scholarly journals Fossil skulls reveal that blood flow rate to the brain increased faster than brain volume during human evolution

2016 ◽  
Vol 3 (8) ◽  
pp. 160305 ◽  
Author(s):  
Roger S. Seymour ◽  
Vanya Bosiocic ◽  
Edward P. Snelling

The evolution of human cognition has been inferred from anthropological discoveries and estimates of brain size from fossil skulls. A more direct measure of cognition would be cerebral metabolic rate, which is proportional to cerebral blood flow rate (perfusion). The hominin cerebrum is supplied almost exclusively by the internal carotid arteries. The sizes of the foramina that transmitted these vessels in life can be measured in hominin fossil skulls and used to calculate cerebral perfusion rate. Perfusion in 11 species of hominin ancestors, from Australopithecus to archaic Homo sapiens , increases disproportionately when scaled against brain volume (the allometric exponent is 1.41). The high exponent indicates an increase in the metabolic intensity of cerebral tissue in later Homo species, rather than remaining constant (1.0) as expected by a linear increase in neuron number, or decreasing according to Kleiber's Law (0.75). During 3 Myr of hominin evolution, cerebral tissue perfusion increased 1.7-fold, which, when multiplied by a 3.5-fold increase in brain size, indicates a 6.0-fold increase in total cerebral blood flow rate. This is probably associated with increased interneuron connectivity, synaptic activity and cognitive function, which all ultimately depend on cerebral metabolic rate.

2015 ◽  
Vol 35 (4) ◽  
pp. 648-654 ◽  
Author(s):  
Laleh Zarrinkoob ◽  
Khalid Ambarki ◽  
Anders Wåhlin ◽  
Richard Birgander ◽  
Anders Eklund ◽  
...  

High-resolution phase—contrast magnetic resonance imaging can now assess flow in proximal and distal cerebral arteries. The aim of this study was to describe how total cerebral blood flow (tCBF) is distributed into the vascular tree with regard to age, sex and anatomic variations. Forty-nine healthy young (mean 25 years) and 45 elderly (mean 71 years) individuals were included. Blood flow rate (BFR) in 21 intra- and extracerebral arteries was measured. Total cerebral blood flow was defined as BFR in the internal carotid plus vertebral arteries and mean cerebral perfusion as tCBF/brain volume. Carotid/vertebral distribution was 72%/28% and was not related to age, sex, or brain volume. Total cerebral blood flow (717±123 mL/min) was distributed to each side as follows: middle cerebral artery (MCA), 21%; distal MCA, 6%; anterior cerebral artery (ACA), 12%, distal ACA, 4%; ophthalmic artery, 2%; posterior cerebral artery (PCA), 8%; and 20% to basilar artery. Deviating distributions were observed in subjects with ‘fetal’ PCA. Blood flow rate in cerebral arteries decreased with increasing age ( P<0.05) but not in extracerebral arteries. Mean cerebral perfusion was higher in women (women: 61±8; men: 55±6 mL/min/100 mL, P<0.001). The study describes a new method to outline the flow profile of the cerebral vascular tree, including reference values, and should be used for grading the collateral flow system.


1985 ◽  
Vol 5 (4) ◽  
pp. 600-608 ◽  
Author(s):  
William J. Powers ◽  
Robert L. Grubb ◽  
Danielle Darriet ◽  
Marcus E. Raichle

This study was undertaken to determine the minimum CBF and CMRO2 required by the human brain to maintain normal function and viability for more than a few hours. Positron emission tomography (PET) was used to perform regional measurements in 50 subjects with varying degrees of cerebral ischemia but no evidence of infarction. There were 24 normal subjects, 24 subjects with arteriographic evidence of vascular disease of the carotid system, and two subjects with reversible ischemic neurological deficits due to cerebral vasospasm. Minimum values found in the 48 subjects with normal neurological function were 19 ml/100 g-min for regional cerebral blood flow (rCBF) and 1.3 ml/100 g-min for regional cerebral metabolic rate of oxygen (rCMRO2). Minimum values for all 50 subjects with viable cerebral tissue were 15 ml/100 g-min for rCBF and 1.3 ml/100 g-min for rCMRO2. Comparison of these measurements with values from 20 areas of established cerebral infarction in 10 subjects demonstrated that 80% (16/20) of infarcted regions had rCMRO2 values below the lower normal limit of 1.3 ml/100g-min. Measurements of rCBF, regional cerebral blood volume, and oxygen extraction fraction were less useful for distinguishing viable from infarcted tissue. These data indicate that quantitative regional measurements of rCMRO2 with PET accurately distinguish viable from nonviable cerebral tissue and may be useful in the prospective identification of patients with reversible ischemia.


