Effect of mannitol on local cerebral blood flow after temporary complete cerebral ischemia in rats

1992 ◽  
Vol 76 (3) ◽  
pp. 486-492 ◽  
Author(s):  
Reizo Shirane ◽  
Philip R. Weinstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
External Carotid ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Content Type ◽  
Arterial Blood ◽  
Permanent Occlusion ◽  
Fine Print

✓ The effects of pretreatment with mannitol on local cerebral blood flow (CBF) after permanent or temporary global cerebral ischemia were evaluated with 14C-iodoantipyrine autoradiography in rats under halothane-N2O endotracheal anesthesia. Blood pressure, pulse rate, arterial blood gas levels, and electroencephalographic (EEG) tracings were monitored throughout the experiments. After permanent occlusion of the basilar artery and both external carotid and pterygopalatine arteries, severe global ischemia was induced by permanent occlusion of the common carotid arteries (CCA's) or by a 30-minute temporary CCA occlusion followed by 5 minutes of reperfusion. Intravenous mannitol (25%, 1 gm/kg) or saline solution was administered 5 minutes before occlusion of the CCA's. Cerebral blood flow was measured in 24 anatomical regions. The EEG tracings flattened within 2 to 3 minutes after the onset of ischemia, and no recovery was observed during reperfusion. In the mannitol-treated rats and the saline-treated controls, autoradiographic studies after permanent occlusion showed no CBF in the forebrain or cerebellum, although brain-stem and spinal cord CBF values were normal. After 5 minutes of reperfusion, CBF in the cortex, basal ganglia, and white matter was 100% to 200% higher in mannitol-treated rats and 50% to 100% higher in saline-injected rats than in the nonischemic anesthetized control group. Heterogeneously distributed areas of no-reflow were seen in all saline-injected rats but were observed in none of the mannitol-treated rats. Pretreatment with mannitol prevented postischemic obstruction of the microcirculation during 5 minutes of recirculation after 30 minutes of severe temporary ischemia, but the EEG signals did not recover. Further studies of the functional and morphological responses to longer periods of postischemic recirculation are needed to verify the extent to which these mannitol-induced effects are protective.

Local cerebral blood flow and glucose utilization after blood exchange with a hemoglobin-based O2 carrier in conscious rats

1993 ◽  
Vol 265 (4) ◽  
pp. H1243-H1248 ◽  
Author(s):  
K. Waschke ◽  
H. Schrock ◽  
D. M. Albrecht ◽  
K. van Ackern ◽  
W. Kuschinsky
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Utilization ◽  
Brain Structures ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Conscious Rats ◽  
Cerebral Glucose Utilization ◽  
Arterial Blood ◽  
Blood Exchange

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.

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.

Effect of chemical sympathectomy on cerebral blood flow in rats

1991 ◽  
Vol 75 (6) ◽  
pp. 906-910 ◽  
Author(s):  
Hidenori Kobayashi ◽  
Minoru Hayashi ◽  
Hirokazu Kawano ◽  
Yuji Handa ◽  
Masanori Kabuto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Systemic Blood Pressure ◽  
Treated Group ◽  
Control Group ◽  
Electron Microscopic ◽  
Content Type ◽  
Left Lateral Ventricle ◽  
6 Hydroxydopamine ◽  
Fine Print

✓ Thirty male Wistar rats, weighing 350 to 400 gm each, received stereotactic injections of 6-hydroxydopamine (300 µg/kg) into the left lateral ventricle. The same amount of saline was injected into a control group of 15 rats. Seven days after this procedure, cerebral blood flow (CBF) was measured by the hydrogen clearance method. A hypertensive condition at a mean arterial pressure of about 160 mm Hg was maintained for 1 hour by intravenous infusion of phenylephrine. In the 6-hydroxydopamine-treated group, CBF increased significantly after the elevation of systemic blood pressure compared with that in the control group, and cerebral autoregulation was impaired. After a 1-hour study, the specific gravity of the cerebral tissue in the treated group significantly decreased; electron microscopic studies at that time revealed brain edema. It is suggested that depletion of brain noradrenaline levels causes a disturbance in cerebral microvascular tone and renders the cerebral blood vessels more vulnerable to hypertension.

