Cerebral Blood Flow and Metabolism during Cardiopulmonary Bypass with Special Reference to Effects of Hypotension Induced by Prostacyclin

Feddersen, Kurt; Arén, Claes; Nilsson, Nils J.; Rådegran, Kjell

doi:10.1016/s0003-4975(10)62694-x

Cited by 22 publications

(10 citation statements)

References 25 publications

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“…Anaerobic metabolism likely plays a pivotal role in providing enhanced energy turnover to sustain cerebral activation (80), although, as in skeletal muscles, it cannot support prolonged activity. Moreover, the brain may release a small amount of lactate at rest and especially during hypoxemia or in response to cerebral hypoperfusion when MAP has become extremely low (25).…”

Section: Cerebral Metabolismmentioning

confidence: 99%

Cerebral blood flow and metabolism during exercise: implications for fatigue

Secher¹,

Seifert²,

Lieshout³

2008

Journal of Applied Physiology

294

281

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Secher NH, Seifert T, Van Lieshout JJ. Cerebral blood flow and metabolism during exercise, implications for fatigue. J Appl Physiol 104: 306 -314, 2008. First published October 25, 2007 doi:10.1152/japplphysiol.00853.2007.-During exercise: the Kety-Schmidt-determined cerebral blood flow (CBF) does not change because the jugular vein is collapsed in the upright position. In contrast, when CBF is evaluated by 133 Xe clearance, by flow in the internal carotid artery, or by flow velocity in basal cerebral arteries, a ϳ25% increase is detected with a parallel increase in metabolism. During activation, an increase in cerebral O 2 supply is required because there is no capillary recruitment within the brain and increased metabolism becomes dependent on an enhanced gradient for oxygen diffusion. During maximal whole body exercise, however, cerebral oxygenation decreases because of eventual arterial desaturation and marked hyperventilation-related hypocapnia of consequence for CBF. Reduced cerebral oxygenation affects recruitment of motor units, and supplemental O 2 enhances cerebral oxygenation and work capacity without effects on muscle oxygenation. Also, the work of breathing and the increasing temperature of the brain during exercise are of importance for the development of so-called central fatigue. During prolonged exercise, the perceived exertion is related to accumulation of ammonia in the brain, and data support the theory that glycogen depletion in astrocytes limits the ability of the brain to accelerate its metabolism during activation. The release of interleukin-6 from the brain when exercise is prolonged may represent a signaling pathway in matching the metabolic response of the brain. Preliminary data suggest a coupling between the circulatory and metabolic perturbations in the brain during strenuous exercise and the ability of the brain to access slow-twitch muscle fiber populations. ammonium; central fatigue; cerebral blood flow; cerebral metabolic ratio; glucose; glycogen; lactate; oxygen; temperature DURING EXERCISE, THERE IS hyperbolic relationship between work intensity and endurance, and A. V. Hill used the relationship to demonstrate that energy turnover can be taken to represent a continuous provision of energy supplemented by an energy store (56). Yet, it is the brain that makes the decision when to slow down or to stop exercise, and from that perspective fatigue is of central origin. Obviously, cerebral metabolism becomes affected if exercise has a duration that lowers blood glucose (74), and, equally, the low O 2 tension faced during mountaineering (47) affects brain function. Perturbation of cerebral metabolism is, however, not restricted to situations where the arterial glucose and O 2 levels are reduced. Recent investigations (3,65,70,90) indicate that also at sea level maximal exercise may be associated with so-called central fatigue as indicated by lower voluntary activation than the force elicited during evoked contractions.The purpose of this review is to address cerebral metabolism in ...

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Section: Cerebral Metabolismmentioning

confidence: 99%

Cerebral blood flow and metabolism during exercise: implications for fatigue

Secher¹,

Seifert²,

Lieshout³

2008

Journal of Applied Physiology

294

281

View full text Add to dashboard Cite

show abstract

“…The brain's capacity for anaerobic metabolism is limited by its phosphocreatine and glycogen stores (5 and 10 mM, respectively) (40), which are small compared with those of skeletal muscles (20 and 70 mM, respectively) (41–43). Yet, significant release of lactate from the brain has only been observed under hypoxic conditions (44–46) and with an extremely low blood pressure (47). However, if anaerobic glycolysis with glycogen as substrate were to sustain normal ATP turnover in the brain, a 10 mmol kg wet wt –1 glycogen store and a 5 mmol kg wet wt ‐1 store of phosphocreatine would last ~3.5 min and produce 20 mmol of lactate (assuming oxygen consumption of 2 μmol O 2 g wet wt ‐1 min ‐1 and P/O = 2.5).…”

