multifunctional mural cells that regulate brain angiogenesis, blood-brain barrier integrity, and vascular stability. Here, the authors analyze the abundance of brain pericytes and their association with vascular changes in sporadic human AVMs.METHODSTissues from bAVMs and from temporal lobe specimens from patients with medically intractable epilepsy (nonvascular lesion controls [NVLCs]) were resected. Immunofluorescent staining with confocal microscopy was performed to quantify pericytes (platelet-derived growth factor receptor–beta [PDGFRβ] and aminopeptidase N [CD13]) and extravascular hemoglobin. Iron-positive hemosiderin deposits were quantified with Prussian blue staining. Syngo iFlow post–image processing was used to measure nidal blood flow on preintervention angiograms.RESULTSQuantitative immunofluorescent analysis demonstrated a 68% reduction in the vascular pericyte number in bAVMs compared with the number in NVLCs (p < 0.01). Additional analysis demonstrated 52% and 50% reductions in the vascular surface area covered by CD13- and PDGFRβ-positive pericyte cell processes, respectively, in bAVMs (p < 0.01). Reductions in pericyte coverage were statistically significantly greater in bAVMs with prior rupture (p < 0.05). Unruptured bAVMs had increased microhemorrhage, as evidenced by a 15.5-fold increase in extravascular hemoglobin compared with levels in NVLCs (p < 0.01). Within unruptured bAVM specimens, extravascular hemoglobin correlated negatively with pericyte coverage (CD13: r = −0.93, p < 0.01; PDGFRβ: r = −0.87, p < 0.01). A similar negative correlation was observed with pericyte coverage and Prussian blue–positive hemosiderin deposits (CD13: r = −0.90, p < 0.01; PDGFRβ: r = −0.86, p < 0.01). Pericyte coverage positively correlated with the mean transit time of blood flow or the time that circulating blood spends within the bAVM nidus (CD13: r = 0.60, p < 0.05; PDGFRβ: r = 0.63, p < 0.05). A greater reduction in pericyte coverage is therefore associated with a reduced mean transit time or faster rate of blood flow through the bAVM nidus. No correlations were observed with time to peak flow within feeding arteries or draining veins.CONCLUSIONSBrain pericyte number and coverage are reduced in sporadic bAVMs and are lowest in cases with prior rupture. In unruptured bAVMs, pericyte reductions correlate with the severity of microhemorrhage. A loss of pericytes also correlates with a faster rate of blood flow through the bAVM nidus. This suggests that pericytes are associated with and may contribute to vascular fragility and hemodynamic changes in bAVMs. Future studies in animal models are needed to better characterize the role of pericytes in AVM pathogenesis.


2002 ◽  
Vol 11 (2) ◽  
pp. 66-71 ◽  
Author(s):  
Thanh G. Phan ◽  
John Huston ◽  
Norbert G. Campeau ◽  
Robert D. Brown ◽  
Jimmy R. Fulgham ◽  
...  

1980 ◽  
Vol 238 (5) ◽  
pp. H745-H749 ◽  
Author(s):  
C. H. Baker ◽  
E. T. Sutton ◽  
D. L. Davis

An indicator dilution technique is described for obtaining time-concentration curves subsequent to bolus injections of sulfhemoglobin red blood cells (SH-RBC), which have a deep greenish-brown color (absorption peak 620 nm vs. 542 and 564 nm for normal red cells). The series- and parallel-coupled microvessels of cat mesentery were studied. This is accomplished by means of video microscopy with a two-window intensity-sensitive video sampler system. The relationship between SH-RBC concentration in blood and optical measurement is linear. Blood flow velocities were calculated from the difference in mean transit times between two points along a vessel. When this technique is used in association with the previously reported method for determining time-concentration curves for the plasma indicator FITC-dextran the mean transit time (t) for red blood cells was less than for plasma in arterioles. The reproducibility of t and flow velocity for both SH-RBC and FITC-dextran from successive injections were reported. The mean transit time ratio of arteriolar SH-RBC to FITC-dextran averages 0.89. Blood flow velocity calculated from SH-RBC is greater than that calculated from FITC-dextran in these same arterioles. The ratio of the velocities averages 1.29.


1987 ◽  
Vol 15 (4) ◽  
pp. 432
Author(s):  
David A. Wilson ◽  
Marco Ferrari ◽  
Daniel F. Hanley ◽  
Mark C. Rogers ◽  
Richard J. Traystman

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