Pentobarbital changes compartmental contribution to cerebral blood flow

1982 ◽  
Vol 56 (4) ◽  
pp. 504-510 ◽  
Author(s):  
John P. Laurent ◽  
Pablo Lawner ◽  
Frederick A. Simeone ◽  
Eugene Fink
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Intracranial Pressure ◽  
Content Type ◽  
Deep White Matter ◽  
Percentage Contribution ◽  
Blood Flows ◽  
Xenon 133 ◽  
Fine Print

✓ Barbiturates were administered to normal dogs, establishing an isoelectric electrocorticogram. Cortical cerebral blood flows (CBF) and deeper CBF's were respectively measured by krypton-85 (85Kr) and xenon-133 (133Xe). Following barbiturate administration, the two methods of measuring CBF showed a poor coefficient of variation (r = 0.12, p < 0.05). The cortical flows decreased less than the fast compartment flows. A shifting of percentage contribution of flow to the slow compartment (60% increase, p < 0.001) was observed after barbiturate infusion. A selective shunting of blood flow to the slower areas may explain the lowering of intracranial pressure and protection of the deep white matter observed by many authors who use barbiturates in clinical and experimental situations.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

Regional cerebral blood flow, sensory evoked potentials, and intracranial pressure in dogs with MCA occlusion by embolization or trapping

1983 ◽  
Vol 58 (4) ◽  
pp. 500-507 ◽  
Author(s):  
Yoshikazu Okada ◽  
Takeshi Shima ◽  
Mitsuo Yamamoto ◽  
Tohru Uozumi
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Evoked Potentials ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Content Type ◽  
Sensory Evoked Potentials ◽  
Sensory Evoked ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF), sensory evoked potentials (SEP), and intracranial pressure (ICP) were investigated in dogs with focal cerebral ischemia produced by a silicone cylinder embolus in the middle cerebral artery (MCA) trunk as compared to that produced by trapping the same vessel. These variables were measured at intervals of 1 hour for a period of 6 hours after MCA occlusion. In the embolized animals, rCBF decreased most extensively at the basal ganglia, from a control level of 53.9 ± 3.9 (mean ± SE) to 21.5 ± 2.7 ml/100 gm/min at the 6th hour. Sensory evoked potentials decreased progressively from the resting level of 100% to 53.0% ± 7.2% at the 3rd hour. Intracranial pressure, measured by epidural pressure on the occluded side, increased rapidly during the first 3 hours, from 10.6 ± 0.3 to about 30 cm H2O. In the animals with trapping, the decreases in rCBF and declines of SEP were significantly less than those in the embolized animals, and no evident brain swelling was observed. This study demonstrates that MCA trunk occlusion by silicone cylinder embolization produces a more marked decrease in deep CBF, with diminution of SEP and increase in ICP, than that produced by trapping.

Effect of reduced cerebral perfusion pressure on cerebral blood flow following inhibition of nitric oxide synthesis

1998 ◽  
Vol 89 (3) ◽  
pp. 448-453 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Nitric Oxide Synthesis ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. The authors tested the hypothesis in a porcine model that inhibition of nitric oxide synthesis during reduced cerebral perfusion pressure (CPP) affected the relative cerebral blood flow (CBF) and the cerebrovascular resistance. Methods. The CPP was reduced by inducing high cerebrospinal fluid pressure and hemorrhagic hypotension. With continuous blood and intracranial pressure monitoring, relative CPP was estimated using the laser Doppler flowmetry technique in nine pigs that received 40 mg/kg nitro-l-arginine methyl ester (l-NAME) and in nine control animals. The l-NAME caused a decrease in relative CBF (p < 0.01) and increases in cerebrovascular resistance (p < 0.01), blood pressure (p < 0.05), and CPP (p < 0.001). During high intracranial pressure there were no significant differences between the treated animals and the controls. After hemorrhage, there was no significant difference between the groups initially, but 30 minutes later the cerebrovascular resistance was decreased in the control group and increased in the l-NAME group relative to baseline (p < 0.05). Combined hemorrhage and high intracranial pressure increased the difference between the two groups with regard to cerebrovascular resistance (p < 0.05). Conclusions. These results suggest that nitric oxide synthesis inhibition affects the autoregulatory response of the cerebral circulation after cardiovascular compensation has taken place. Nitric oxide synthesis inhibition enhanced the undesirable effects of high intracranial pressure during hypovolemia.

Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients

2001 ◽  
Vol 94 (3) ◽  
pp. 403-411 ◽  
Author(s):  
Sarah B. Rockswold ◽  
Gaylan L. Rockswold ◽  
Janet M. Vargo ◽  
Carla A. Erickson ◽  
Richard L. Sutton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Hyperbaric Oxygenation ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Brain Injured ◽  
Csf Lactate ◽  
Injured Patients ◽  
Fine Print

Object. Hyperbaric oxygenation (HBO) therapy has been shown to reduce mortality by 50% in a prospective randomized trial of severely brain injured patients conducted at the authors' institution. The purpose of the present study was to determine the effects of HBO on cerebral blood flow (CBF), cerebral metabolism, and intracranial pressure (ICP), and to determine the optimal HBO treatment paradigm. Methods. Oxygen (100% O2, 1.5 atm absolute) was delivered to 37 patients in a hyperbaric chamber for 60 minutes every 24 hours (maximum of seven treatments/patient). Cerebral blood flow, arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), ventricular cerebrospinal fluid (CSF) lactate, and ICP values were obtained 1 hour before and 1 hour and 6 hours after a session in an HBO chamber. Patients were assigned to one of three categories according to whether they had reduced, normal, or raised CBF before HBO. In patients in whom CBF levels were reduced before HBO sessions, both CBF and CMRO2 levels were raised 1 hour and 6 hours after HBO (p < 0.05). In patients in whom CBF levels were normal before HBO sessions, both CBF and CMRO2 levels were increased at 1 hour (p < 0.05), but were decreased by 6 hours after HBO. Cerebral blood flow was reduced 1 hour and 6 hours after HBO (p < 0.05), but CMRO2 was unchanged in patients who had exhibited a raised CBF before an HBO session. In all patients AVDO2 remained constant both before and after HBO. Levels of CSF lactate were consistently decreased 1 hour and 6 hours after HBO, regardless of the patient's CBF category before undergoing HBO (p < 0.05). Intracranial pressure values higher than 15 mm Hg before HBO were decreased 1 hour and 6 hours after HBO (p < 0.05). The effects of each HBO treatment did not last until the next session in the hyperbaric chamber. Conclusions. The increased CMRO2 and decreased CSF lactate levels after treatment indicate that HBO may improve aerobic metabolism in severely brain injured patients. This is the first study to demonstrate a prolonged effect of HBO treatment on CBF and cerebral metabolism. On the basis of their data the authors assert that shorter, more frequent exposure to HBO may optimize treatment.

Cerebral blood flow and glucose metabolism in experimental brain edema

1989 ◽  
Vol 71 (6) ◽  
pp. 868-874 ◽  
Author(s):  
Leslie N. Sutton ◽  
David Barranco ◽  
Joel Greenberg ◽  
Stephen Dante ◽  
Sandra Florin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Vasogenic Edema ◽  
Tissue Water ◽  
Content Type ◽  
Control Value ◽  
Experimental Brain Edema ◽  
Fine Print ◽  
Edematous Brain

✓ The relationship between cerebral blood flow (CBF) and cerebral metabolic rate of glucose (CMR gl) in the white matter was studied in a plasma infusion model of vasogenic edema in cats. Local CBF, as determined by iodoantipyrine testing, was found to be significantly decreased in edematous white matter (mean ± standard error of the mean: 17.3 ± 1.5 ml/100 gm/min) when compared with CBF in the contralateral control white matter (24.8 ± 1.8 ml/100 gm/min). When the values for edematous brain were corrected for dilution, however, the local CBF averaged 25.3 ± 1.7 ml/100 gm/min, which was similar to the control value. Local CMRgl was found to be significantly increased in plasma-infused white matter (16.3 ± 2.2 µmol/100 gm/min) compared with that in control white matter (10.7 ± 1.3 µmol/100 gm/min). This difference remained, despite correction for dilution and recalculation of local CMRgl values based on altered kinetic constants found in edematous brain. A similar increase in local CMRgl was noted with saline-infusion edema. It is concluded that the increased tissue water level does not alter CBF, but does induce an increase in anaerobic metabolism.

The effect of intracarotid infusion of dexamethasone and 5-hydroxytryptamine on cerebral blood flow and metabolism in baboons

1978 ◽  
Vol 48 (4) ◽  
pp. 594-600 ◽  
Author(s):  
A. David Mendelow ◽  
Benjamin H. Eidelman ◽  
Thomas A. McCalden
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Internal Carotid ◽  
Cerebral Oxygen ◽  
Oxygen Utilization ◽  
Content Type ◽  
Baseline Values ◽  
Xenon 133 ◽  
Fine Print ◽  
Clearance Technique

✓ The effect of intracarotid infusion of dexamethasone on cerebral blood flow and cerebral oxygen utilization was measured in baboons using the xenon-133 clearance technique. The cerebrovascular response to intracarotid infusion of 5-hydroxytryptamine (5-HT) was then determined during simultaneous infusion of the steroid. Infusion of dexamethasone alone and infusion with 5-HT produced no significant change in cerebral blood flow or cerebral oxygen utilization when compared to baseline values. The study indicates that neither dexamethasone nor 5-HT with dexamethasone modify cerebral blood flow when infused via the internal carotid artery.

