Quantitative agreement between [15O]H2O PET and model free QUASAR MRI-derived cerebral blood flow and arterial blood volume

2016 ◽  
Vol 29 (4) ◽  
pp. 519-526 ◽  
Author(s):  
D.F.R. Heijtel ◽  
E.T. Petersen ◽  
H.J.M.M. Mutsaerts ◽  
E. Bakker ◽  
P. Schober ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Quantitative Agreement ◽  
Model Free ◽  
Arterial Blood ◽  
Arterial Blood Volume

scholarly journals Regional Cerebral Blood Flow and Arterial Blood Volume and Their Reactivity to Hypercapnia in Hypertensive and Normotensive Rats

2013 ◽  
Vol 34 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Tae Kim ◽  
J Richard Jennings ◽  
Seong-Gi Kim
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Vascular Reactivity ◽  
Early Stage ◽  
Blood Oxygenation ◽  
Chronic Hypertension ◽  
Arterial Blood ◽  
Wistar Kyoto ◽  
Arterial Blood Volume

Chronic hypertension induces cerebrovascular remodeling, changing the inner diameter and elasticity of arterial vessels. To examine cerebrovascular morphologic changes and vasodilatory impairment in early-stage hypertension, we measured baseline (normocapnic) cerebral arterial blood volume ( CBVa) and cerebral blood flow ( CBF) as well as hypercapnia-induced dynamic vascular responses in animal models. All experiments were performed with young (3 to 4 month old) spontaneously hypertensive rats (SHR) and control Wistar–Kyoto rats (WKY) under ∼1% isoflurane anesthesia at 9.4 Tesla. Baseline regional CBF values were similar in both animal groups, whereas SHR had significantly lower CBVa values, especially in the hippocampus area. As CBF is maintained by adjusting arterial diameters within the autoregulatory blood pressure range, CBVa is likely more sensitive than CBF for detecting hypertensive-mediated alterations. Unexpectedly, hypercapnia-induced CBF and blood-oxygenation-level-dependent (BOLD) response were significantly higher in SHR as compared with WKY, and the CBF reactivity was highly correlated with the BOLD reactivity in both groups. The higher reactivity in early-stage hypertensive animals indicates no significant vascular remodeling occurred. At later stages of hypertension, the reduced vascular reactivity is expected. Thus, CBF and CBVa mapping may provide novel insights into regional cerebrovascular impairment in hypertension and its progression as hypertension advances.

Relationship of cerebral blood flow to cardiac output, mean arterial pressure, blood volume, and alpha and beta blockade in cats

1980 ◽  
Vol 52 (6) ◽  
pp. 745-754 ◽  
Author(s):  
Dudley H. Davis ◽  
Thoralf M. Sundt
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Cerebral Autoregulation ◽  
Major Change ◽  
Beta Blockade ◽  
Content Type ◽  
Therapeutic Implications ◽  
Arterial Blood

✓ The relationship among cerebral blood flow (CBF), blood volume, cardiac output (CO), and mean arterial blood pressure (MABP) at varying levels of arterial CO2 tensions (PaCO2) were studied in 70 normal cats. The CBF was measured from the clearance curve of xenon−133 and CO with a thermal dilution catheter placed in the pulmonary artery. The CBF, CO, and MABP values varied appropriately with changes in PaCO2, confirming the reliability of the preparations and the presence of normal autoregulatory responses. Moderate hypovolemia that did not change MABP did, nevertheless, significantly decrease CO and CBF. In an effort to determine if this decrease in CO and CBF were coupled responses, the effects of beta stimulation, hypervolemia, and alpha and beta blockade were investigated. Propranolol, in a dosage insufficient to change MABP, decreased both CO and CBF. This agent abolished the CO response to elevations in PaCO2 but not the CBF response, making it unlikely that this CBF reduction resulted from impaired cerebral autoregulation. Isoproterenol, which, in contrast to propranolol, does not cross the normal blood-brain barrier, alone or in combination with phenoxybenzamine, produced a 38% and 72% increase in CO, respectively, without a change in CBF. Alpha blockade (no major change in CO) and beta blockade (major decrease in CO) did not significantly effect cerebral autoregulation to changes in MABP from angiotensin. The ability of the brain to resist increases in MABP and CO and maintain normal CBF is explained by normal cerebral autoregulation. However, its vulnerability to modest decreases in blood volume, which cannot be attributed to variations in perfusion pressure, is unexplained but obviously has important therapeutic implications. This may be related to reduction in CO, changes in autonomic activity, or a decrease in the size of the perfused capillary bed.

scholarly journals Phasic changes in arterial blood volume is influenced by collateral blood flow: implications for the quantification of coronary stenosis at rest

Heart ◽  
2007 ◽  
Vol 93 (4) ◽  
pp. 438-443 ◽  
Author(s):  
M. Pascotto ◽  
K. Wei ◽  
A. Micari ◽  
T. Bragadeesh ◽  
N. Craig Goodman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Coronary Stenosis ◽  
Collateral Blood Flow ◽  
Arterial Blood ◽  
Arterial Blood Volume

Reflection photoplethysmography of arterial-blood-volume pulses

1977 ◽  
Vol 15 (1) ◽  
pp. 22-31 ◽  
Author(s):  
J. Weinman ◽  
A. Hayat ◽  
G. Raviv
Keyword(s):  
Blood Volume ◽  
Arterial Blood ◽  
Arterial Blood Volume

scholarly journals Examination of Potential Mechanisms in the Enhancement of Cerebral Blood Flow by Hypoglycemia and Pharmacological Doses of Deoxyglucose

1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Plasma Lactate ◽  
Insulin Hypoglycemia ◽  
Glucose Levels ◽  
Arterial Blood ◽  
Arterial Plasma

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.

Hyperacute Stroke: Simultaneous Measurement of Relative Cerebral Blood Volume, Relative Cerebral Blood Flow, and Mean Tissue Transit Time

Radiology ◽  
1999 ◽  
Vol 210 (2) ◽  
pp. 519-527 ◽  
Author(s):  
A. Gregory Sorensen ◽  
William A. Copen ◽  
Leif Østergaard ◽  
Ferdinando S. Buonanno ◽  
R. Gilberto Gonzalez ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Transit Time ◽  
Simultaneous Measurement ◽  
Cerebral Blood Volume ◽  
Hyperacute Stroke ◽  
Relative Cerebral Blood Volume
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