Section: Anaerobic Metabolismmentioning

confidence: 99%

Lactate fuels the human brain during exercise

Quistorff¹,

Secher²,

2008

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The human brain releases a small amount of lactate at rest, and even an increase in arterial blood lactate during anesthesia does not provoke a net cerebral lactate uptake. However, during cerebral activation associated with exercise involving a marked increase in plasma lactate, the brain takes up lactate in proportion to the arterial concentration. Cerebral lactate uptake, together with glucose uptake, is larger than the uptake accounted for by the concomitant O(2) uptake, as reflected by the decrease in cerebral metabolic ratio (CMR) [the cerebral molar uptake ratio O(2)/(glucose+(1/2) lactate)] from a resting value of 6 to <2. The CMR also decreases when plasma lactate is not increased, as during prolonged exercise, cerebral activation associated with mental activity, or exposure to a stressful situation. The CMR decrease is prevented with combined beta(1)- and beta(2)-adrenergic receptor blockade but not with beta(1)-adrenergic blockade alone. Also, CMR decreases in response to epinephrine, suggesting that a beta(2)-adrenergic receptor mechanism enhances glucose and perhaps lactate transport across the blood-brain barrier. The pattern of CMR decrease under various forms of brain activation suggests that lactate may partially replace glucose as a substrate for oxidation. Thus, the notion of the human brain as an obligatory glucose consumer is not without exceptions.

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“…It should be considered that under these conditions, the effects of MAP and CO on CBF cannot be examined separately. As an example, when CO is rigorously controlled as is the case during cardiopulmonary bypass surgery, CBF is independent from CPP for a range of pressures (36,114).…”

Section: Regulation Of Cerebral Blood Flowmentioning

confidence: 99%

Syncope, cerebral perfusion, and oxygenation

Lieshout

Wieling

Karemaker

et al. 2003

Journal of Applied Physiology

324

293

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During standing, both the position of the cerebral circulation and the reductions in mean arterial pressure (MAP) and cardiac output challenge cerebral autoregulatory (CA) mechanisms. Syncope is most often associated with the upright position and can be provoked by any condition that jeopardizes cerebral blood flow (CBF) and regional cerebral tissue oxygenation (cO(2)Hb). Reflex (vasovagal) responses, cardiac arrhythmias, and autonomic failure are common causes. An important defense against a critical reduction in the central blood volume is that of muscle activity ("the muscle pump"), and if it is not applied even normal humans faint. Continuous tracking of CBF by transcranial Doppler-determined cerebral blood velocity (V(mean)) and near-infrared spectroscopy-determined cO(2)Hb contribute to understanding the cerebrovascular adjustments to postural stress; e.g., MAP does not necessarily reflect the cerebrovascular phenomena associated with (pre)syncope. CA may be interpreted as a frequency-dependent phenomenon with attenuated transfer of oscillations in MAP to V(mean) at low frequencies. The clinical implication is that CA does not respond to rapid changes in MAP; e.g., there is a transient fall in V(mean) on standing up and therefore a feeling of lightheadedness that even healthy humans sometimes experience. In subjects with recurrent vasovagal syncope, dynamic CA seems not different from that of healthy controls even during the last minutes before the syncope. Redistribution of cardiac output may affect cerebral perfusion by increased cerebral vascular resistance, supporting the view that cerebral perfusion depends on arterial inflow pressure provided that there is a sufficient cardiac output.

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Cerebral Blood Flow and Metabolism during Cardiopulmonary Bypass with Special Reference to Effects of Hypotension Induced by Prostacyclin

Cited by 22 publications

References 25 publications

Cerebral blood flow and metabolism during exercise: implications for fatigue

Cerebral blood flow and metabolism during exercise: implications for fatigue

Lactate fuels the human brain during exercise

Syncope, cerebral perfusion, and oxygenation

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