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.

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.

Nonuniform brain blood flow response to hypoxia in unanesthetized cats

1984 ◽  
Vol 57 (6) ◽  
pp. 1803-1808 ◽  
Author(s):  
J. A. Neubauer ◽  
N. H. Edelman
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Sympathetic Innervation ◽  
Brain Blood Flow ◽  
Intact Side ◽  
Flow Response ◽  
Regional Brain ◽  
Sympathetic Nervous ◽  
The Brain ◽  
Increased Blood Flow

In seven unanesthetized cats, radiolabeled microspheres were used to determine regional brain blood flow (rBBF) to the medulla-pons (M-P), midbrain-thalamus (M-T), cerebellum (Cb), and cortex (Cx) during three conditions: 1) control [arterial O2 tension (PaO2) = 81 Torr, arterial CO2 tension (PaCO2) = 26 Torr]; 2) hypocapnic hypoxia (PaO2 = 39 Torr, PaCO2 = 22 Torr); and 3) isocapnic hypoxia (PaO2 = 47 Torr, PaCO2 = 26 Torr). Hypoxia increased blood flow significantly more in the caudal brain stem (M-P) than in the Cx (P less than 0.05) during both hypocapnic hypoxia (M-P/Cx: +33/ +17 ml X min-1 X 100 g-1) and isocapnic hypoxia (M-P/Cx: +13/ -2 ml X min-1 X 100 g-1). Since sympathetic innervation is greater anatomically to rostral than to caudal vessels, we examined the rBBF response to hypocapnic hypoxia in seven additional cats after unilateral superior cervical gangliectomy. All seven cats had a reduction in the cortical-to-caudal brain stem trend on the denervated side of the brain (M-P/Cx: +27/+28 ml X min-1 X 100 g-1) compared with the intact side of the brain (M-P/Cx: +34/+24 ml X min-1 X 100 g-1) owing to both increases in Cx and decreases in M-P flows. We conclude that in unanesthetized cats hypoxia causes a greater increase in the caudal brain stem compared with cortical blood flow, and this differential response is related to modulation by the sympathetic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of exercise on the cerebral circulation and metabolism

1965 ◽  
Vol 20 (6) ◽  
pp. 1289-1293 ◽  
Author(s):  
Eldred G. Zobl ◽  
Frederick N. Talmers ◽  
Raymond C. Christensen ◽  
Lesem J. Baer
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Physical Exercise ◽  
Cerebral Metabolism ◽  
Peripheral Resistance ◽  
Hypertensive Patients ◽  
Total Body ◽  
Cerebral Resistance ◽  
The Brain ◽  
Cerebral Vascular Resistance

Cerebral hemodynamics and metabolism were studied in 13 normal patients and 14 hypertensive patients at rest and during vigorous physical exercise. Cerebral blood flow was determined by the nitrous oxide method. The cerebral vascular resistance in normal and hypertensive patients remained remarkably constant during exercise despite a marked reduction in total peripheral resistance. Cerebral blood flow was relatively unaffected by the marked increase in cardiac output and the cerebral metabolism did not share in the increased total body metabolism. During vigorous physical exercise the brain behaved as a steady-state organ. cerebral resistance; cerebral blood flow; cerebral oxygen consumption; exercise Submitted on February 4, 1965

Changes in Brain Blood Flow and Oxidative Metabolism During Mental Activity

Physiology ◽  
1987 ◽  
Vol 2 (4) ◽  
pp. 120-124 ◽  
Author(s):  
PE Roland
Keyword(s):  
Blood Flow ◽  
Oxidative Metabolism ◽  
Regional Cerebral Blood Flow ◽  
Mental Activity ◽  
Brain Blood Flow ◽  
Regional Cerebral Blood ◽  
Different Types ◽  
The Brain ◽  
Cerebral Oxidative Metabolism ◽  
Different Parts

Until recently mental activity was regarded as too subtle to have any effect on energy metabolism of the brain. Recent measurements show that when subjects perform pure mental activity regional cerebral oxidative metabolism and regional cerebral blood flow (which are dynamically coupled) increase in several areas of the brain, including the cerebellum. Different types of mental activity cause such increases in different parts of the brain.

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.

Ventral medullary extracellular fluid pH and blood flow during hypoxia

1982 ◽  
Vol 242 (3) ◽  
pp. R195-R198 ◽  
Author(s):  
W. F. Nolan ◽  
P. C. Houck ◽  
J. L. Thomas ◽  
D. G. Davies
Keyword(s):  
Blood Flow ◽  
Extracellular Fluid ◽  
Brain Blood Flow ◽  
Vascular Response ◽  
Radioactive Microspheres ◽  
Vascular Responses ◽  
Control Value ◽  
Total Brain ◽  
The Brain ◽  
Ph Microelectrodes

