Changes In Cerebral Vascular Resistance Research Articles

AltitudeOmics: the effect of high altitude ascent and acclimatisation on cerebral blood flow regulation (885.1)

Adequate oxygen supply to the brain is critical to maintain brain function. Hypoxia presents a unique challenge in maintaining sufficient cerebral oxygen delivery (DO2). We assessed by ultrasound cerebral blood flow (CBF: internal carotid, vertebral arteries and middle cerebral artery velocity [MCAv]) and arterial blood pressure (index of cerebral autoregulation; CA) during rest and hypercapnic breathing (MCAv‐CO2 slope; index of cerebrovascular function) in 21 healthy subjects at sea‐level (SL) and upon arrival at 5260m (ALT1) and after 16 days of acclimatisation (ALT16). Cerebral DO2 was calculated as the product of arterial oxygen content (CaO2) and flow in each respective artery and summed to estimate global CBF. Global CBF increased ~70% upon arrival at ALT1 (P<0.05) and returned to SL values at ALT16 as a result of changes in cerebral vascular resistance. A reciprocal pattern in CaO2 maintained global cerebral DO2 across acclimatisation. MCAv‐CO2 slope was elevated by ~79% upon arrival at ALT1 and further increased by ~89% at ALT16 (P<0.05). Indexes of CA were reduced upon arrival at ALT1 (P<0.05), but did not change with acclimatisation at ALT16 (P>0.10). Cerebral DO2 was well maintained upon acute exposure and acclimatisation to hypoxia. Cerebrovascular function was enhanced with acclimatisation to high altitude, but these changes did not mitigate the reduction in CA associated with hypoxic exposure.Grant Funding Source: Supported by U.S. Department of Defense

AltitudeOmics: effect of ascent and acclimatization to 5260 m on regional cerebral oxygen delivery

Cerebral hypoxaemia associated with rapid ascent to high altitude can be life threatening; yet, with proper acclimatization, cerebral function can be maintained well enough for humans to thrive. We investigated adjustments in global and regional cerebral oxygen delivery (DO2) as 21 healthy volunteers rapidly ascended and acclimatized to 5260m. Ultrasound indices of cerebral blood flow in internal carotid and vertebral arteries were measured at sea level, upon arrival at 5260m (ALT1; atmospheric pressure 409mmHg) and after 16days of acclimatization (ALT16). Cerebral DO2 was calculated as the product of arterial oxygen content and flow in each respective artery and summed to estimate global cerebral blood flow. Vascular resistances were calculated as the quotient of mean arterial pressure and respective flows. Global cerebral blood flow increased by ∼70% upon arrival at ALT1 (P<0.001) and returned to sea-level values at ALT16 as a result of changes in cerebral vascular resistance. A reciprocal pattern in arterial oxygen content maintained global cerebral DO2 throughout acclimatization, although DO2 to the posterior cerebral circulation was increased by ∼25% at ALT1 (P=0.032). We conclude that cerebral DO2 is well maintained upon acute exposure and acclimatization to hypoxia, particularly in the posterior and inferior regions of the brain associated with vital homeostatic functions. This tight regulation of cerebral DO2 was achieved through integrated adjustments in local vascular resistances to alter cerebral perfusion during both acute and chronic exposure to hypoxia.

Pediatric Head Injury

1. Jeff E. Schunk, MD* 2. Sara A. Schutzman, MD† 1. *Professor, Division of Pediatric Emergency Medicine, Department of Pediatrics, University of Utah School of Medicine, Primary Children’s Medical Center, Salt Lake City, UT. 2. †Assistant Professor, Department of Pediatrics, Harvard Medical School, Senior Associate Physician in Medicine, Division of Emergency Medicine, Department of Medicine, Children’s Hospital Boston, Boston, MA. * Abbreviations: BSF: : basilar skull fracture CSF: : cerebrospinal fluid CT: : computed tomography EDH: : epidural hemorrhage GCS: : Glasgow Coma Scale ICI: : intracranial injury ICP: : intracranial pressure PECARN: : Pediatric Emergency Care Applied Research Network SAH: : subarachnoid hemorrhage SDH: : subdural hemorrhage TBI: : traumatic brain injury Recent studies have provided updated guidelines for the diagnosis of head injury and the management of patients who experience concussions. A multidisciplinary panel has recently issued new guidelines for return to play after head injury. After reading this article, readers should be able to: 1. Understand the anatomy and pathophysiology relevant to pediatric head injuries. 2. Take an appropriate history, perform an appropriate physical examination, and decide what imaging, if any, is warranted in the case of a child with a head injury. 3. Know the characteristics of the various types of intracranial injuries. 4. Understand the proper management of both minor and severe head injuries in children. Pediatric head injury is extremely common. Although the vast majority of children with head trauma have minor injuries, a small number, even among well-appearing children, will have more serious injuries with the potential for deterioration and significant sequelae. The clinician is challenged to discern which few among the many injured are at high risk for intracranial complications. Clinical symptoms are neither completely sensitive nor specific for significant injury: vomiting may be associated with intracranial injury (ICI), but most children who experience vomiting do not have a complication. Computed tomography (CT) accurately identifies ICIs requiring intervention, but also identifies minor lesions with unclear clinical importance (ie, not requiring intervention) and exposes developing brains to ionizing radiation with the associated risks. Although clinical decision rules determine which children are at highest risk and provide a useful clinical framework, they may not necessarily direct care. Additionally, in this era of reliance on imaging, it is important to remember what the clinical examination tells us regarding brain function, information that …