1994 ◽  
Vol 14 (5) ◽  
pp. 877-881 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson ◽  
Peter L. Lutz

The exceptional ability of the turtle brain to survive prolonged anoxia makes it a unique model for studying anoxic survival mechanisms. We have used epiillumination microscopy to record blood flow rate in venules on the cortical surface of turtles ( Trachemys scripta). During anoxia, blood flow rate increased 1.7 times after 45–75 min, whereupon it fell back, reaching preanoxic values after 115 min of anoxia. Topical super-fusion with adenosine (50 μ M) during normoxia caused a 3.8-fold increase in flow rate. Superfusing the brain with the adenosine receptor blocker aminophylline (250 μ M) totally inhibited the effects of both adenosine and anoxia, while aminophylline had no effect on normoxic flow rate. None of the treatments affected systemic blood pressure. These results indicate an initial adenosine-mediated increase in cerebral blood flow rate during anoxia, probably representing an emergency response before deep metabolic depression sets in.


1994 ◽  
Vol 267 (2) ◽  
pp. R590-R595 ◽  
Author(s):  
G. E. Nilsson ◽  
P. Hylland ◽  
C. O. Lofman

The crucian carp (Carassius carassius) has the rare ability to survive prolonged anoxia, indicating an extraordinary capacity for glycolytic ATP production, especially in a highly energy-consuming organ like the brain. For the brain to be able to increase its glycolytic flux during anoxia and profit from the large liver glycogen store, an increased glucose delivery from the blood would be expected. Nevertheless, the effect of anoxia on brain blood flow in crucian carp has never been studied previously. We have used epireflection microscopy to directly observe and measure blood flow rate on the brain surface (optic lobes) during normoxia and anoxia in crucian carp. We have also examined the possibility that adenosine participates in the regulation of brain blood flow rate in crucian carp. The results showed a 2.16-fold increase in brain blood flow rate during anoxia. A similar increase was seen after topical application of adenosine during normoxia, while adenosine was without effect during anoxia. Moreover, superfusing the brain with the adenosine receptor blocker aminophylline inhibited the effect of anoxia on brain blood flow rate, clearly suggesting a mediatory role of adenosine in the anoxia-induced increase in brain blood flow rate.


2021 ◽  
Author(s):  
George Hyde-Linaker ◽  
Pauline Hall Barrientos ◽  
Sokratis Stoumpos ◽  
Asimina Kazakidi

Abstract Despite arteriovenous fistulae (AVF) being the preferred vascular access for haemodialysis, high primary failure rates (30-70%) and low one-year patency rates (40-70%) hamper their use. The haemodynamics within the vessels of the fistula change significantly following surgical creation of the anastomosis and can be a surrogate of AVF success or failure. Computational fluid dynamics (CFD) can crucially predict AVF outcomes through robust analysis of a fistula’s haemodynamic patterns, which is impractical in-vivo. We present a proof-of-concept CFD framework for characterising the AVF blood flow prior and following surgical creation of a successful left radiocephalic AVF in a 20-year-old end-stage kidney disease patient. The reconstructed vasculature was generated utilising multiple contrast-enhanced magnetic resonance imaging (MRI) datasets. Large eddy simulations were conducted for establishing the extent of arterial and venous remodelling. Following anastomosis creation, a significant 2-3-fold increase in blood flow rate was induced downstream of the left subclavian artery. This was validated through comparison with post-AVF patient-specific phase-contrast data. The increased flow rate yielded an increase in time-averaged wall shear stress (TAWSS), a key marker of adaptive vascular remodelling. We have demonstrated TAWSS and oscillatory shear distributions of the transitional-flow in the venous anastomosis are predictive of AVF remodelling.


1990 ◽  
Vol 258 (2) ◽  
pp. H408-H413 ◽  
Author(s):  
W. M. Armstead ◽  
C. W. Leffler ◽  
D. W. Busija ◽  
R. Mirro

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.


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