Vascular responses of the ventral medulla and total brain to 30-60 min of isocapnic hypoxia (PaO2 = 32 +/- 2 Torr) were examined using radioactive microspheres in anesthetized, paralyzed, and artificially ventilated cats. Ventral medullary extracellular fluid (ECF) pH was measured using pH microelectrodes with tip diameters of 1-2 micrometers. Total brain blood flow (Q) increased significantly from a control value of 53 +/- 8 (mean +/- SE) to 160 +/- 42 ml.100 g-1.min-1 following 30-60 min of hypoxia. Ventral medullary Q increased from 28 +/- 5 to 97 +/- 20 ml.100 g-1.min-1 and ECF pH decreased by 0.15 +/- 0.06 pH U. Q responses are attributable to decreased vascular resistance as arterial pressure remained constant. The sensitivity of the ventral medullary vasculature to isocapnic hypoxia did not differ from that of the brain as a whole. The results show that under the conditions of our experiment, the ventral medullary vascular response to hypoxia is not sufficient to stabilize local ECF pH. The observation of simultaneously reduced pH and increased Q is consistent with a role for ECF H+ in mediating the cerebrovascular response to hypoxia.

scholarly journals Role of Nitric Oxide in the Elevation of Cerebral Blood Flow Induced by Acetylcholine and Anoxia in the Turtle

1996 ◽  
Vol 16 (2) ◽  
pp. 290-295 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson ◽  
Peter L. Lutz
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Freshwater Turtle ◽  
Brain Blood Flow ◽  
Brain Surface ◽  
Synthase Inhibitor ◽  
The Brain

Nitric oxide (NO)-dependent regulation of brain blood flow has hitherto not been studied in reptiles. By observing the brain surface (telencephalon) of the freshwater turtle (Trachemys scripta) with epiillumination microscopy, we show that topical application of acetylcholine (ACh) induces an increase in CBF velocity that can be completely blocked by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). The effect of L-NAME was reversed by L-arginine. Also, sodium nitroprusside (SNP), which decomposes to liberate NO, caused an increase in CBF velocity. By contrast, L-NAME could not block the increase in blood flow velocity caused by anoxia. Interestingly, superfusing the brain with ACh or SNP during anoxia had no effect on the blood flow velocity. The results suggest that NO is an endogenous vasodilator in the turtle brain, mediating the effects of ACh during normoxia. By contrast, anoxia does not rely on NO as a vasodilator.

Regional distribution of cerebral blood flow during exercise in dogs

1980 ◽  
Vol 48 (2) ◽  
pp. 213-217 ◽  
Author(s):  
P. M. Gross ◽  
M. L. Marcus ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Distribution ◽  
Moderate Intensity ◽  
Regional Cerebral Blood ◽  
Arterial Pco2 ◽  
Regional Flow ◽  
Arterial Blood ◽  
The Brain ◽  
Cerebral Vascular Resistance

This study was performed to determine whether exercise produces vasodilatation in regions of the brain that are associated with motor functions despite the associated vasoconstrictor effect of hypocapnia. Total and regional cerebral blood flow (CBF) were measured with microspheres in dogs during treadmill exercise of moderate intensity. Flow was also measured at rest after stimulation of ventilation with doxapram. During moderate exercise, total CBF was not changed significantly, but regional flow was increased in structures associated with motor-sensory control; blood flow to motor-sensory cortex, neocerebellar and paleocerebellar cortex, and spinal cord increased 30 +/- 7%, 39 +/- 8%, and 29 +/- 4%, respectively (P less than 0.05). After doxapram, which increased arterial blood pressure and decreased arterial PCO2 to levels similar to those during exercise, total CBF decreased and there was no redistribution of CBF. These results indicate that exercise in conscious dogs increases blood flow in regions of the brain associated with movement despite the associated vasoconstrictor stimulus of arterial hypocapnia. Thus, during exercise, local dilator influences that presumably result from increases in metabolism predominate over a potent constrictor stimulus in regulation of cerebral vascular resistance.

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.

The contribution of carotid rete variability to brain temperature variability in sheep in a thermoneutral environment

2007 ◽  
Vol 292 (3) ◽  
pp. R1298-R1305 ◽  
Author(s):  
Shane K. Maloney ◽  
Duncan Mitchell ◽  
Dominique Blache
Keyword(s):  
Blood Flow ◽  
Temperature Difference ◽  
Heat Production ◽  
Brain Temperature ◽  
Brain Blood Flow ◽  
Tight Coupling ◽  
Hypothalamic Temperature ◽  
Arterial Blood ◽  
Carotid Arterial ◽  
The Brain

The degree of variability in the temperature difference between the brain and carotid arterial blood is greater than expected from the presumed tight coupling between brain heat production and brain blood flow. In animals with a carotid rete, some of that variability arises in the rete. Using thermometric data loggers in five sheep, we have measured the temperature of arterial blood before it enters the carotid rete and after it has perfused the carotid rete, as well as hypothalamic temperature, every 2 min for between 6 and 12 days. The sheep were conscious, unrestrained, and maintained at an ambient temperature of 20–22°C. On average, carotid arterial blood and brain temperatures were the same, with a decrease in blood temperature of 0.35°C across the rete and then an increase in temperature of the same magnitude between blood leaving the rete and the brain. Rete cooling of arterial blood took place at temperatures below the threshold for selective brain cooling. All of the variability in the temperature difference between carotid artery and brain was attributable statistically to variability in the temperature difference across the rete. The temperature difference between arterial blood leaving the rete and the brain varied from −0.1 to 0.9°C. Some of this variability was related to a thermal inertia of the brain, but the majority we attribute to instability in the relationship between brain blood flow and brain heat production.

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