Leaky vessels: how the brain deals with pregnancy under pressure

Leaky vessels: how the brain deals with pregnancy under pressure

Impact of Pump Flow Rate During Selective Cerebral Perfusion on Cerebral Hemodynamics and Metabolism

Although hypothermic selective cerebral perfusion (SCP) is widely used for cerebral protection during aortic surgery, little is known about the ideal pump-flow management during this procedure. This study explored cerebral hemodynamics and metabolism at two different flow rates. Fourteen pigs (33 to 38 kg) were cooled on cardiopulmonary bypass to 25°C. After 10 minutes of hypothermic circulatory arrest, the animals were randomly assigned to 60 minutes of SCP at two different pump flow rates: 8 mL·kg(-1)·min(-1) (n = 7) and 18 mL·kg(-1)·min(-1) (n = 7). Microspheres were injected at baseline, coolest temperature, and at 5, 15, 25, and 60 minutes of SCP to calculate cerebral blood flow, cerebral vascular resistance, metabolic rate, and intracranial pressure. Cerebral blood flow decreased during cooling to 41% of the baseline value (from 57 ± 10 to 23 ± 4 mL·min(-1)·100 g(-1)). It recovered during the initial 15 minutes of SCP, showing a significantly higher increase (p = 0.017) at high-flow versus low-flow perfusion (139 ± 41 versus 75 ± 22 mL·min(-1)·100 g(-1)). After 60 minutes of SCP the cerebral blood flow almost returned to baseline values in the low-flow group (43 ± 25 mL·min(-1)·100 g(-1)), but showed an unexpected decrease (30 ± 7 mL·min(-1)·100 g(-1)) in the high-flow group. The highest regional cerebral blood flow was seen in the cortex (66 ± 12 mL·min(-1)·100 g(-1)), followed by the cerebellum (63 ± 12 mL·min(-1)·100 g(-1)), the pons (51 ± 17 mL·min(-1)·100 g(-1)), and the hippocampus (36 ± 9 mL·min(-1)·100 g(-1)). Intracranial pressure increased from 11 ± 3 to 13 ± 5 mm Hg during cooling on cardiopulmonary bypass. During low-flow SCP, it stayed stable at baseline values, whereas high-flow perfusion resulted in significantly higher intracranial pressures (17 ± 3 mm Hg; p = 0.001). Changes in cerebral vascular resistance and metabolic rate showed no significant differences between the groups. High-flow SCP provides no benefit during long-term SCP at 25°C. Higher cerebral blood flow during the initial SCP period leads to cerebral edema, with no profit in metabolic rate.

Role of Prostanoids in the Regulation of Cerebral Blood Flow During Normoxia and Hypoxia in the Fetal Sheep

The fetal cardiovascular responses to hypoxia include decreased peripheral blood flow and increased cerebral, cardiac, and adrenal blood flow. Prostanoids, metabolites of cyclooxygenase enzyme activity, have potent effects on vascular tone in both the adult and the fetus. To examine the role of prostanoids in the regulation of fetal cerebral blood flow (CBF) during acute hypoxic stress, eight near term fetal sheep were studied after infusing vehicle or diclofenac, a cyclooxygenase inhibitor, followed by a 30-min period of hypoxia (arterial Po(2) 12 Torr). In the control experiments, CBF, measured continuously with laser Doppler flowmetry, increased to 148% of baseline values (p < 0.01) and cerebral vascular resistance decreased to 70% of baseline values after 30 min of hypoxic stress. During diclofenac infusion, hypoxia resulted in a CBF increase to only 129% of baseline, a significant attenuation (p < 0.05), accompanied by decreased plasma prostanoid concentrations. Increases in mean arterial blood pressure during hypoxia were also attenuated by diclofenac infusion. Flow and pressure responses were not accompanied by changes in cerebral vascular resistance. These results indicate that prostanoids indirectly modulate fetal CBF responses to hypoxia, but that their effects are mediated through modulation of systemic rather than cerebral vascular tone.

