Erratum

1994 ◽  
Vol 14 (5) ◽  
pp. 884-884
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ground Squirrel ◽  
Weighted Average ◽  
Ground Squirrels ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Correct Number ◽  
Natural Tolerance ◽  
The Brain

Local Cerebral Blood Flow During Hibernation, a Model of Natural Tolerance to “Cerebral Ischemia” Kai U. Frerichs, Charles Kennedy, Louis Sokoloff and John M. Hallenbeck [ originally published in Journal of Cerebral Blood Flow and Metabolism 1994;14(2):193–205] The weighted average cerebral blood flow in the brains of hibernating and nonhibernating ground squirrels appeared in three places in the article cited above. The numbers varied to some extent in each of the three places that they were displayed. The correct number for the active ground squirrel group was 62 ± 18 ml 100 g−1 min−1. The correct number for the hibernating group was 7 ± 4 ml 100 g−1 min−1. These numbers should be inserted on page 193 in the abstract so that the sentence would read, “Mean (± SD) mass-weighted CBF in the brain was 62 ± 18 ml 100 g−1 min−1 (n = 4) in the control group but was reduced to ischemic levels, 7 ± 4 ml 100 g−1 min−1 (n = 4), in the hibernating animals (p < 0.001).” The same numbers should be inserted into the sentence that begins at the bottom of page 198, “Average blood flow (± SD) in the brain as a whole in the hibernating animals was reduced to about 1/10 (7 ± 4 ml 100 g−1 min−1) of the level in active animals (62 ± 18 ml 100 g−1 min−1) (Table 4).” Finally, on page 201 at the bottom of Table 4 below “Weighted average in brain as a whole,” the readings should be 62 ± 18 for active and 7 ± 4 for hibernating.

scholarly journals Local Cerebral Blood Flow during Hibernation, a Model of Natural Tolerance to “Cerebral Ischemia”

1994 ◽  
Vol 14 (2) ◽  
pp. 193-205 ◽  
Author(s):  
Kai U. Frerichs ◽  
Charles Kennedy ◽  
Louis Sokoloff ◽  
John M. Hallenbeck
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Body Temperature ◽  
Physiological State ◽  
Ground Squirrels ◽  
Control Group ◽  
Spermophilus Tridecemlineatus ◽  
Destructive Processes ◽  
Natural Tolerance

The breakdown of cellular homeostasis and progressive neuronal destruction in cerebral ischemia appears to be mediated by a complex network of causes that are intricately interrelated. We have investigated a physiological state existing normally in nature in which mammals appear to tolerate the ordinarily detrimental effects of ischemia with reduced oxygen availability and to resist activation of self-destructive processes, i.e., mammalian hibernation. Ground squirrels (Spermophilus tridecemlineatus) were chronically implanted with arterial and venous catheters and telemetry devices for electroencephalography, electrocardiography, and monitoring of body temperature. The animals were placed in an environmental chamber at an ambient temperature of 5°C. Entrance into hibernation was characterized by a drop in heart rate followed by a gradual decline in body temperature and an isoelectric electroencephalogram. Cold-adapted active animals that were not hibernating served as controls. Cerebral blood flow (CBF) was measured in both groups with the autoradiographic [14C]iodoantipyrine method. Mean (±SD) mass-weighted CBF in the brain as a whole was 62 ± 16 ml/100 g/min (n = 4) in the control group but was reduced to ischemic levels, 7 ± 4 ml/100 g/min (n = 4), in the hibernating animals (p < 0.001). No neuropathological changes were found in similarly hibernating animals aroused from hibernation. Hibernation appears to be actively regulated, and hormonal factors may be involved. The identification and characterization of such factors and of the mechanisms used by hibernating species to increase ischemic tolerance and to blunt the destructive effects of ischemia may enable us to prevent or minimize the loss of homeostatic control during and after cerebral ischemia in other species.

Cerebral blood flow, glucose use, and CSF ionic regulation in potassium-depleted rats

1988 ◽  
Vol 254 (2) ◽  
pp. H250-H257
Author(s):  
H. Schrock ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Local Cerebral Blood Flow ◽  
Arterial Pco2 ◽  
Average Decrease ◽  
K Concentration ◽  
Low K ◽  
The Brain ◽  
K Depletion

Rats were kept on a low-K+ diet for 25 or 70 days. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 31 different structures of the brain by means of the [14C]iodoantipyrine and [14C]2-deoxy-D-glucose method. After 25 and 70 days of K+ depletion LCBF was decreased significantly in 27 and 30 structures, respectively, the average decrease being 19 and 25%. In contrast, average LCGU was not changed. Cisternal cerebrospinal fluid (CSF) K+ concentration decreased significantly from 2.65 +/- 0.02 mM in controls to 2.55 +/- 0.02 mM and 2.47 +/- 0.02 mM in the two treated groups (P less than 0.01). CSF [HCO3-], pH, and PCO2 were increased in K+-depleted animals. These data show that K+ depletion induces an increase in CSF pH and a decrease in CSF K+ concentration, both of which cause a reduction in cerebral blood flow. The increased CSF PCO2 is secondary to the reduction of blood flow, since brain metabolism and arterial PCO2 remained constant.

