Cerebral Blood Flow and Cerebral Metabolism in Normal and Intrauterine Growth Retarded Neonatal Piglets

1983 ◽  
Vol 64 (2) ◽  
pp. 161-165 ◽  
Author(s):  
P. A. Flecknell ◽  
R. Wootton ◽  
Muriel John
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Partition Coefficient ◽  
Cerebral Metabolism ◽  
Liver Weight ◽  
Arterial Oxygen ◽  
Intrauterine Growth ◽  
Neonatal Piglets ◽  
Fick Principle ◽  
The Brain

1. Cerebral blood flow and cerebral metabolism were measured in conscious, normally grown neonatal piglets and in littermates which had undergone intrauterine growth retardation. 2. Cerebral blood flow was measured by the Kety-Schmidt technique using [125I]iodoantipyrine as the tracer. The tissue: blood partition coefficient of this tracer was measured in separate groups of growth retarded and normal animals. Cerebral utilization rates of glucose and oxygen were calculated from the arteriovenous concentration differences on the Fick principle. 3. The mean body weight of the growth retarded animals was about half that of their normally grown littermates, and liver weight was reduced in proportion. Brain weight was slightly but significantly lower in the growth retarded animals. 4. Cerebral blood flow was lower in the growth retarded piglets but the rates of cerebral utilization of oxygen and glucose were not significantly different in the two groups. The fractional extraction of arterial oxygen by the brain was significantly higher in the growth retarded animals. 5. The partition coefficient of ipdoantipyrine was significantly lower in the growth retarded animals, being about 75% of the normal value. It is clear that had the partition coefficients been assumed to have been the same in both groups the calculated cerebral blood flows would have been identical. 6. It is concluded that growth retarded neonatal piglets have relatively normal sized brains, with a rate of glucose and oxygen consumption that is not significantly different from normal, despite a reduction in cerebral blood flow of about 35%. Consequently the fractional extraction rate of arterial oxygen by the brain is increased from 50% to 70%.

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

scholarly journals Overview of Monitoring of Cerebral Blood Flow and Metabolism after Severe Head Injury

1994 ◽  
Vol 21 (S1) ◽  
pp. S6-S11 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Marc L. Schröder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Severe Head Injury ◽  
Cerebral Metabolism ◽  
Jugular Bulb ◽  
Cerebral Metabolic Rate ◽  
Venous Oxygen Saturation ◽  
Arteriovenous Difference ◽  
The Brain ◽  
Pressure Autoregulation

AbstractThe relationships between cerebral blood flow (CBF), cerebral metabolism (cerebral metabolic rate of oxygen, CMRO2) and cerebral oxygen extraction (arteriovenous difference of oxygen, AVDO2) are discussed, using the formula CMRO2 = CBF × AVDO2. Metabolic autoregulation, pressure autoregulation and viscosity autoregulation can all be explained by the strong tendency of the brain to keep AVDO2 constant. Monitoring of CBF, CMRO2 or AVDO2 very early after injury is impractical, but the available data indicate that cerebral ischemia plays a considerable role at this stage. It can best be avoided by not "treating" arterial hypertension and not using too much hyperventilation, while generous use of mannitol is probably beneficial. Once in the ICU, treatment can most practically be guided by monitoring of jugular bulb venous oxygen saturation. If saturation drops below 50%, the reason for this must be found (high intracranial pressure, blood pressure not high enough, too vigorous hyperventilation, arterial hypoxia, anemia) and must be treated accordingly.

Cerebral Metabolism of Nitric Oxide during Retrograde Cerebral Perfusion

2002 ◽  
Vol 10 (3) ◽  
pp. 223-227 ◽  
Author(s):  
Katsuhito Ueno ◽  
Shinichi Takamoto ◽  
Takeshi Miyairi ◽  
Tetsuro Morota ◽  
Ko Shibata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Cerebral Perfusion ◽  
Cerebral Metabolism ◽  
Oxidation Products ◽  
Retrograde Cerebral Perfusion ◽  
Ph Stat ◽  
The Brain

