scholarly journals Cerebral blood flow during hypoxic hypoxia with plasma-based hemoglobin at reduced hematocrit

1998 ◽  
Vol 274 (6) ◽  
pp. H1933-H1942 ◽  
Author(s):  
John A. Ulatowski ◽  
Enrico Bucci ◽  
Anna Razynska ◽  
Richard J. Traystman ◽  
Raymond C. Koehler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Hemoglobin Concentration ◽  
Hypoxic Hypoxia ◽  
Control Group ◽  
Hemoglobin Solution ◽  
Sagittal Sinus ◽  
Wide Range ◽  
Anemia Group ◽  
The Brain

We determined whether cerebral blood flow (CBF) remained related to arterial O2 content ([Formula: see text]) during hypoxic hypoxia when hematocrit and hemoglobin concentration were independently varied with cell-free, tetramerically stabilized hemoglobin transfusion. Three groups of pentobarbital sodium-anesthetized cats were studied with graded reductions in arterial O2saturation to 50%: 1) a control group with a hematocrit of 31 ± 1% (mean ± SE; n = 7); 2) an anemia group with a hematocrit of 21 ± 1% that underwent an isovolumic exchange transfusion with an albumin solution ( n = 8); and 3) a group transfused with an intramolecularly cross-linked hemoglobin solution to decrease hematocrit to 21 ± 1% ( n = 10). Total arterial hemoglobin concentration (g/dl) after hemoglobin transfusion (8.8 ± 0.2) was intermediate between that of the control (10.3 ± 0.3) and albumin (7.2 ± 0.4) groups. Forebrain CBF increased after albumin and hemoglobin transfusion at normoxic O2 tensions to levels attained at equivalent reductions in [Formula: see text] in the control group during graded hypoxia. Over a wide range of arterial O2 saturation and sagittal sinus[Formula: see text], CBF remained greater in the albumin group. When CBF was plotted against[Formula: see text] for all three groups, a single relationship was formed. Cerebral O2 transport, O2 consumption, and fractional O2 extraction were constant during hypoxia and equivalent among groups. We conclude that CBF remains related to [Formula: see text] during hypoxemia when hematocrit is reduced with and without proportional reductions in O2-carrying capacity. Thus O2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O2 saturation.

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.

Cerebral blood flow and end-tidal PCO2 during prolonged acetazolamide treatment in humans

1990 ◽  
Vol 258 (4) ◽  
pp. H954-H959 ◽  
Author(s):  
L. Friberg ◽  
J. Kastrup ◽  
D. Rizzi ◽  
J. B. Jensen ◽  
N. A. Lassen
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Mountain Sickness ◽  
Hemoglobin Concentration ◽  
Intracellular Acidosis ◽  
Drug Induced ◽  
Control Value ◽  
Healthy Humans ◽  
Ventilatory Drive ◽  
The Brain

One oral dose of 1,000 mg of acetazolamide caused an acute 38% increase in cerebral blood flow (CBF) in eight healthy volunteers. During the following 10 days the subjects took 1,000 mg acetazolamide daily. CBF normalized within the first 2 days. The drug induced mild hyperventilation, gradually decreasing alveolar PCO2 to 70% of the control value at the end of the treatment period. In healthy humans the hyperventilation will not increase brain oxygenation significantly at sea level. But at high altitudes the enhanced ventilatory drive will improve oxygenation of the brain, and this may account for the beneficial effects of the drug on the symptoms of acute mountain sickness. During the treatment there was a significant 10% decrease of the hematocrit but an unaltered hemoglobin concentration. In combination with data in the literature our studies suggest that the initial CBF increase is a consequence of a transient extracellular acidosis dilating brain arterioles, whereas increased ventilatory drive results from a gradually increasing mild intracellular acidosis in 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.

The Cerebral Pharmacokinetics of Meperidine and Alfentanil in Conscious Sheep 

1997 ◽  
Vol 86 (6) ◽  
pp. 1317-1325 ◽  
Author(s):  
Richard N. Upton ◽  
Guy L. Ludbrook ◽  
Elke C. Gray ◽  
Clifford Grant
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Distribution Volume ◽  
Concentration Gradients ◽  
Variable Effect ◽  
Rate Of Penetration ◽  
Sagittal Sinus ◽  
Conscious Sheep ◽  
Kinetics Of ◽  
The Brain

