Relationship of cerebral blood flow to cardiac output, mean arterial pressure, blood volume, and alpha and beta blockade in cats

1980 ◽  
Vol 52 (6) ◽  
pp. 745-754 ◽  
Author(s):  
Dudley H. Davis ◽  
Thoralf M. Sundt
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Cerebral Autoregulation ◽  
Major Change ◽  
Beta Blockade ◽  
Content Type ◽  
Therapeutic Implications ◽  
Arterial Blood

✓ The relationship among cerebral blood flow (CBF), blood volume, cardiac output (CO), and mean arterial blood pressure (MABP) at varying levels of arterial CO2 tensions (PaCO2) were studied in 70 normal cats. The CBF was measured from the clearance curve of xenon−133 and CO with a thermal dilution catheter placed in the pulmonary artery. The CBF, CO, and MABP values varied appropriately with changes in PaCO2, confirming the reliability of the preparations and the presence of normal autoregulatory responses. Moderate hypovolemia that did not change MABP did, nevertheless, significantly decrease CO and CBF. In an effort to determine if this decrease in CO and CBF were coupled responses, the effects of beta stimulation, hypervolemia, and alpha and beta blockade were investigated. Propranolol, in a dosage insufficient to change MABP, decreased both CO and CBF. This agent abolished the CO response to elevations in PaCO2 but not the CBF response, making it unlikely that this CBF reduction resulted from impaired cerebral autoregulation. Isoproterenol, which, in contrast to propranolol, does not cross the normal blood-brain barrier, alone or in combination with phenoxybenzamine, produced a 38% and 72% increase in CO, respectively, without a change in CBF. Alpha blockade (no major change in CO) and beta blockade (major decrease in CO) did not significantly effect cerebral autoregulation to changes in MABP from angiotensin. The ability of the brain to resist increases in MABP and CO and maintain normal CBF is explained by normal cerebral autoregulation. However, its vulnerability to modest decreases in blood volume, which cannot be attributed to variations in perfusion pressure, is unexplained but obviously has important therapeutic implications. This may be related to reduction in CO, changes in autonomic activity, or a decrease in the size of the perfused capillary bed.

Early changes measured by magnetic resonance imaging in cerebral blood flow, blood volume, and blood-brain barrier permeability following dexamethasone treatment in patients with brain tumors

1999 ◽  
Vol 90 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Leif Østergaard ◽  
Fred H. Hochberg ◽  
James D. Rabinov ◽  
A. Gregory Sorensen ◽  
Michael Lev ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Brain Tumors ◽  
Mr Imaging ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Clinical Effects ◽  
Content Type ◽  
Fine Print

Object. In this study the authors assessed the early changes in brain tumor physiology associated with glucocorticoid administration. Glucocorticoids have a dramatic effect on symptoms in patients with brain tumors over a time scale ranging from minutes to a few hours. Previous studies have indicated that glucocorticoids may act either by decreasing cerebral blood volume (CBV) or blood-tumor barrier (BTB) permeability and thereby the degree of vasogenic edema.Methods. Using magnetic resonance (MR) imaging, the authors examined the acute changes in CBV, cerebral blood flow (CBF), and BTB permeability to gadolinium-diethylenetriamine pentaacetic acid after administration of dexamethasone in six patients with brain tumors. In patients with acute decreases in BTB permeability after dexamethasone administration, changes in the degree of edema were assessed using the apparent diffusion coefficient of water.Conclusions. Dexamethasone was found to cause a dramatic decrease in BTB permeability and regional CBV but no significant changes in CBF or the degree of edema. The authors found that MR imaging provides a powerful tool for investigating the pathophysiological changes associated with the clinical effects of glucocorticoids.