Effect of α-adrenergic blockade on the cerebrovascular response to increased intracranial pressure after hemorrhage

1998 ◽  
Vol 89 (3) ◽  
pp. 454-459 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Blood Loss ◽  
Treated Group ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. In this study the authors tested the hypothesis that hemorrhagic hypotension and high intracranial pressure induce an increase in cerebrovascular resistance that is caused by sympathetic compensatory mechanisms and can be modified by α-adrenergic blockade. Methods. Continuous measurements of cerebral blood flow were obtained using laser Doppler microprobes placed in the cerebral cortex in anesthetized pigs during induced hemorrhagic hypotension and high cerebrospinal fluid pressure. Eight pigs received 2 mg/kg phentolamine in 10 ml saline, and 13 pigs served as control animals. During high intracranial pressure occurring after blood loss, cerebral perfusion pressure (CPP) (p < 0.01) and cerebral blood flow (p < 0.01) decreased in both groups. Cerebrovascular resistance increased (p < 0.05) in the control group and decreased < 0.005) in the phentolamine-treated group. The cerebrovascular resistance was significantly lower in the phentolamine-treated group (p < 0.05) than in the control group. Cerebrovascular resistance increased at lower CPPs in the control group (linear correlation, r = 0.39, p < 0.01) and decreased with decreasing CPP in the phentolamine-treated group (linear correlation, r = 0.76, p < 0.001). Conclusions. This study shows that the deleterious effects on cerebral hemodynamics induced by blood loss in combination with high intracranial pressure are inhibited by α-adrenergic blockade. This suggests that these responses are caused by α-adrenergically mediated cerebral vasoconstriction.

High level of extracellular potassium and its correlates after severe human head injury: relationship to high intracranial pressure

2000 ◽  
Vol 93 (5) ◽  
pp. 800-807 ◽  
Author(s):  
Michael Reinert ◽  
Ahmad Khaldi ◽  
Alois Zauner ◽  
Egon Doppenberg ◽  
Sung Choi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Fatal Outcome ◽  
Cell Swelling ◽  
Simultaneous Increase ◽  
Extracellular Potassium ◽  
Content Type ◽  
Amperometric Method ◽  
Fine Print

Object. Disturbed ionic and neurotransmitter homeostasis are now recognized as probably the most important mechanisms contributing to the development of secondary brain swelling after traumatic brain injury (TBI). Evidence obtained in animal models indicates that posttraumatic neuronal excitation by excitatory amino acids leads to an increase in extracellular potassium, probably due to ion channel activation. The purpose of this study was therefore to measure dialysate potassium in severely head injured patients and to correlate these results with measurements of intracranial pressure (ICP), patient outcome, and levels of dialysate glutamate and lactate, and cerebral blood flow (CBF) to determine the role of ischemia in this posttraumatic ion dysfunction.Methods. Eighty-five patients with severe TBI (Glasgow Coma Scale Score < 8) were treated according to an intensive ICP management-focused protocol. All patients underwent intracerebral microdialyis. Dialysate potassium levels were analyzed using flame photometry, and dialysate glutamate and dialysate lactate levels were measured using high-performance liquid chromatography and an enzyme-linked amperometric method in 72 and 84 patients, respectively. Cerebral blood flow studies (stable xenon computerized tomography scanning) were performed in 59 patients.In approximately 20% of the patients, dialysate potassium values were increased (dialysate potassium > 1.8 mM) for 3 hours or more. A mean amount of dialysate potassium greater than 2 mM throughout the entire monitoring period was associated with ICP above 30 mm Hg and fatal outcome, as were progressively rising levels of dialysate potassium. The presence of dialysate potassium correlated positively with dialysate glutamate (p < 0.0001) and lactate (p < 0.0001) levels. Dialysate potassium was significantly inversely correlated with reduced CBF (p = 0.019).Conclusions. Dialysate potassium was increased after TBI in 20% of measurements. High levels of dialysate potassium were associated with increased ICP and poor outcome. The simultaneous increase in dialysate potassium, together with dialysate glutamate and lactate, supports the concept that glutamate induces ionic flux and consequently increases ICP, which the authors speculate may be due to astrocytic swelling. Reduced CBF was also significantly correlated with increased levels of dialysate potassium. This may be due to either cell swelling or altered vasoreactivity in cerebral blood vessels caused by higher levels of potassium after trauma. Additional studies in which potassium-sensitive microelectrodes are used are needed to validate these ionic events more clearly.

