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.

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.

scholarly journals Model-derived assessment of cerebrovascular resistance and cerebral blood flow following traumatic brain injury

2010 ◽  
Vol 235 (4) ◽  
pp. 539-545 ◽  
Author(s):  
Michael L Daley ◽  
Nithya Narayanan ◽  
Charles W Leffler
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Cerebral Perfusion ◽  
The State ◽  
Cerebrovascular Resistance ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Cerebrovascular Regulation

The published guidelines point out the need for the development of methods that individualize patient cerebral perfusion management and minimize secondary ischemic complications associated with traumatic brain injury. A laboratory method has been developed to determine model-derived assessments of cerebrovascular resistance (mCVR) and cerebral blood flow (mCBF) from cerebrovascular pressure transmission, and the dynamic relationship between arterial blood pressure (ABP) and intracranial pressure (ICP). The aim of this two-fold study is to (1) evaluate relative changes in the model-derived parameters of mCVR and mCBF with the corresponding changes in the pial arteriolar vascular parameters of pial arteriolar resistance (PAR) and relative pial arteriolar blood flow (rPABF); and (2) examine the efficacy of the proposed modeling methodology for continuous assessment of the state of cerebrovascular regulation by evaluating relative changes in the model-derived parameters of CBF and cerebrovascular resistance in relation to changes of cerebral perfusion pressure prior to and following fluid percussion brain injury. Changes of ABP, ICP, PAR, relative arteriolar blood flow (rPABF) and the corresponding model-derived parameters of mCBF and mCVR induced by acute hypertensive challenge were evaluated before and following fluid percussion injury in piglets equipped with cranial windows. Before fluid percussion, hypertensive challenge resulted in a significant increase of PAR and mCVR, whereas both rPABF and mCBF remained constant. Following fluid percussion, hypertensive challenge resulted in a significant decrease of PAR and mCVR and consistent with impaired cerebrovascular regulation. Hypertensive challenge significantly increased both rPABF and mCBF, which approximately doubled with increased CPP with correlation values of r = 0.96 ( P < 0.01) and r = 0.97 ( P ≤ 0.01), respectively. The assessment of model-derived cerebrovascular resistance and CBF with changes of CPP provides a means to monitor continuously the state of cerebrovascular regulation.

Cerebral blood flow decreased by adrenergic stimulation of cerebral vessels in anesthetized newborn pigs with traumatic brain injury

1993 ◽  
Vol 79 (5) ◽  
pp. 696-704 ◽  
Author(s):  
Masaaki Shibata ◽  
Stephanie Einhaus ◽  
John B. Schweitzer ◽  
Samuel Zuckerman ◽  
Charles W. Leffler
Keyword(s):  
Blood Pressure ◽  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Parietal Cortex ◽  
Adrenergic Blockade ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Arteriolar Diameter

✓ Changes in cerebral blood flow (CBF), pial arteriolar diameter, and arterial blood pressure, gases, and pH were examined before and for 3 hours after fluid-percussion brain injury in α-chloralose-anesthetized piglets. The brain injury was induced by a percussion of 2.28 ± 0.06 atm applied for 23.7 ± 0.5 msec to the right parietal cortex. Regional CBF was measured with radiolabeled microspheres, and changes in pial arteriolar diameter were monitored in the left parietal cortex using closed cranial windows. Immediately following brain injury, mean blood pressure transiently (for approximately 10 minutes) either increased or decreased and then exhibited a prolonged decrease in all of the animals. The brains showed changes consistent with traumatic brain injury such as subarachnoid hemorrhage, contusions, or reactive axonal swelling; none showed histological evidence of a global alternative pathogenetic mechanism such as hypoxic ischemic damage. While CBF of uninjured control animals did not change over a 3-hour observation period, after brain injury blood flow decreased 30% ± 1% below the baseline level within 10 minutes and remained there for 2 to 3 hours posttrauma. After adrenergic blockade, CBF did not decrease at any time during the 3-hour period in either the uninjured control or the injured animals. Concomitant with the decreased blood flow after brain injury, pial arteriolar diameter decreased 14% below the preinjury level. However, in piglets treated with adrenoceptor antagonists, uninjured control and brain-injured animals did not show a decrease in pial arteriolar diameter. The present results support the hypothesis that increased sympathetic outflow to the cephalic vasculature following the fluid-percussion brain injury causes cerebral vasoconstriction decreasing pial arteriolar diameter and regional CBF.

Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood

1976 ◽  
Vol 44 (3) ◽  
pp. 353-358 ◽  
Author(s):  
Albert N. Martins ◽  
Norwyn Newby ◽  
Thomas F. Doyle ◽  
Arthur I. Kobrine ◽  
Archimedes Ramirez
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Subarachnoid Injection ◽  
Ischemic Encephalopathy ◽  
Hydrogen Clearance

✓ The hydrogen clearance method was used to measure total and focal cerebral blood flow (CBF) in the monkey before and for 5 hours after a simulated subarachnoid hemorrhage (SAH). Some monkeys also received 0.2 to 1.0 mg/kg phentolamine intracisternally 3 hours after SAH. Results show that SAH did not change cerebrovascular resistance, but as cerebral perfusion pressure decreased, CBF fell transiently. Phentolamine injected intracisternally 3 hours after SAH produced a significant fall in arterial blood pressure; cerebrovascular resistance did not change but CBF decreased significantly. These data indicate that intracisternal phentolamine cannot be considered potentially useful to treat ischemic encephalopathy after SAH.