Preservation of static and dynamic cerebral autoregulation after mild hypothermic cardiopulmonary bypass

Dysfunction of cerebral autoregulation might contribute to neurological morbidity after cardiac surgery. In this study, our aim was to assess the preservation of cerebral autoregulation after cardiac surgery involving cardiopulmonary bypass (CPB). Dynamic and static components of cerebral autoregulation were evaluated in 12 patients undergoing coronary artery bypass graft surgery, anaesthetized with midazolam, fentanyl, and propofol, and using mild hypothermic CPB (31-33 degrees C). Arterial pressure (ABP), central venous pressure (CVP), and blood flow velocity in the middle cerebral artery (CBFV) were recorded. The cerebral perfusion pressure (CPP) was calculated as a difference between mean ABP and CVP. Rapid decrease of CPP was caused by a sudden change of patients' position from Trendelenburg to reverse Trendelenburg. Cerebral vascular resistance (CVR) was calculated by dividing CPP by CBFV. Index of static cerebral autoregulation (CAstat) was calculated as the change of CVR related to change of CPP during the manoeuvre. Dynamic rate of autoregulation (RoRdyn) was determined as the change in CVR per second during the first 4 s immediately after a decrease in CPP, related to the change of CPP. Measurements were obtained after induction of anaesthesia, and 15, 30, and 45 min after termination of CPB. No significant changes were found in CAstat or RoRdyn after CPB. Significant changes in CVR could be explained by concomitant changes in body temperature and haematocrit. Autoregulation of cerebral blood flow remains preserved after mild hypothermic CPB.

Transcranial Doppler ultrasound analysis of resistive index in rostral and caudal cerebral arteries in dogs

Transcranial Doppler (TCD) was carried out to determine the resistive index (RI) values of normal canine cerebral arteries and its reproducibility and to evaluate the change of cerebral vascular resistance following diuretics administration. RI values of rostral cerebral artery (RCA) were compared between fontanelle window and temporal window. Normal ranges and reproducibility of the RI values were examined in the rostal cerebral artery (RCA) and caudal cerebral artery (CCA). And after administration of diuretics, TCD-derived RI values were measured at RCA and CCA. Cerebral vascular RI values of RCA and CCA were 0.55 +/- 0.05 and 0.55 +/- 0.03 in the normal dogs, respectively. There was no significant difference of RI between male and female; between fontanelle window and temporal window. Reproducibility of RI measurements between intraobserver and interobserver were relatively high. The RI of RCA and CCA were significantly increased 15 minutes after mannitol administration (p<0.01) and returned to baseline values by 30 minutes, but it did not significantly change after furosemide and saline administration. The results suggest that TCD is a useful test which can obtain reproducible results from any window and has the advantage of detecting subtle changes in cerebral vascular resistance.

Cerebral response to haemodilution during cardiopulmonary bypass in dogs: the role of nitric oxide synthase

During cardiopulmonary bypass, haemodilution is standard practice and is accompanied by increases in cerebral blood flow (CBF). We investigated if changes in cerebral vascular resistance (CVR) during cardiopulmonary bypass-haemodilution are dependent on nitric oxide synthase. The cerebral response to haemodilution in nine dogs treated with the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), was compared with a control group (n = 8). Both groups underwent serial isovolaemic haemodilution (target packed cell volumes 0.39, 0.26, 0.19 and 0.14) using 6% dextran 70. CBF, CVR and cerebral metabolic rate for oxygen (CMRO2) were measured. While initial CVR was different in the two groups, haemodilution-dependent reductions in CVR were equivalent and the curves describing the packed cell volume-CVR relationship were parallel in control and nitric oxide synthase inhibition groups. Our data indicate that nitric oxide synthase does not play a primary role in the cerebral response to haemodilution.