Effect of stable xenon inhalation on intracranial pressure during measurement of cerebral blood flow in head injury

1994 ◽  
Vol 81 (6) ◽  
pp. 822-828 ◽  
Author(s):  
Jan Plougmann ◽  
Jens Astrup ◽  
Jens Pedersen ◽  
Carsten Gyldensted
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Stable Xenon ◽  
The Mean ◽  
Injured Patients ◽  
Fine Print

✓ Xenon-enhanced computerized tomography (CT) is well suited for measurements of cerebral blood flow (CBF) in head-injured patients. Previous studies indicated divergent results on whether inhalation of xenon may cause a clinically relevant increase in intracranial pressure (ICP). The authors employed Xe-enhanced CT/CBF measurements to study the effect of 20 minutes of inhalation of 33% xenon in oxygen on ICP, cerebral perfusion pressure (CPP), and arteriovenous oxygen difference (AVDO2) in 13 patients 3 days (mean 1 to 5 days) after severe head injury (Glasgow Coma Scale score ≤ 7). The patients were moderately hyperventilated (mean PaCO2 4.3 kPa or 32.3 mm Hg). Six patients were studied before and during additional hyperventilation. All 13 patients reacted with an increase in ICP and 11 with a decrease in CPP. The mean ICP increment was 6.9 ± 7.7 (range 2 to 17 mm Hg). The mean CPP decrement was −9.7 ± −14.6 (range 17 to 47 mm Hg). The time course of the ICP changes indicated that ICP increased rapidly during the first 5 to 6 minutes, then declined to a plateau (peak-plateau type in four of 13 patients), remained at a plateau (plateau type in six of 13), or continued to increase in three of 13, indicating individual variance in xenon reactivity. Additional hyperventilation had no effect on the xenon-induced increments in ICP but these occurred at lower ICP and higher CPP baseline levels. The AVDO2 values, an index of flow in relation to metabolism, indicated a complex effect of xenon on CBF as well as on metabolism. This study indicates that xenon inhalation for Xe-CT CBF measurements in head-injured patients according to our protocol causes clinically significant increments in ICP and decrements in CPP. It is suggested that the effect of xenon is analogous to anesthesia induction. Individual variations were observed indicating possible individual tolerance, possible influence of type and extent of the cerebral injury, disturbances in cerebrovascular reactivity, and possible influence of medication. These effects of xenon suggest that hyperventilation should be ensured in patients with evidence of reduced compliance or high ICP. On the other hand, inhalation of stable xenon is not believed to pose a risk because no signs of cerebral oligemia or ischemia were indicated in the AVDO2 values.

Relationship of early cerebral blood flow and metabolism to outcome in acute head injury

1990 ◽  
Vol 72 (2) ◽  
pp. 176-182 ◽  
Author(s):  
Jurg L. Jaggi ◽  
Walter D. Obrist ◽  
Thomas A. Gennarelli ◽  
Thomas W. Langfitt
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Vegetative State ◽  
Closed Head Injury ◽  
Total Sample ◽  
Prognostic Indicators ◽  
Content Type ◽  
Blood Flows ◽  
Fine Print

✓ Cerebral blood flow (CBF) measurements were obtained acutely in 96 comatose patients with closed head injury, using the intravenous 133Xe technique. Arteriojugular venous oxygen differences and cerebral metabolic rate for oxygen (CMRO2) were determined in a subgroup of 66 patients. The relationship between each of these variables and outcome at 6 months was analyzed, using the Glasgow Outcome Scale. The CMRO2 was significantly depressed in patients who subsequently died or remained in a vegetative state, whereas higher values were obtained in patients who later regained consciousness. Although CBF was not predictive of outcome in the total sample, omission of patients with acute hyperemia resulted in a significant relationship that paralleled the metabolic findings. Follow-up studies in the survivors revealed a correlation between CBF and degree of functional recovery, the lowest blood flows being obtained among patients with severe disability. Age, initial Glasgow Coma Scale score, and occurrence of intracranial hypertension were each found to be predictive of outcome, thus confirming previous reports. When these variables were combined with CMRO2 in a logistic regression analysis, the probability of recovery was correctly predicted in 82% of the cases. The CMRO2 was relatively independent of the other prognostic indicators and, next to age, contributed most to the prediction.

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