Background Different opioids have different delays (hysteresis) between their concentrations in blood and their cerebral effects. Possible mechanisms include differences in their rate of penetration into the brain and differences in their distribution volume in the brain. There have been few in vivo studies of the cerebral kinetics of opioids to differentiate these mechanisms. Methods The cerebral kinetics of meperidine and alfentanil were examined using conscious sheep that were fitted with long-term monitoring equipment to measure relative changes in cerebral blood flow and opioid concentration gradients across the brain through frequent sampling of arterial and sagittal sinus blood. The data were compared using hybrid physiologic modeling with membrane-limited (consistent with mechanism 1) and flow-limited (consistent with mechanism 2) models of cerebral kinetics. Results Alfentanil had a variable effect on relative cerebral blood flow, whereas meperidine induced a transient increase. The arteriovenous concentration gradients were small after alfentanil but large after meperidine. The flow-limited model gave acceptable descriptions of observed sagittal sinus concentrations for alfentanil and meperidine, whereas the membrane-limited model collapsed to a flow-limited model. The half-lives of equilibrium between blood and brain were 6.3 and 0.8 min for meperidine and alfentanil, respectively: Conclusions The rate of penetration of both opioids into the brain was rapid and not rate-limiting. Large differences in the cerebral distribution volume of meperidine and alfentanil accounted for the respective delays in their peak brain concentration relative to blood.

scholarly journals An Ultrasonic Doppler Venous Outflow Method for the Continuous Measurement of Cerebral Blood Flow in Conscious Sheep

1994 ◽  
Vol 14 (4) ◽  
pp. 680-688 ◽  
Author(s):  
Richard Upton ◽  
Cliff Grant ◽  
Guy Ludbrook
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Continuous Measurement ◽  
Venous Outflow ◽  
Sagittal Sinus ◽  
Global Cerebral Blood Flow ◽  
Conscious Sheep ◽  
End Tidal ◽  
The Brain

A pulsed ultrasonic Doppler venous outflow method was developed for the continuous measurement of global cerebral blood flow (CBF) in conscious sheep. The sheep were prepared under anesthesia with a “suture down”-style ultrasonic flow probe on the dorsal sagittal sinus placed via a trephine hole. Angiographic and dye studies showed that the dorsal sagittal sinus at the point of placement of the probe collected the majority of the blood from the cerebral hemispheres. Studies of the blood velocity profile across the sinus showed that the dimensions of the dorsal sagittal sinus changed minimally with changes in CBF in vivo. The velocity measurements were calibrated under anesthesia against an in vivo direct venous outflow method. Control CBF values for six sheep ranged from 31 to 53 ml/min for the area of brain described above; for two sheep in which the weight of the brain was determined, this gave total CBF values of approximately 34 and 30 ml min−1 100 g−1. The CBF measured varied in the expected manner with changes in the end-tidal CO2 concentration in expired breath and showed transient reductions with the barbiturate thiopentone and transient increases with the opiate alfentanil. It is concluded that the method is simple and accurate.

scholarly journals Influence of different qualitative composition of infusion solutions on cerebral hemodynamics in patients with acute ischemic stroke

2020 ◽  
Vol 73 (2) ◽  
pp. 272-277
Author(s):  
Andrii I. Semenenko ◽  
Halyna I. Khrebtii ◽  
Svetlana L. Malyk ◽  
Dmytro V. Dmytriiev ◽  
Roksolana Ya. Bodnar ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ischemic Stroke ◽  
Cerebral Arteries ◽  
Cerebral Hemodynamics ◽  
Control Group ◽  
Qualitative Composition ◽  
Infusion Solution ◽  
Brain Substance ◽  
The Brain

The aim: Investigate the effect of 0.9% NaCl, HES 130, HAES-LX-5% and mannitol 15% on cerebral hemodynamics in patients with AIS. Materials and methods: The study included 100 patients with AIS. As the investigated solutions were used: isosmolar 0.9% NaCl, hyperosmolar mannitol 15%, colloid-isoosmolar HES 130, colloid-hyperosmolar HAES-LX-5%. The control group received only 0.9% NaCl compared: 0.9% NaCl+HES 130, 0.9% NaCl+HAES-LX-5%, 0.9% NaCl+mannitol 15%. Evaluation of cerebral hemodynamic (indexes of cerebral blood flow) was performed using doppler ultrasound of cerebral arteries. Results: The dynamics of specific volume velocity of blood flow per 100 grams of brain substance indicates that in the group of 0.9% NaCl and 0.9% NaCl+mannitol is the tendency to decrease the blood flow of the brain during 7 days of treatment, respectively: 2.8% and 7.5%. In patients with HES 130 solution cerebral blood flow increases by 14.2%, whereas when applied HAES-LX-5% during 7 days, it increases by 43.2% (p=0.004). Conclusions: The analysis of the data of treatment the patients with AIS showed the best effect (p=0.004) of improvement of the cerebral circulation in the use of the polyfunctional infusion solution HAES-LX-5% unlike the 0.9% NaCl group and group of 0.9% NaCl+mannitol where was a decrease of the dynamics of cerebral blood flow, which could lead to hypoperfusion of the brain.