The aim of this study was to determine whether alpha- or pH-stat protects the brain during deep hypothermic retrograde cerebral perfusion. Fifteen anesthetized dogs on cardiopulmonary bypass were cooled to 18°C under alpha-stat and underwent retrograde cerebral perfusion for 90 minutes under alpha-stat or pH-stat, or underwent antegrade cardiopulmonary bypass under alpha-stat as the control. Cerebral blood flow of the cortex was monitored and serial analyses of blood gases and total nitric oxide oxidation products made. Cerebral blood flow and cerebral metabolic rate for oxygen were significantly higher and plasma levels of nitric oxide oxidation products in the outflow from the brain were significantly lower in retrograde cerebral perfusion under pH-stat than under alpha-stat. This study shows that reduced levels of nitric oxide oxidation products may protect against neuronal damage induced by nitric oxide and that increased cerebral blood flow under pH-stat may lead to a reduction of nitric oxide oxidation products. Under retrograde cerebral perfusion, pH-stat is thus better than alpha-stat for protecting the brain.

A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury

2010 ◽  
Vol 112 (5) ◽  
pp. 1080-1094 ◽  
Author(s):  
Sarah B. Rockswold ◽  
Gaylan L. Rockswold ◽  
David A. Zaun ◽  
Xuewei Zhang ◽  
Carla E. Cerra ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Tissue ◽  
Cerebral Metabolism ◽  
Treatment Session ◽  
Control Group ◽  
Normobaric Hyperoxia ◽  
The Brain

Object Oxygen delivered in supraphysiological amounts is currently under investigation as a therapy for severe traumatic brain injury (TBI). Hyperoxia can be delivered to the brain under normobaric as well as hyperbaric conditions. In this study the authors directly compare hyperbaric oxygen (HBO2) and normobaric hyperoxia (NBH) treatment effects. Methods Sixty-nine patients who had sustained severe TBIs (mean Glasgow Coma Scale Score 5.8) were prospectively randomized to 1 of 3 groups within 24 hours of injury: 1) HBO2, 60 minutes of HBO2 at 1.5 ATA; 2) NBH, 3 hours of 100% fraction of inspired oxygen at 1 ATA; and 3) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Brain tissue PO2, microdialysis, and intracranial pressure were continuously monitored. Cerebral blood flow (CBF), arteriovenous differences in oxygen, cerebral metabolic rate of oxygen (CMRO2), CSF lactate and F2-isoprostane concentrations, and bronchial alveolar lavage (BAL) fluid interleukin (IL)–8 and IL-6 assays were obtained pretreatment and 1 and 6 hours posttreatment. Mixed-effects linear modeling was used to statistically test differences among the treatment arms as well as changes from pretreatment to posttreatment. Results In comparison with values in the control group, the brain tissue PO2 levels were significantly increased during treatment in both the HBO2 (mean ± SEM, 223 ± 29 mm Hg) and NBH (86 ± 12 mm Hg) groups (p < 0.0001) and following HBO2 until the next treatment session (p = 0.003). Hyperbaric O2 significantly increased CBF and CMRO2 for 6 hours (p ≤ 0.01). Cerebrospinal fluid lactate concentrations decreased posttreatment in both the HBO2 and NBH groups (p < 0.05). The dialysate lactate levels in patients who had received HBO2 decreased for 5 hours posttreatment (p = 0.017). Microdialysis lactate/pyruvate (L/P) ratios were significantly decreased posttreatment in both HBO2 and NBH groups (p < 0.05). Cerebral blood flow, CMRO2, microdialysate lactate, and the L/P ratio had significantly greater improvement when a brain tissue PO2 ≥ 200 mm Hg was achieved during treatment (p < 0.01). Intracranial pressure was significantly lower after HBO2 until the next treatment session (p < 0.001) in comparison with levels in the control group. The treatment effect persisted over all 3 days. No increase was seen in the CSF F2-isoprostane levels, microdialysate glycerol, and BAL inflammatory markers, which were used to monitor potential O2 toxicity. Conclusions Hyperbaric O2 has a more robust posttreatment effect than NBH on oxidative cerebral metabolism related to its ability to produce a brain tissue PO2 ≥ 200 mm Hg. However, it appears that O2 treatment for severe TBI is not an all or nothing phenomenon but represents a graduated effect. No signs of pulmonary or cerebral O2 toxicity were present.

