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Radiology Nov 2019
Topics: Blood Volume; Kidney
PubMed: 31577176
DOI: 10.1148/radiol.2019192035 -
Journal of Cerebral Blood Flow and... Dec 2022Non-invasive mapping of cerebral perfusion is critical for understanding neurovascular and neurodegenerative diseases. However, perfusion MRI methods cannot be easily...
Non-invasive mapping of cerebral perfusion is critical for understanding neurovascular and neurodegenerative diseases. However, perfusion MRI methods cannot be easily implemented for whole-brain studies in mice because of their small size. To overcome this issue, a transient hypoxia stimulus was applied to induce a bolus of deoxyhemoglobins as an endogenous paramagnetic contrast in blood oxygenation level-dependent (BOLD) MRI. Based on stimulus-duration-dependent studies, 5 s anoxic stimulus was chosen, which induced a decrease in arterial oxygenation to 59%. Dynamic susceptibility changes were acquired with whole-brain BOLD MRI using both all-vessel-sensitive gradient-echo and microvascular-sensitive spin-echo readouts. Cerebral blood flow (CBF) and cerebral blood volume (CBV) were quantified by modeling BOLD dynamics using a partial-volume-corrected arterial input function. In the mouse under ketamine/xylazine anesthesia, total CBF and CBV were 112.0 ± 15.0 ml/100 g/min and 3.39 ± 0.59 ml/100 g (n = 15 mice), respectively, whereas microvascular CBF and CBV were 85.8 ± 6.9 ml/100 g/min and 2.23 ± 0.27 ml/100 g (n = 7 mice), respectively. Regional total vs. microvascular perfusion metrics were highly correlated but a slight mismatch was observed in the large-vessel areas and cortical depth profiles. Overall, this non-invasive, repeatable, simple hypoxia BOLD-MRI approach is viable for perfusion mapping of rodents.
Topics: Animals; Mice; Blood Volume; Magnetic Resonance Imaging; Brain; Cerebrovascular Circulation; Perfusion; Hypoxia
PubMed: 35903000
DOI: 10.1177/0271678X221117008 -
British Medical Journal Mar 1968
Topics: Aged; Blood Volume; Humans; Hypotension; Infusions, Parenteral
PubMed: 5641500
DOI: 10.1136/bmj.1.5595.839-a -
Anesthesiology Nov 2015Cerebral blood flow (CBF) is rigorously regulated by various powerful mechanisms to safeguard the match between cerebral metabolic demand and supply. The question of how... (Review)
Review
Cerebral blood flow (CBF) is rigorously regulated by various powerful mechanisms to safeguard the match between cerebral metabolic demand and supply. The question of how a change in cardiac output (CO) affects CBF is fundamental, because CBF is dependent on constantly receiving a significant proportion of CO. The authors reviewed the studies that investigated the association between CO and CBF in healthy volunteers and patients with chronic heart failure. The overall evidence shows that an alteration in CO, either acutely or chronically, leads to a change in CBF that is independent of other CBF-regulating parameters including blood pressure and carbon dioxide. However, studies on the association between CO and CBF in patients with varying neurologic, medical, and surgical conditions were confounded by methodologic limitations. Given that CBF regulation is multifactorial but the various processes must exert their effects on the cerebral circulation simultaneously, the authors propose a conceptual framework that integrates the various CBF-regulating processes at the level of cerebral arteries/arterioles while still maintaining autoregulation. The clinical implications pertinent to the effect of CO on CBF are discussed. Outcome research relating to the management of CO and CBF in high-risk patients or during high-risk surgeries is needed.
