Anoxia and adenosine induce increased cerebral blood flow rate in crucian carp

1994 ◽  
Vol 267 (2) ◽  
pp. R590-R595 ◽  
Author(s):  
G. E. Nilsson ◽  
P. Hylland ◽  
C. O. Lofman
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Crucian Carp ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Liver Glycogen ◽  
Glycolytic Flux ◽  
Brain Blood Flow ◽  
Atp Production ◽  
The Brain

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.

scholarly journals Time Course of Anoxia-Induced Increase in Cerebral Blood Flow Rate in Turtles: Evidence for a Role of Adenosine

1994 ◽  
Vol 14 (5) ◽  
pp. 877-881 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson ◽  
Peter L. Lutz
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Rate ◽  
Time Course ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Systemic Blood Pressure ◽  
The Brain ◽  
Survival Mechanisms

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.

scholarly journals Patient-specific computational haemodynamics associated with surgical creation of an arteriovenous fistula

2021 ◽  
Author(s):  
George Hyde-Linaker ◽  
Pauline Hall Barrientos ◽  
Sokratis Stoumpos ◽  
Asimina Kazakidi
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Disease Patient ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Transitional Flow ◽  
Patient Specific ◽  
Venous Anastomosis ◽  
End Stage

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.

Changes in local cerebral blood flow following profound systemic hypotension

1976 ◽  
Vol 44 (2) ◽  
pp. 215-225 ◽  
Author(s):  
Francis W. Gamache ◽  
Ronald E. Myers ◽  
Esteban Monell
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Rate ◽  
Rank Order ◽  
Blood Flow Rate ◽  
Rapid Onset ◽  
Border Zone ◽  
Local Cerebral Blood Flow ◽  
Content Type ◽  
The Brain

✓ The authors studied local cerebral blood flow in monkeys rendered hypotensive by infusion of a ganglionic blocking agent. Application of the 14C-antipyrine method demonstrated that the blood flow: 1) normally varies reproducibly from one structure to another within the brain; 2) appears at its lowest level in all structures during the early minutes of a rapid-onset hypotension; 3) maintains the same general rank order of blood flow rate during hypotension as was present during normotension; and 4) returns to supranormal levels immediately following the rapid restoration of blood pressure. The values for local cerebral blood flow remain close-to-normal in some animals and diminish significantly in others during late recovery from hypotension. The close-to-normal values accompany uncomplicated recoveries while the diminished values appear in those animals which became neurologically depressed. Areas of the brain considered predisposed to hypotensive injury did not exhibit depressions in blood flow rate during hypotension more markedly than did other brain areas. The present results are interpreted as strong evidence against the “border zone” hypothesis.

scholarly journals Evidence That Acetylcholine Mediates Increased Cerebral Blood Flow Velocity in Crucian Carp through a Nitric Oxide—Dependent Mechanism

1995 ◽  
Vol 15 (3) ◽  
pp. 519-524 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Crucian Carp ◽  
Cerebral Blood Flow Velocity ◽  
Early Event ◽  
Brain Blood Flow ◽  
The Brain

Nitric oxide (NO)–dependent regulation of brain blood flow has not been proven to exist in fish or other ectothermic vertebrates. Using epi-illumination microscopy on the brain surface (optic lobes) of crucian carp ( Carassius carassius), we show that superfusing the brain with acetylcholine (ACh) induces an increase in cerebral blood flow velocity that can be completely blocked by the NO synthase inhibitors NG-nitro-l-arginine methylester (L-NAME) and NG-nitro-l-arginine. Also, sodium nitroprusside, which decomposes to liberate NO, causes an increase in cerebral blood flow velocity. By contrast, L-NAME does not block the increase in blood flow velocity caused by anoxia. The results suggest that NO is an endogenous vasodilator in crucian carp brain that mediates the effects of ACh. Because teleost fish deviated from other vertebrates 400 million years ago, these results suggest that NO-dependent brain blood flow regulation was an early event in vertebrate evolution.

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
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Flow Rate ◽  
Brain Volume ◽  
Brain Size ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Cerebral Tissue ◽  
Cerebral Metabolic Rate

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.

Contribution of hypercapnia and trigeminal stimulation to cerebrovascular dilation during simulated diving

1998 ◽  
Vol 274 (4) ◽  
pp. R921-R930 ◽  
Author(s):  
G. P. Ollenberger ◽  
N. H. West
Keyword(s):  
Blood Flow ◽  
Fold Increase ◽  
Brain Blood Flow ◽  
Relative Contribution ◽  
Trigeminal Stimulation ◽  
Hemodynamic Profile ◽  
The Brain ◽  
Cerebral Vascular Resistance ◽  
Dive Response ◽  
Flow Tracer

We investigated the relative contribution of humoral (carbon dioxide) and neural (trigeminal stimulation) inputs in the cerebrovasodilatory response to simulated diving in the rat. The cerebral hemodynamic profile of rats was determined using the brain blood flow tracer N-[14C]isopropyl- p-iodoamphetamine. During a simulated dive response, cerebral vascular resistance (CVR) decreased 63.1%, resulting in a 1.5-fold increase in cerebral blood flow (CBF). To investigate the contribution of hypercapnia to the decrease in CVR during simulated diving, we measured CBF during simulated diving in rats with preexisting hypocapnia. To investigate the contribution of trigeminal input, we measured CBF during periods of trigeminal stimulation alone with continued ventilation. Preexisting hypocapnia abolished the cerebrovasodilatory response to simulated diving. Trigeminal stimulation alone did not produce a significant increase in CBF from control values in any brain region, suggesting that trigeminal input does not contribute to the cerebrovascular response to simulated diving in rats. These results suggest that the cerebrovasodilatory response observed during diving in small mammals is driven primarily by progressive hypercapnia associated with asphyxia.

The Effect of Furosemide on the Intrarenal Blood Flow Distribution in the Dog

1972 ◽  
Vol 50 (8) ◽  
pp. 774-783 ◽  
Author(s):  
Serge Carrière ◽  
Michel Desrosiers ◽  
Jacques Friborg ◽  
Michèle Gagnan Brunette
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Urine Volume ◽  
Flow Distribution ◽  
Blood Flow Rate ◽  
Initial Distribution ◽  
Blood Flow Distribution ◽  
Intrarenal Blood Flow ◽  
Femoral Blood ◽  
Furosemide Administration

Furosemide (40 μg/min) was perfused directly into the renal artery of dogs in whom the femoral blood pressure was reduced (80 mm Hg) by aortic clamping above the renal arteries. This maneuver, which does not influence the intrarenal blood flow distribution, produced significant decreases of the urine volume, natriuresis, Ccreat, and CPAH, and prevented the marked diuresis normally produced by furosemide. Therefore the chances that systemic physiological changes occurred, secondary to large fluid movements, were minimized. In those conditions, however, furosemide produced a significant increase of the urine output and sodium excretion in the experimental kidney whereas Ccreat and CPAH were not affected. The outer cortical blood flow rate (ml/100 g-min) was modified neither by aortic constriction (562 ± 68 versus 569 ± 83) nor by the subsequent administration of furosemide (424 ± 70). The blood flow rate of the outer medulla in these three conditions remained unchanged (147 ± 52 versus 171 ± 44 versus 159 ± 54). The initial distribution of the radioactivity in each compartment remained comparable in the three conditions. In parallel with the results from the krypton-85 disappearance curves, the autoradiograms, silicone rubber casts, and EPAH did not suggest any change in the renal blood flow distribution secondary to furosemide administration.

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