Coupling of Cerebral Blood Flow and Oxygen Metabolism in Infant Pigs during Selective Brain Hypothermia

2000 ◽  
Vol 20 (8) ◽  
pp. 1215-1224 ◽  
Author(s):  
Bernd Walter ◽  
Reinhard Bauer ◽  
Gernot Kuhnen ◽  
Harald Fritz ◽  
Ulrich Zwiener
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Metabolism ◽  
Oxygen Metabolism ◽  
Metabolic Effects ◽  
Main Determinant ◽  
Cerebral Hemodynamic ◽  
Systemic Hypothermia ◽  
C 30 ◽  
The Brain

Studies documenting the cerebral hemodynamic consequences of selective brain hypothermia (SBH) have yielded conflicting data. Therefore, the authors have studied the effect of SBH on the relation of cerebral blood flow (CBF) and CMRO2 in the forebrain of pigs. Selective brain hypothermia was induced in seven juvenile pigs by bicarotid perfusion of the head with extracorporally cooled blood. Cooling and stepwise rewarming of the brain to a Tbrain of 38°C, 25°C, 30°C, and 38°C at normothermic Ttrunk (38°C) decreased CBF from 71 ± 12 mL 100 g−1 min−1 at normothermia to 26 ± 3 mL 100 g−1 min−1 and 40 ± 12 mL 100 g−1 min−1 at a Tbrain of 25°C and 30°C, respectively. The decrease of CMRO2 during cooling of the brain to a Tbrain of 25°C resulted in a mean Q10 of 2.8. The ratio between CBF and CMRO2 was increased at a Tbrain of 25°C indicating a change in coupling of flow and metabolism. Despite this change, regional perfusion remained coupled to regional temperatures during deep cerebral hypothermia. The data demonstrate that SBH decreases CBF and oxygen metabolism to a degree comparable with the cerebrovascular and metabolic effects of systemic hypothermia. The authors conclude that, irrespective of a change in coupling of blood flow and metabolism during deep cerebral hypothermia, cerebral metabolism is a main determinant of CBF during SBH.

scholarly journals Lack of Dependence of Cerebral Blood Flow on Blood Viscosity after Blood Exchange with a Newtonian O2 Carrier

1994 ◽  
Vol 14 (5) ◽  
pp. 871-876 ◽  
Author(s):  
K. F. Waschke ◽  
H. Krieter ◽  
G. Hagen ◽  
D. M. Albrecht ◽  
K. Van Ackern ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Blood Substitute ◽  
Brain Structures ◽  
Arterial Oxygen ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Blood Exchange ◽  
The Brain

Whether the increase in cerebral blood flow measured after hemodilution is mediated by a decrease in blood viscosity or in oxygen delivery to the brain is debated. In the present study, blood was replaced by an oxygen-carrying blood substitute, ultrapurified, polymerized, bovine hemoglobin (UPBHB). In contrast to normal blood, UPBHB yields a constant and defined viscosity in the brain circulation, since its viscosity is not dependent on the shear rate. CBF was determined after blood exchange with UPBHB in one group of conscious rats (UPBHB group) and in another group of blood-exchanged conscious rats in which viscosity was increased fourfold by the addition of 2% polyvinylpyrrolidone (PVP), mw 750,000 (UPBHB-PVP group). Local CBF (LCBF) was measured in 34 brain structures by means of the quantitative iodo(14C)antipyrine method. After blood replacement, systemic parameters such as cardiac index, arterial blood pressure, blood gases, and acid-base status were not different between the UPBHB and the UPBHB-PVP groups. In particular, arterial oxygen content was similar in both groups. Compared with a control group without blood exchange, LCBF was increased after blood exchange in the different brain structures by 60–102% (UPBHB group) and by 33–101% (UPBHB-PVP group). Mean CBF was increased by 77% in the UPBHB group and by 69% in the UPBHB-PVP group. No significant differences were observed in the values of LCBF or mean CBF between the UPBHB group and the UPBHB-PVP group. The results show that a fourfold variation in the viscosity of a Newtonian blood substitute does not result in differences in CBF values. It is concluded that blood viscosity is less important to CBF than hitherto postulated.