Topics: Adult; Blood Flow Velocity; Blood Volume; Brain; Cardiac Output; Cerebrovascular Circulation; Homeostasis; Humans
PubMed: 26402848
DOI: 10.1097/ALN.0000000000000872 -
Anesthesiology Sep 2013
Topics: Arterial Pressure; Blood Volume; Cardiac Output; Female; Humans; Male; Perioperative Period
PubMed: 23962932
DOI: 10.1097/ALN.0b013e31829e094e -
Anesthesiology Sep 2013
Topics: Arterial Pressure; Blood Volume; Cardiac Output; Female; Humans; Male; Perioperative Period
PubMed: 23962931
DOI: 10.1097/ALN.0b013e31829e090c -
Anesthesiology 1965
Review
Topics: Blood Volume; Delivery, Obstetric; Female; Humans; Postpartum Period; Pregnancy
PubMed: 14313451
DOI: 10.1097/00000542-196507000-00004 -
Kidney International Nov 2016It is widely held that in response to high salt diets, normal individuals are acutely and chronically resistant to salt-induced hypertension because they rapidly excrete... (Review)
Review
It is widely held that in response to high salt diets, normal individuals are acutely and chronically resistant to salt-induced hypertension because they rapidly excrete salt and retain little of it so that their blood volume, and therefore blood pressure, does not increase. Conversely, it is also widely held that salt-sensitive individuals develop salt-induced hypertension because of an impaired renal capacity to excrete salt that causes greater salt retention and blood volume expansion than that which occurs in normal salt-resistant individuals. Here we review results of both acute and chronic salt-loading studies that have compared salt-induced changes in sodium retention and blood volume between normal subjects (salt-resistant normotensive control subjects) and salt-sensitive subjects. The results of properly controlled studies strongly support an alternative view: during acute or chronic increases in salt intake, normal salt-resistant subjects undergo substantial salt retention and do not excrete salt more rapidly, retain less sodium, or undergo lesser blood volume expansion than do salt-sensitive subjects. These observations: (i) directly conflict with the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension, and (ii) have implications for contemporary understanding of how various genetic, immunologic, and other factors determine acute and chronic blood pressure responses to high salt diets.
Topics: Blood Volume; Case-Control Studies; Humans; Hypertension; Sodium; Sodium Chloride, Dietary
PubMed: 27546606
DOI: 10.1016/j.kint.2016.05.032 -
American Journal of Physiology.... Feb 2006We have previously shown that both plasma protein restitution and plasma volume restitution are significantly enhanced in female rats hemorrhaged during the proestrus...
We have previously shown that both plasma protein restitution and plasma volume restitution are significantly enhanced in female rats hemorrhaged during the proestrus phase of the estrous cycle. Estradiol and progesterone levels are markedly elevated during proestrus and also increase during pregnancy. The present studies were therefore designed to determine whether the ability to restore plasma protein and blood volume after hemorrhage is augmented during pregnancy and by chronically elevated estradiol levels. The response to moderate hemorrhage (22-23% blood loss) was evaluated in conscious pregnant rats during early and midgestation and compared with that of virgin female rats studied during metestrus. At 22 h posthemorrhage, plasma volume had increased to greater than basal levels, and blood volume was restored to 93 +/- 1% (metestrus), 91 +/- 2% (early pregnancy), and 98 +/- 2% (midgestation) of control (P > 0.05). Animals hemorrhaged during metestrus or early pregnancy restored the same amount of protein to the plasma as had been removed, whereas those hemorrhaged during midgestation restored nearly 50% more plasma protein than had been removed (P < 0.01). In ovariectomized animals with chronic steroid replacement that maintained plasma progesterone at metestrus levels (15 +/- 2 ng/ml) but raised plasma estradiol to twofold that of midgestation (22 +/- 3 pg/ml), the blood volume and plasma protein restitution responses to hemorrhage did not differ from those of ovariectomized animals with no steroid replacement. In summary, posthemorrhage restoration of plasma protein content is significantly augmented during midgestation, but not during early pregnancy. This augmented response cannot be attributed to chronic elevation of plasma estradiol levels alone.
Topics: Animals; Blood Pressure; Blood Proteins; Blood Volume; Body Weight; Estradiol; Female; Heart Rate; Hematocrit; Hemorrhage; Hormone Replacement Therapy; Ovariectomy; Pregnancy; Progesterone; Rats; Rats, Sprague-Dawley; Time Factors
PubMed: 16166212
DOI: 10.1152/ajpregu.00011.2005 -
American Journal of Physiology. Heart... Aug 2017
Topics: Atrial Pressure; Blood Volume; Cardiac Output; Cardiopulmonary Bypass
PubMed: 28626078
DOI: 10.1152/ajpheart.00315.2017