EEG MONITORING: INTRAOPERATIVE APPLICATION

Intraoperative monitoring of electroencephalograms (EEGs) is becoming more commonplace as the technology advances,7, 39 making it easier and less costly to apply.48 Although the cardiovascular status and systemic perfusion are routinely monitored during anesthesia, the brain, which is the target organ of general anesthesia, is generally not monitored. Instead, it is generally assumed that without prior known pathology, adequate cerebral perfusion can be assumed by maintaining adequate mean arterial pressure.72 Cerebral blood flow is not only dependent on adequate cerebral perfusion pressure, which is decreased by elevations in intracranial pressure, but also by changes in cerebral vascular resistance and cerebral vascular pathology.74 Monitoring for cerebral perfusion, however, is not the only application for intraoperative EEG monitoring. EEG can also be used to monitor the depth of sedation and the degree of burst suppression produced by barbiturate infusion, as well as monitoring for the occurrence of seizures while the patients are under the influence of muscle relaxants.20 Each of these applications are discussed in this article, but for intraoperative EEG to be most effectively applied, a number of fundamental principles must first be addressed.

Cardiopulmonary Bypass in a Patient with Moyamoya Disease

Cardiopulmonary Bypass in a Patient with Moyamoya Disease

Neonatal cerebral doppler flow velocity waveforms in the pre-term infant with cerebral pathology

In a longitudinal study of 217 infants delivering at < 37 completed weeks gestation, Doppler flow velocity waveforms were obtained, and resistance index (RI) values calculated from the middle (MCA) and anterior (ACA) cerebral arteries during the first 10 days of life. Sixty infants demonstrated ultrasound evidence of cerebral pathology, of which five cases were congenital, and an additional 13 cases were complicated by patent ductus arteriosus during the study period. The Doppler data obtained during the first week of life from the remaining 42 infants who developed cerebral pathology, and 15 infants who had evidence of metabolic acidosis at delivery without ultrasound evidence of cerebral pathology were compared with local reference data obtained from non-acidotic infants with normal cranial ultrasound from 24 h of age. In those infants who had evidence of minor periventricular haemorrhage alone (Grade I/II PVH), there was no significant difference between the ACA or MCA RI during the study period compared with the reference data. In those groups of infants who demonstrated major PVH (Grade III/IV) or persistent periventricular flares, the ACA and MCA RI was found to be consistently significantly higher than the reference group throughout the study period. In those infants who developed ultrasound evidence of periventricular cystic leukomalacia (PVCL), the MCA RI was significantly lower than the reference data between 48 and 72 h of age, there being no significant difference in the ACA RI. The Doppler findings in those infants with evidence of metabolic acidosis at delivery (umbilical arterial pH < 7.20; BD > 8 mmol/1) but with normal ultrasound findings were similar to those infants who developed PVCL, namely a significant fall in MCA RI between 48 and 72 h of life, with no significant difference in the ACA RI during the study period. These findings suggest that variable changes in cerebral vascular resistance occur with the evolution of, or as a consequence of the development of cerebral pathology in the pre-term infant, and these changes of increased and decreased vascular resistance are discussed. Further investigation of the changes occurring in the cerebral circulation in the early neonatal period of infants who develop PVCL is required to clarify the vascular changes taking place, but if the findings of this study are confirmed, this technique may provide a means of identifying infants at risk of developing ischaemic cerebral pathology at an early stage when it may be possible to initiate therapeutic intervention to limit the cerebral damage.

Hypoxemia lowers cerebrovascular resistance without changing brain and blood [H+

We designed the present study to see whether, during acute moderate isocapnic hypoxemia, changes in cerebral vascular resistance (CVR) and brain extracellular fluid (ECF) [H+] can or cannot be dissociated from each other. In seven anesthetized and paralyzed dogs we measured brain ECF pH with surface electrodes (n = 4) or double-barreled microelectrodes (n = 3) with tip diameters of less than 30 micron inserted 5 mm below the surface. Cerebral blood flow (CBF) was measured by radioactive microspheres during normoxemia and moderate hypoxemia, whereas brain ECF pH was measured continuously. In six of the seven dogs brain pH did not change during moderate hypoxemia of 4-20 min duration. In these six animals the mean arterial O2 partial pressure decreased from 84.8 +/- 12.9 (SD) to 46.7 +/- 10.2 Torr during hypoxic gas breathing, resulting in a significant drop in CVR from 3.88 +/- 1.88 to 3.27 +/- 1.97 Torr X ml-1 X min X 100 g and a rise in CBF from 31.7 +/- 12.7 to 47.8 +/- 31.5 ml X min-1 X 100 g-1. The mean brain ECF [H+] was 57.4 +/- 8.2 nmol/l (pH = 7.24) during normoxemia and did not change significantly during hypoxic gas breathing [56.6 +/- 7.7 nmol/l (pH = 7.25)]. Furthermore, arterial and sagittal venous blood and cisternal cerebrospinal fluid (CSF) pH did not change significantly during hypoxic gas breathing. We conclude that during acute moderate hypoxemia reduction in CVR can occur independently from increases in brain ECF, cisternal CSF, and arterial and sagittal venous blood [H+] and PCO2.