Local cerebral blood flow and glucose utilization after blood exchange with a hemoglobin-based O2 carrier in conscious rats

1993 ◽  
Vol 265 (4) ◽  
pp. H1243-H1248 ◽  
Author(s):  
K. Waschke ◽  
H. Schrock ◽  
D. M. Albrecht ◽  
K. van Ackern ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Brain Structures ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Conscious Rats ◽  
Cerebral Glucose Utilization ◽  
Arterial Blood ◽  
Blood Exchange

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.

scholarly journals The Effect of Local Infusion of Adenosine and Adenosine Analogues on Local Cerebral Blood Flow

1989 ◽  
Vol 9 (4) ◽  
pp. 556-562 ◽  
Author(s):  
David G. L. Van Wylen ◽  
T. S. Park ◽  
Rafael Rubio ◽  
Robert M. Berne
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Receptor Activation ◽  
Local Cerebral Blood Flow ◽  
Caudate Nuclei ◽  
Adenosine Concentration ◽  
The Brain ◽  
Adenosine Receptor Activation ◽  
Dialysis Technique ◽  
Hydrogen Clearance

The purpose of this study was to determine the effects of local infusion of adenosine (ADO) and non-metabolized ADO analogues on local cerebral blood flow (CBF) and interstitial fluid (ISF) ADO levels. The brain dialysis technique was used to (a) deliver drugs locally to brain tissue, (b) estimate cerebral ISF ADO levels, and (c) measure local CBF (hydrogen clearance). Dialysis probes were implanted bilaterally in the caudate nuclei of ketamine-anesthetized rats. The probe on one side was perfused with artificial CSF while the contralateral probe was perfused with artificial CSF containing ADO ( n = 5), or the ADO agonists 2-chloroadenosine (2-CADO; n = 4) or 5'-N-ethylcarboxamide adenosine (NECA; n = 4). When ADO was included in the artificial CSF at 10−5, 10−4, or 10−3 M, a 30% increase in local CBF was detected only with 10−3 M ADO. During perfusion with ADO, dialysate inosine and hypoxanthine levels increased, indicating that the cells adjacent to the probe metabolized the exogenous ADO. With 2-CADO included in the artificial CSF at 10−6, 10−5, or 10−4 M, local CBF increased 18, 131, and 201%, respectively. Perfusion with artificial CSF containing 10−7, 10−6, or 10−5 M NECA resulted in a 35, 112, and 187% increase in local CBF, respectively. In a separate group of rats ( n = 6), perfusion with artificial CSF containing 10−6 M NECA resulted in a sustained twofold increase in local CBF and 40% decrease in dialysate adenosine concentration, both of which could be reversed by including 8-( p-sulfophenyl)-theophylline, an ADO receptor antagonist, in the artificial CSF. These results are consistent with the known vascular actions of ADO and ADO analogues and suggest that there is a basal level of ISF ADO that can be reduced by increased CBF and/or adenosine receptor activation.

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 Measurement of Local Cerebral Blood Flow with [14C]Iodoantipyrine in the Mouse

1988 ◽  
Vol 8 (1) ◽  
pp. 121-129 ◽  
Author(s):  
Therese M. Jay ◽  
Giovanni Lucignani ◽  
Alison M. Crane ◽  
Jane Jehle ◽  
Louis Sokoloff
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Local Cerebral Blood Flow ◽  
Sources Of Error ◽  
Arterial Blood ◽  
Appropriate Care ◽  
Rapid Removal ◽  
The Brain

Local cerebral blood flow was measured in the mouse by means of the [14C]iodoantipyrine method. This method has been previously used in the monkey, dog, cat, and rat, but its application to small mammals such as the mouse requires special attention to potential sources of error. The small size of the mouse brain requires special attention to the rapid removal and freezing of the brain to minimize effects of postmortem diffusion of tracer in the tissue. Because of the relatively low diameter/length ratios of the catheters needed for arterial sampling in small animals, substantial errors can occur in the determination of the time course of the [14C]iodoantipyrine concentration in the arterial blood unless corrections for lag time and dead space washout in the catheter are properly applied. Local cerebral blood flow was measured in seven awake mice with appropriate care to minimize these sources of error. The values were found to vary from 48 ml/100 g/min in the corpus callosum to 198 ml/100 g/min in the inferior colliculus. The results demonstrate that the [14C]iodoantipyrine method can be used to measure local cerebral blood flow in the mouse and that the values in that species are, in general, somewhat higher than those in the rat.

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.

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