A venous outflow method for continuously monitoring cerebral blood flow in the rat

1986 ◽  
Vol 250 (2) ◽  
pp. H304-H312
Author(s):  
S. Morii ◽  
A. C. Ngai ◽  
K. R. Ko ◽  
H. R. Winn
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Venous Blood ◽  
Tracer Technique ◽  
Excellent Correlation ◽  
Venous Outflow ◽  
Sagittal Sinus ◽  
Wide Range ◽  
Microsphere Method

We analyzed the retroglenoid venous outflow (VOF) technique in the rat to document the validity of this method of measuring cerebral blood flow (CBF). Stereotypic changes in CBF were obtained with VOF during hypercarbia and hypotension. O2 content of retroglenoid venous blood did not differ significantly from O2 content of blood obtained from the sagittal sinus, suggesting minimal extracerebral contamination of the retroglenoid venous blood. This lack of extracerebral contamination was further analyzed using a double tracer technique (125I-labeled serum albumin, 22Na) that quantitated minimal extracerebral contamination in the retroglenoid vein. CBF measurements were made simultaneously using microsphere and VOF methods, and excellent correlation was found between the two techniques over a wide range of CBF during normoxia, hypoxia, and normoxic hypocarbia and hypercarbia. However, a decrease in the ratio of VOF to microsphere CBF was observed during severe normoxic hypotension (mean arterial pressure = 41 +/- 4 mmHg). VOF represented 18% of total CBF as measured by microsphere method. This study indicates that the retroglenoid outflow technique in rats is a valid method of measuring CBF.

Hypoxia, alpha 2-adrenergic, and nitric oxide-dependent interactions on canine cerebral blood flow

1994 ◽  
Vol 266 (2) ◽  
pp. H476-H482 ◽  
Author(s):  
R. W. McPherson ◽  
R. C. Koehler ◽  
R. J. Traystman
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Methyl Ester ◽  
No Synthase ◽  
Hypoxic Hypoxia ◽  
Control Group ◽  
O2 Transport ◽  
Anesthetized Dogs

We tested the hypothesis that NO synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) and alpha 2-adrenoreceptor stimulation with dexmedetomidine (Dex) decreases the cerebral blood flow (CBF) response to hypoxia. In isoflurane-anesthetized dogs, CBF was measured during two episodes of hypoxic hypoxia. In a control group (n = 6), CBF increased similarly from 83 +/- 4 to 210 +/- 30 ml.min-1 x 100 g-1 and from 88 +/- 7 to 205 +/- 27 (+/- SE) ml.min-1 x 100 g-1 during two hypoxic episodes. In a second group (n = 6), hypoxia increased CBF from 88 +/- 15 to 204 +/- 38 ml.min-1 x 100 g-1. Dex (10 micrograms/kg i.v.) reduced normoxic CBF to 54 +/- 8 ml.min-1 x 100 g-1, and subsequent hypoxia increased CBF to 97 +/- 14 ml.min-1 x 100 g-1. In a third group pretreated with L-NAME (40 mg/kg i.v.) 1 h before anesthesia (n = 6), normoxic CBF was less than in the control group (52 +/- 2 vs. 83 +/- 4 ml.min-1 x 100 g-1). Hypoxia increased CBF to 177 +/- 13 ml.min-1 x 100 g-1. Dex after L-NAME further decreased normoxic CBF to 37 +/- 3 ml.min-1 x 100 g-1, and subsequent hypoxia increased CBF to 106 +/- 18 ml.min-1 x 100 g-1. Dex, L-NAME, and Dex + L-NAME each reduced cerebral O2 transport (CBF x arterial O2 content) during normoxia, but the increase in CBF during hypoxia was sufficient to prevent further decreases in O2 transport. Thus the response to hypoxia remained proportional to normoxic levels of CBF.(ABSTRACT TRUNCATED AT 250 WORDS)

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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