Transient changes in cerebral vascular resistance during the Valsalva maneuver in man.

Measurements of cerebral spinal fluid pressure, arterial pressure, and internal carotid artery blood flow were obtained in a series of patients during a Valsalva maneuver. During straining (phase II), an 11% reduction in mean arterial pressure was associated with a 21% decrease in internal carotid flow from control values; and following release (phase IV), the 19% increase in mean arterial pressure produced a 22% increase in internal carotid artery flow. Perfusion pressure computed as the mean arterial pressure minus cerebral spinal fluid pressure and internal carotid artery blood flow were used to calculate an index of cerebral vascular resistance. The data indicate that a modest but significant decrease in vascular resistance occurred during phases II and III followed by return to control levels during phase IV. These changes in vascular resistance were not rapid enough or of sufficient magnitude to maintain constant cerebral perfusion during the Valsalva maneuver.

Production, metabolism and possible functions of adenosine in brain tissue in situ.

Adenosine and H+ may act synergistically to regulate cerebral blood flow because adenosine production is enhanced under various experimental conditions associated with an imbalance between oxygen supply and oxygen need. Direct application of adenosine dilates the pial vessels, but changes in cerebral vascular resistance are not observed when adenosine is infused intraarterially. This is because adenosine does not readily cross the blood-brain barrier. The studies reported here show that in dogs the adenosine released into the interstitium is partly reincorporated into adenine nucleotides via an adenosine kinase (EC 2.7.1.20) reaction (salvage pathway) and partly degraded to inosine and hypoxanthine. However, in contrast to other tissues, the accumulation of iosine and hypoxanthine in brain tissue proceeds at a rate slower than that of adenosine because one of the degradative enzymes, namely purine-nucleoside phosphorylase (EC 2.4.2.1) is located only in the vessel wall, which is not readily permeable to adenosine. Thus, the slow access of adenosine to its degradative enzymes delays the appearance of its products, inosine and hypoxanthine.

Neurogenic control of cerebral blood flow

In experiments on 15 isolated dog brains, cerebral blood flow could be influenced by short (20 sec) supramaximal, unilateral electrical stimulation of the vagoysympathetic trunk, the trigeminal nerve and the medulla oblongata. The changes in cerebral vascular resistance and cerebral oxygen consumption developed 2 sec after onset of the stimulation, reaching their peak 30 sec later and lasted up to 3 min. During sympathetic stimulation cerebral blood flow decreased from 47.2 ml to 42.0 ml 100 g tissue/min and cerebral vascular resistance increased about 18%. This constrictor effect was completely blocked by phentolamine. During vagal stimulation no effect could be observed. During trigeminal stimulation cerebral blood flow increased from 44.0 ml to 48.9 ml 100 g tissue/min, cerebral vascular resistance decreased about 19%, and cerebral oxygen consumption increased about 12%. Reliable inhibition of this dilating response was not achieved with either propranolol or atropine and it is assumed that there are no vasodilator fibers in the trigeminal nerve. During medullary stimulation cerebral blood flow increased from 42.0 ml to 54.7 ml 100 g tissue/min, cerebral vascular resistance decreased about 45% and cerebral oxygen consumption increased about 23%. The diminishing effects of propranolol and atropine on this dilating response was not statistically significant. A restricted region in the medulla is presented from which changes in cerebral blood flow produced by electrical stimulation were not associated with changes in the electrical pattern of the brain. Observations that the vascular and functional reactions of the brain can be dissociated point to a role of the medulla in regulating cerebral blood flow, but do not elucidate the mechanism. In general, the results support evidence that a double—metabolic and neurogenic—mechanism is involved in the control of cerebral blood flow. It is suggested that the effects during vagosympathetic stimulation are completely neurogenic, the effects during trigeminal stimulation mainly metabolic, and the effects during medullary stimulation both metabolic and neurogenic in origin.

Demonstration of alpha and beta adrenergic receptors in canine cerebral vasculature.