Melatonin improves cerebral circulation security margin in rats

1998 ◽  
Vol 275 (1) ◽  
pp. H139-H144 ◽  
Author(s):  
Olivier Régrigny ◽  
Philippe Delagrange ◽  
Elizabeth Scalbert ◽  
Jeffrey Atkinson ◽  
Isabelle Lartaud-Idjouadiene
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Mean Arterial Blood Pressure ◽  
Pressure Level ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation

Because melatonin is a cerebral vasoconstrictor agent, we tested whether it could shift the lower limit of cerebral blood flow autoregulation to a lower pressure level, by improving the cerebrovascular dilatory reserve, and thus widen the security margin. Cerebral blood flow and cerebrovascular resistance were measured by hydrogen clearance in the frontal cortex of adult male Wistar rats. The cerebrovasodilatory reserve was evaluated from the increase in the cerebral blood flow under hypercapnia. The lower limit of cerebral blood flow autoregulation was evaluated from the fall in cerebral blood flow following hypotensive hemorrhage. Rats received melatonin infusions of 60, 600, or 60,000 ng ⋅ kg−1 ⋅ h−1, a vehicle infusion, or no infusion ( n= 9 rats per group). Melatonin induced concentration-dependent cerebral vasoconstriction (up to 25% of the value for cerebrovascular resistance of the vehicle group). The increase in vasoconstrictor tone was accompanied by an improvement in the vasodilatory response to hypercapnia (+50 to +100% vs. vehicle) and by a shift in the lower limit of cerebral blood flow autoregulation to a lower mean arterial blood pressure level (from 90 to 50 mmHg). Because melatonin had no effect on baseline mean arterial blood pressure, the decrease in the lower limit of cerebral blood flow autoregulation led to an improvement in the cerebrovascular security margin (from 17% in vehicle to 30, 55, and 55% in the low-, medium-, and high-dose melatonin groups, respectively). This improvement in the security margin suggests that melatonin could play an important role in the regulation of cerebral blood flow and may diminish the risk of hypoperfusion-induced cerebral ischemia.

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.

Beagle pup model of brain injury: regional cerebral blood flow and cerebral prostaglandins

1987 ◽  
Vol 67 (2) ◽  
pp. 278-283 ◽  
Author(s):  
Laura R. Ment ◽  
William B. Stewart ◽  
Charles C. Duncan ◽  
Bruce R. Pitt ◽  
Judith Cole
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
White Matter ◽  
Regional Cerebral Blood Flow ◽  
Ventilatory Support ◽  
Periventricular White Matter ◽  
Regional Cerebral Blood ◽  
Content Type ◽  
Carbon 14

✓ Asphyxia is the most common cause of severe brain injury in very young children, and frequently results in lesions of the periventricular white matter in addition to other neuropathological changes. This study examines the effects of asphyxia on regional cerebral blood flow (rCBF) and the role of prostaglandins (PG's) in its control in the newborn beagle pup. Pups were anesthetized, tracheotomized, paralyzed, artificially ventilated, and randomly assigned to two groups: asphyxial insult produced by discontinuing ventilatory support, and no insult. Experiments for carbon-14-iodoantipyrine autoradiographic determination of rCBF and regional cerebral PG determination were performed on separate groups of pups. These studies demonstrated a significant increase in cortical gray PGE2 levels at a time when rCBF was significantly impaired in response to severe asphyxial insult. No such increase was noted in the periventricular white matter zones.

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.

scholarly journals Continuous non-invasive optical monitoring of cerebral blood flow and oxidative metabolism after acute brain injury

2019 ◽  
Vol 39 (8) ◽  
pp. 1469-1485 ◽  
Author(s):  
Wesley B Baker ◽  
Ramani Balu ◽  
Lian He ◽  
Venkaiah C Kavuri ◽  
David R Busch ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Acute Brain Injury ◽  
Oxygen Extraction Fraction ◽  
Cerebral Microdialysis ◽  
Optical Monitoring ◽  
Non Invasive ◽  
Arterial Blood ◽  
Brain Injured

Rapid detection of ischemic conditions at the bedside can improve treatment of acute brain injury. In this observational study of 11 critically ill brain-injured adults, we employed a monitoring approach that interleaves time-resolved near-infrared spectroscopy (TR-NIRS) measurements of cerebral oxygen saturation and oxygen extraction fraction (OEF) with diffuse correlation spectroscopy (DCS) measurement of cerebral blood flow (CBF). Using this approach, we demonstrate the clinical promise of non-invasive, continuous optical monitoring of changes in CBF and cerebral metabolic rate of oxygen (CMRO2). In addition, the optical CBF and CMRO2 measures were compared to invasive brain tissue oxygen tension (PbtO2), thermal diffusion flowmetry CBF, and cerebral microdialysis measures obtained concurrently. The optical CBF and CMRO2 information successfully distinguished between ischemic, hypermetabolic, and hyperemic conditions that arose spontaneously during patient care. Moreover, CBF monitoring during pressor-induced changes of mean arterial blood pressure enabled assessment of cerebral autoregulation. In total, the findings suggest that this hybrid non-invasive neurometabolic optical monitor (NNOM) can facilitate clinical detection of adverse physiological changes in brain injured patients that are otherwise difficult to measure with conventional bedside monitoring techniques.

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.

Sign in / Sign up

Export Citation Format

Share Document