Cerebral blood flow and interstitial fluid adenosine during hemorrhagic hypotension

1988 ◽  
Vol 255 (5) ◽  
pp. H1211-H1218 ◽  
Author(s):  
D. G. Van Wylen ◽  
T. S. Park ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Adenosine Receptor ◽  
Cerebral Autoregulation ◽  
Interstitial Fluid ◽  
Adenosine Receptor Antagonist ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Adenosine Concentration ◽  
Group 2

This study was designed to assess the role of adenosine in autoregulation of cerebral blood flow (CBF) with the use of the brain dialysis technique to sample cerebral interstitial fluid (ISF) and hydrogen clearance to measure local CBF in ketamine-anesthetized rats. In group 1 (n = 11), animals were hemorrhaged to reduce mean arterial blood pressure (MABP) from control levels (MABP = 101.1 +/- 2.6) to 80, 70, 60, 50, 40, and 30 mmHg. Cerebral autoregulation was evidenced by no significant decrease in CBF until MABP decreased to 60 mmHg. However, dialysate adenosine concentration did not increase until MABP decreased to 50 mmHg. In group 2 (bilateral dialysis; n = 11), in which the left carotid artery was ligated before reductions in MABP, left-side dialysate adenosine concentration increased at a MABP of 70 mmHg. In group 3 (bilateral dialysis; n = 6), one dialysis probe was perfused with artificial cerebrospinal fluid containing 10(-3) M 8(p-sulfophenyl)theophylline (8-SPT), an adenosine receptor antagonist, during reduction of MABP to 50 mmHg. Although there were similar reductions in CBF with or without adenosine receptor blockade, dialysate adenosine concentration was greater on the side of locally infused 8-SPT at a MABP of 50 mmHg. These data suggest that adenosine is not responsible for cerebral autoregulation at blood pressures greater than 50 mmHg but may contribute to the decrease in cerebral vascular resistance observed at arterial pressures below the autoregulatory range.

Effects of fluid-percussion brain injury on regional cerebral blood flow and pial arteriolar diameter

1986 ◽  
Vol 64 (5) ◽  
pp. 787-794 ◽  
Author(s):  
Douglas S. DeWitt ◽  
Larry W. Jenkins ◽  
Enoch P. Wei ◽  
Harry Lutz ◽  
Donald P. Becker ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Pial Arterioles ◽  
High Level ◽  
Arteriolar Diameter

✓ The effects of two levels of fluid-percussion brain injury on cerebral blood flow (CBF) and pial arteriolar diameter were investigated in cats. Regional CBF was measured using the radioactive microsphere technique. Experimental brain injury resulted in changes in arterial blood pressure, CBF, and pial arteriolar diameter that were related to the severity of the injury. Low-level injury (1.88 ± 0.11 atm, mean ± standard error of the mean) resulted in a slight transient increase in CBF which had returned to preinjury levels by 30 minutes. High-level injury (2.68 ± 0.19 atm) resulted in larger, statistically significant (p < 0.01) increases in whole-brain CBF, decreases in cerebrovascular resistance, and increases in pial arteriolar diameter 1 minute postinjury. One hour after injury, CBF had returned to preinjury levels while cerebral perfusion pressure was significantly (p < 0.01) reduced. There was no evidence of reduced CBF in any region studied. Pial arterioles dilated during the posttraumatic hypertensive period and then returned to control diameters within 1 hour after injury. Changes in the diameter of pial arterioles were significantly correlated with posttraumatic changes in CBF.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Alterations in cerebral autoregulation and cerebral blood flow velocity during acute hypoxia: rest and exercise

2007 ◽  
Vol 292 (2) ◽  
pp. H976-H983 ◽  
Author(s):  
Philip N. Ainslie ◽  
Alice Barach ◽  
Carissa Murrell ◽  
Mike Hamlin ◽  
John Hellemans ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Autoregulation ◽  
Cerebral Oxygenation ◽  
Cerebral Blood Flow Velocity ◽  
Arterial Blood ◽  
Cerebrovascular Function ◽  
Hypoxic Exercise