The cerebral vascular effects of various adrenomimetic agents were examined in 12 isolated canine brains perfused with blood at constant flow. Changes in cerebral vascular resistance (CVR) and the magnitude of pressor or depressor responses observed following drug injection were examined. The presence of alpha adrenergic receptors in this vascular bed is indicated by the increased CVR observed when phenylephrine, norepinephrine, and epinephrine were administered and by the reduced or reversed pressor actions of these compounds following treatment with the alpha adrenergic blocking drug phenoxybenzamine HCl. The presence of beta adrenergic receptors in this vascular bed is indicated by the decreased CVR noted when isoproterenol was given and by the reduced depressor actions of this compound following treatment with the beta adrenergic blocking drug propranolol. Further evidence for the presence of beta adrenergic receptors is demonstrated by the vasomotor reversal to epinephrine which was observed following alpha suppression with phenoxybenzamine. As catecholamine blood levels in intact dogs are low in comparison to those achieved in these studies, it appears doubtful that circulating catecholamines play an important physiological role in the regulation of CVR. Possible explanations are considered for the lower response of the cerebral vasculature to catecholamines when this response is compared to that observed in other vascular beds.

Respiratory and cerebral circulatory control during exercise at .21 and 2.0 atmospheres inspired p02.

Respiratory and cerebral hemodynamic responses to leg exercise during respiration of air at 1.0 atm. and O2 at 2.0 atm. were studied in relation to changes in arterial and internal jugular venous blood oxygen composition, pH, pCO2 and bicarbonate concentration. The hyperpnea of exercise at 1.0 atm. was accompanied by arterial and venous acidemia and hypocapnia. Oxygen administration during exercise at 2.0 atm. lowered ventilation, restored arterial pH and pCO2 toward resting levels and caused venous pCO2 to rise above the resting level; cerebral venous cH remained elevated in spite of reduction of blood fixed acid concentration. The ventilatory response to exercise showed positive correlations with work load, oxygen consumption, and with changes in arterial and internal jugular venous cH and fixed acid. The observed negative correlations of changes in respiratory minute volume with changes in arterial and internal jugular venous pCO2 and bicarbonate concentration suggest that these factors are functions, rather than primary determinants, of ventilation in exercise. Cerebral hemodynamics and oxygen consumption were not significantly altered by exercise at 1.0 atm. The data suggest either a slight elevation of cerebral blood flow or reduction in the rate of cerebral oxygen consumption during exercise breathing O2 at 2.0 atm., without gross elevation of cerebral venous pO2. Observed changes in cerebral vascular resistance during exercise at .21 and 2.0 atm. inspired pO2 appear related to concomitant alterations in arterial pCO2, with no detectable relationship either to brain oxygen requirement of cerebral venous acid-base composition. Submitted on November 25, 1958

METABOLISM OF L-THYROXINE AND L-3:5:3′-TRIIODOTHYRONINE BY BRAIN TISSUE PREPARATIONS1

THYROID gland preparations have been known for many years to have a marked effect on the development and function of the central nervous system (1). More recently, the thyroid hormones, l-thyroxine and l-3:5:3′-triiodothyronine, have been shown to increase the excitability of the brain, as measured by the threshold for electric shock seizures (2, 3). Both substances also influence the electrolyte distribution and in particular, the distribution of sodium in the brain tissue (3). Absence of the thyroid gland has marked effects on the electroencephalogram and causes profound changes in cerebral vascular resistance and blood flow (4). Moreover, changes in mental activity, mood and even psychosis maybe associated with either over- or under-activity of the thyroid (5, 6, 7, 8). There is, however, no change in oxygen consumption in brain tissue removed from either thyroidectomized or hyperthyroid rats (9) although hyperthyroidism may effect a slight change in succinoxidase activity (10).

Effects of vigorous physical exercise on cerebral circulation and metabolism

1. 1. The effects of vigorous muscular exercise in the upright posture were studied in thirteen normal subjects and compared with the changes resulting from motionless standing. 2. 2. Exercise resulted in a decrease in cerebral vascular resistance and an increase in cerebral oxygen consumption. The decrease in mean cerebral blood flow which results from motionless standing did not occur with exercise. There was no change in cerebral respiratory quotient. 3. 3. Although exercise resulted in a striking fall in blood carbon dioxide content and pH, no correlations could be made between these changes and the alterations in cerebral circulatory or metabolic functions. There was a close correlation between changes in cerebral vascular resistance and cerebral oxygen consumption, though the reason for this is not known.