Effects of local pressure on cortical electrical activity and cortical vessels in the dog

1970 ◽  
Vol 33 (4) ◽  
pp. 381-387 ◽  
Author(s):  
Mitsuo Numoto ◽  
R. M. Peardon Donaghy
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Intracranial Pressure ◽  
Electrical Activity ◽  
Applied Pressure ◽  
Local Blood Flow ◽  
Local Pressure ◽  
Content Type ◽  
Cortical Electrical Activity ◽  
Fine Print

✓ Suppression of the cortical electrical activity and resistance of cortical vessels to collapse were investigated under various pressures applied locally by an inflatable balloon over the cerebral cortex of dogs. The locally applied pressure and the transmitted general intracranial pressure were measured by a special pressure switch. To produce a 50% suppression of the electrical activity required an average of 45.4 mm Hg local pressure; for 100% suppression, an average of 164 mm Hg. Thus, suppression of the cortical electrical activity is proportional to the pressure applied. In separate experiments with transparent cranial windows, collapse of the cortical veins was produced by an average local pressure of 48.5 mm Hg and collapse of the cortical arteries by an average of 188 mm Hg. It is concluded that the cortical electrical activity is suppressed as a result of changes in local blood flow which are in turn a result of local compression and tissue distortion.

Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury

2002 ◽  
Vol 97 (5) ◽  
pp. 1045-1053 ◽  
Author(s):  
Matthias Oertel ◽  
Daniel F. Kelly ◽  
Jae Hong Lee ◽  
David L. McArthur ◽  
Thomas C. Glenn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Induced Hypertension ◽  
Metabolic Suppression ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

Object. Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. Methods. Thirty-three patients with a mean age of 33 ± 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 ± 5 to 27 ± 5 mm Hg and in ICP from 20 ± 11 to 13 ± 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 ± 5 mm Hg and ICP increased from 16 ± 9 to 19 ± 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 ± 10 to 16 ± 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. Conclusions Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.

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.

Dissociation of cerebral blood flow, glucose metabolism, and electrical activity in pediatric brain death

1993 ◽  
Vol 79 (5) ◽  
pp. 752-755 ◽  
Author(s):  
Michael D. Medlock ◽  
William C. Hanigan ◽  
Robert P. Cruse
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Brain Death ◽  
Electrical Activity ◽  
Closed Head Injury ◽  
Content Type ◽  
Positron Emission ◽  
Mononuclear Cell Infiltrates ◽  
Fine Print

✓ A 2-month-old infant demonstrated clinical brain death 48 hours after suffering a closed head injury accompanied by cardiac arrest. Two nuclear cerebral blood flow (CBF) studies demonstrated normal perfusion. On the 11th day following injury, cerebral electrical activity ceased and a normal glucose metabolic gradient between gray and white matter was documented on positron emission tomography. Autopsy revealed widespread necrosis with mononuclear cell infiltrates throughout all cerebral cortical layers. Nine children have previously been described with clinical brain death, electrocerebral silence, and evidence of CBF by radionuclide scan. The dissociation between cerebral electrical activity and blood flow may be explained by an increase in cranial volume allowed by the expansile neonatal skull, preventing both intracranial hypertension and a reduction in perfusion pressure. The persistence of glucose metabolism may be associated with the presence of inflammatory microglial cells in the ischemic cortex. The authors conclude that persistence of CBF and glucose metabolism in brain-dead children may not indicate neuronal survival. If repeated neurological examinations with or without electroencephalography support the diagnosis of brain death, the presence of CBF and glucose metabolism should not alter this conclusion.

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.

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.

The impact of raised intracranial pressure on cerebral venous hemodynamics: a prospective venous transcranial Doppler ultrasonography study

1999 ◽  
Vol 91 (5) ◽  
pp. 744-749 ◽  
Author(s):  
Benedikt G. H. Schoser ◽  
Nils Riemenschneider ◽  
H. Christian Hansen
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Linear Relationship ◽  
Transcranial Doppler ◽  
Venous Blood ◽  
Venous Blood Flow ◽  
Monitoring Tool ◽  
Content Type ◽  
Basal Vein Of Rosenthal ◽  
Fine Print

Object. The effect of increased intracranial pressure (ICP) on cerebral venous blood flow has been the subject of very few clinical and experimental studies. The authors assessed the usefulness of venous transcranial Doppler (TCD) ultrasonography as a noninvasive monitoring tool for predicting raised ICP.Methods. Serial venous TCD studies of the basal vein of Rosenthal and the straight sinus (SS) were prospectively performed in 30 control volunteers and 25 patients with raised ICP. Correlations with ICP data were calculated using a multivariate regression model. Venous blood flow velocities (BFVs) in the basal vein of Rosenthal showed, within a certain range, a linear relationship between mean ICP and maximal venous BFV (r = 0.645; p < 0.002). Moreover, a linear relationship was found for maximal venous BFVs in the SS and mean ICP (r = 0.928; p < 0.0003).Conclusions. Venous TCD studies may provide an additional noninvasive monitoring tool for raised ICP and give further insights into the cerebral venous hemodynamics present during raised ICP.

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.

Sign in / Sign up

Export Citation Format

Share Document