We examined the relationship between changes in cardiorespiratory and cerebrovascular function in 14 healthy volunteers with and without hypoxia [arterial O2 saturation (SaO2) ∼80%] at rest and during 60–70% maximal oxygen uptake steady-state cycling exercise. During all procedures, ventilation, end-tidal gases, heart rate (HR), arterial blood pressure (BP; Finometer) cardiac output (Modelflow), muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasound) were measured continuously. The effect of hypoxia on dynamic cerebral autoregulation was assessed with transfer function gain and phase shift in mean BP and MCAV. At rest, hypoxia resulted in increases in ventilation, progressive hypocapnia, and general sympathoexcitation (i.e., elevated HR and cardiac output); these responses were more marked during hypoxic exercise ( P < 0.05 vs. rest) and were also reflected in elevation of the slopes of the linear regressions of ventilation, HR, and cardiac output with SaO2 ( P < 0.05 vs. rest). MCAV was maintained during hypoxic exercise, despite marked hypocapnia (44.1 ± 2.9 to 36.3 ± 4.2 Torr; P < 0.05). Conversely, hypoxia both at rest and during exercise decreased cerebral oxygenation compared with muscle. The low-frequency phase between MCAV and mean BP was lowered during hypoxic exercise, indicating impairment in cerebral autoregulation. These data indicate that increases in cerebral neurogenic activity and/or sympathoexcitation during hypoxic exercise can potentially outbalance the hypocapnia-induced lowering of MCAV. Despite maintaining MCAV, such hypoxic exercise can potentially compromise cerebral autoregulation and oxygenation.

Autoregulation of cerebral blood flow after experimental fluid percussion injury of the brain

1980 ◽  
Vol 53 (4) ◽  
pp. 500-511 ◽  
Author(s):  
W. Lewelt ◽  
L. W. Jenkins ◽  
J. Douglas Miller
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Injury ◽  
Content Type ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Fluid Percussion Injury ◽  
The Brain

✓ To test the hypothesis that concussive brain injury impairs autoregulation of cerebral blood flow (CBF), 24 cats were subjected to hemorrhagic hypotension in 10-mm Hg increments while measurements were made of arterial and intracranial pressure, CBF, and arterial blood gases. Eight cats served as controls, while eight were subjected to mild fluid percussion injury of the brain (1.5 to 2.2 atmospheres) and eight to severe injury (2.8 to 4.8 atmospheres). Injury produced only transient changes in arterial and intracranial pressure, and no change in resting CBF. Impairment of autoregulation was found in injured animals, more pronounced in the severe-injury group. This could not be explained on the basis of intracranial hypertension, hypoxemia, hypercarbia, or brain damage localized to the area of the blood flow electrodes. It is, therefore, concluded that concussive brain injury produces a generalized loss of autoregulation for at least several hours following injury.

Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury

1978 ◽  
Vol 48 (5) ◽  
pp. 689-703 ◽  
Author(s):  
Erna M. Enevoldsen ◽  
Finn T. Jensen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Damage ◽  
Severely Injured ◽  
Content Type ◽  
Cerebrovascular Autoregulation ◽  
Decerebrate Rigidity ◽  
Arterial Blood ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with impaired CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.

scholarly journals Metoprolol Reduces Cerebral Tissue Oxygen Tension after Acute Hemodilution in Rats

2009 ◽  
Vol 111 (5) ◽  
pp. 988-1000 ◽  
Author(s):  
Tenille E. Ragoonanan ◽  
W Scott Beattie ◽  
C David Mazer ◽  
Albert K.Y. Tsui ◽  
Howard Leong-Poi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Oxygen Tension ◽  
Tissue Oxygen Tension ◽  
Beta Blockade ◽  
Tissue Oxygen ◽  
Cerebral Tissue ◽  
Protein Levels