The tissue–blood partition coefficient of iodoantipyrine in pig brain and its change with age

1983 ◽  
Vol 61 (6) ◽  
pp. 595-598 ◽  
Author(s):  
R. Wootton ◽  
P. A. Flecknell ◽  
J. P. Royston ◽  
M. John
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Partition Coefficient ◽  
Partition Coefficients ◽  
Brain Lipid ◽  
Neonatal Piglets ◽  
Pig Brain ◽  
Accuracy Of Measurement ◽  
The Mean ◽  
Sexually Mature

The tissue–blood partition coefficient of 125I-labelled iodoantipyrine was measured in pig brain. The mean coefficient for 11 neonatal piglets (aged 0.5 to 4 days) was 0.718 mL/g (SD 0.083). Measurements in a further 11 animals up to 144 days old (at which time pigs are sexually mature), showed that the partition coefficient increased significantly with age, possibly as a result of the accumulation of brain lipid during growth. The change in partition coefficient with age was curvilinear, rising to unity as the animals reached maturity. There were significant differences between the partition coefficients in grey and in white matter, but these were so small relative to the differences between pigs that they could be neglected for all practical purposes. Since the accuracy of measurement of cerebral blood flow (CBF) by the Kety–Schmidt technique depends directly on the partition coefficient of the tracer, it is important to confirm that apparent changes of CBF do not simply reflect alterations in the partition coefficient rather than real changes in blood flow.

Vorläufige Ergebnisse von 99mTc-HMPAO-SPECT-Untersuchungen bei endogenen Psychosen

1989 ◽  
Vol 28 (03) ◽  
pp. 88-91
Author(s):  
J. Schröder ◽  
H. Henningsen ◽  
H. Sauer ◽  
P. Georgi ◽  
K.-R. Wilhelm
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Regions Of Interest ◽  
Post Mortem ◽  
Regional Cerebral Blood ◽  
Hmpao Spect ◽  
Endogenous Psychoses ◽  
The Brain ◽  
99Mtc Hmpao

18 psychopharmacologically treated patients (7 schizophrenics, 5 schizoaffectives, 6 depressives) were studied using 99mTc-HMPAO-SPECT of the brain. The regional cerebral blood flow was measured in three transversal sections (infra-/supraventricular, ventricular) within 6 regions of interest (ROI) respectively (one frontal, one parietal and one occipital in each hemisphere). Corresponding ROIs of the same section in each hemisphere were compared. In the schizophrenics there was a significantly reduced perfusion in the left frontal region of the infraventricular and ventricular section (p < 0.02) compared with the data of the depressives. The schizoaffectives took an intermediate place. Since the patients were treated with psychopharmaca, the result must be interpreted cautiously. However, our findings seem to be in accordance with post-mortem-, CT- and PET-studies presented in the literature. Our results suggest that 99mTc-HMPAO-SPECT may be helpful in finding cerebral abnormalities in endogenous psychoses.

Neuroimaging in Drug Discovery and Development: Paradigms for Accelerating New Drug Availability

2001 ◽  
Vol 14 (5) ◽  
pp. 407-415
Author(s):  
John T. Metz ◽  
Malcolm D. Cooper ◽  
Terry F. Brown ◽  
Leann H. Kinnunen ◽  
Declan J. Cooper
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Phase Ii ◽  
New Drugs ◽  
Central Effects ◽  
Drug Discovery And Development ◽  
Psychological Tasks ◽  
The Brain ◽  
Phase Iv

The process of discovering and developing new drugs is complicated. Neuroimaging methods can facilitate this process. An analysis of the conceptual bases and practical limitations of different neuroimaging modalities reveals that each technique can best address different kinds of questions. Radioligand studies are well suited to preclinical and Phase II questions when a compound is known or suspected to affect well-understood mechanisms; they are also useful in Phase IV to characterize effective agents. Cerebral blood flow studies can be extremely useful in evaluating the effects of a drug on psychological tasks (mostly in Phase IV). Glucose metabolism studies can answer the simplest questions about whether a compound affects the brain, where, and how much. Such studies are most useful in confirming central effects (preclinical and early clinical phases), in determining effective dose ranges (Phase II), and in comparing different drugs (Phase IV).

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