Background Perioperative beta-blockade and anemia are independent predictors of increased stroke and mortality by undefined mechanisms. This study investigated the effect of beta-blockade on cerebral tissue oxygen delivery in an experimental model of blood loss and fluid resuscitation (hemodilution). Methods Anesthetized rats were treated with metoprolol (3 mg x kg) or saline before undergoing hemodilution with pentastarch (1:1 blood volume exchange, 30 ml x kg). Outcomes included cardiac output, cerebral blood flow, and brain (PBrO2) and kidney (PKO2) tissue oxygen tension. Hypoxia inducible factor-1alpha (HIF-1alpha) protein levels were assessed by Western blot. Systemic catecholamines, erythropoietin, and angiotensin II levels were measured. Results Hemodilution increased heart rate, stroke volume, cardiac output (60%), and cerebral blood flow (50%), thereby maintaining PBrO2 despite an approximately 50% reduction in blood oxygen content (P &lt; 0.05 for all). By contrast, PKO2 decreased (50%) under the same conditions (P &lt; 0.05). Beta-blockade reduced baseline heart rate (20%) and abolished the compensatory increase in cardiac output after hemodilution (P &lt; 0.05). This attenuated the cerebral blood flow response and reduced PBrO2 (50%), without further decreasing PKO2. Cerebral HIF-1alpha protein levels were increased in beta-blocked hemodiluted rats relative to hemodiluted controls (P &lt; 0.05). Systemic catecholamine and erythropoietin levels increased comparably after hemodilution in both groups, whereas angiotensin II levels increased only after beta-blockade and hemodilution. Conclusions Cerebral tissue oxygen tension is preferentially maintained during hemodilution, relative to the kidney, despite elevated systemic catecholamines. Acute beta-blockade impaired the compensatory cardiac output response to hemodilution, resulting in a reduction in cerebral tissue oxygen tension and increased expression of HIF-1alpha.

Continuous monitoring of regional cerebral blood flow: experimental and clinical validation of a novel thermal diffusion microprobe

2000 ◽  
Vol 93 (2) ◽  
pp. 265-274 ◽  
Author(s):  
Peter Vajkoczy ◽  
Harry Roth ◽  
Peter Horn ◽  
Thomas Lucke ◽  
Claudius Thomé ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Thermal Diffusion ◽  
Regional Cerebral Blood Flow ◽  
Linear Regression Analysis ◽  
Secondary Brain Injury ◽  
Regional Cerebral Blood ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

Object. Current clinical neuromonitoring techniques lack adequate surveillance of cerebral perfusion. In this article, a novel thermal diffusion (TD) microprobe is evaluated for the continuous and quantitative assessment of intraparenchymal regional cerebral blood flow (rCBF).Methods. To characterize the temporal resolution of this new technique, rCBF measured using the TD microprobe (TD-rCBF) was compared with rCBF levels measured by laser Doppler (LD) flowmetry during standardized variations of CBF in a sheep model. For validation of absolute values, the microprobe was implanted subcortically (20 mm below the level of dura) into 16 brain-injured patients, and TD-rCBF was compared with simultaneous rCBF measurements obtained using stable xenon-enhanced computerized tomography scanning (sXe-rCBF). The two techniques were compared using linear regression analysis as well as the Bland and Altman method.Stable TD-rCBF measurements could be obtained throughout all 3- to 5-hour sheep experiments. During hypercapnia, TD-rCBF increased from 49.3 ± 15.8 ml/100 g/min (mean ± standard deviation) to 119.6 ± 47.3 ml/100 g/min, whereas hypocapnia produced a decline in TD-rCBF from 51.2 ± 12.8 ml/100 g/min to 39.3 ± 5.6 ml/100 g/min. Variations in mean arterial blood pressure revealed an intact autoregulation with pressure limits of approximately 65 mm Hg and approximately 170 mm Hg. After cardiac arrest TD-rCBF declined rapidly to 0 ml/100 g/min. The dynamics of changes in TD-rCBF corresponded well to the dynamics of the LD readings. A comparison of TD-rCBF and sXe-rCBF revealed a good correlation (r = 0.89; p <0.0001) and a mean difference of 1.1 ± 5.2 ml/100 g/min between the two techniques.Conclusions. The novel TD microprobe provides a sensitive, continuous, and real-time assessment of intraparenchymal rCBF in absolute flow values that are in good agreement with sXe-rCBF measurements. This study provides the basis for the integration of TD-rCBF into multimodal monitoring of patients who are at risk for secondary brain injury.

Sign in / Sign up

Export Citation Format

Share Document