Spinal cord stimulation reducing infarct volume in a model of focal cerebral ischemia in rats

2003 ◽  
Vol 99 (1) ◽  
pp. 131-137 ◽  
Author(s):  
Oren Sagher ◽  
Dah-Luen Huang ◽  
Richard F. Keep
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Spinal Cord Stimulation ◽  
Focal Cerebral Ischemia ◽  
Doppler Flowmetry ◽  
Content Type ◽  
Baseline Values ◽  
Fine Print

Object. The authors previously showed that spinal cord stimulation (SCS) increases cerebral blood flow in rats, indicating that this technique may be useful in the treatment of focal cerebral ischemia. In the present study, the neuroprotective potential of SCS in the setting of middle cerebral artery occlusion (MCAO) was investigated. Methods. The authors induced permanent, focal cerebral ischemia by using either suture-induced occlusion or direct division of the MCA in Sprague—Dawley rats. Electrical stimulation of the cervical spinal cord was performed during cerebral ischemia. Cerebral blood flow was assessed using both laser Doppler flowmetry (LDF) and quantitative radiotracer analysis. Stroke volumes were analyzed after 6 hours of ischemia. Spinal cord stimulation resulted in a 52.7 ± 13.3% increase in LDF values (nine animals). Following MCAO, LDF values decreased by 64.1 ± 3.6% from baseline values (10 animals). Spinal cord stimulation subsequently increased LDF values to 30.9 ± 13.5% below original baseline values. These findings were corroborated using radiotracer studies. Spinal cord stimulation in the setting of transcranial MCAO significantly reduced stroke volumes as well (from 203 ± 33 mm3 [control] to 32 ± 8 mm3 [MCAO plus SCS], seven animals in each group, p < 0.001). Similarly, after suture-induced MCAO, SCS reduced stroke volumes (from 307 ± 29 mm3 [control] to 78 ± 22 mm3 [MCAO plus SCS], 10 animals in each group, p < 0.001). Conclusions. A strategy of performing SCS for the prevention of critical ischemia is feasible and may have the potential for the treatment and prevention of stroke.

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.

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.

Experimental intracerebral mass: time-related effects on local cerebral blood flow

1987 ◽  
Vol 67 (5) ◽  
pp. 732-738 ◽  
Author(s):  
Thomas A. Kingman ◽  
A. David Mendelow ◽  
David I. Graham ◽  
Graham M. Teasdale
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Local Cerebral Blood Flow ◽  
Ischemic Lesion ◽  
Content Type ◽  
Local Ischemia ◽  
Carbon 14 ◽  
Autoradiographic Technique ◽  
Space Occupying Lesion ◽  
Fine Print

✓ Cerebral blood flow (CBF) was measured at different times during the first 150 minutes following an experimental space-occupying lesion produced with a 50-µl microballoon in rats. Local CBF was measured with the carbon-14-labeled iodoantipyrine quantitative autoradiographic technique. A region of local ischemia developed around the mass, while the remote effects of the mass were minimal. The focal ischemic lesion enlarged with time, and simulated removal of the lesion within this design did not alleviate the ischemia.

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.

Differences in critical cerebral blood flow with age in swine

1991 ◽  
Vol 75 (1) ◽  
pp. 103-107 ◽  
Author(s):  
Jun Harada ◽  
Akira Takaku ◽  
Shunro Endo ◽  
Naoya Kuwayama ◽  
Osamu Fukuda
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Content Type ◽  
Neonatal Pigs ◽  
S 100 ◽  
Newborn Pigs ◽  
Electroencephalogram Eeg ◽  
The Brain ◽  
Fine Print

✓ Normal cerebral blood flow (CBF), critical CBF at a flat reading of the electroencephalogram (EEG), and reversibility of the flat EEG after reperfusion were investigated in a total of 59 pigs, including seven newborns (1 to 3 days of age), 38 juveniles (1 month old), and 14 adults (7 months old). The CBF was determined by the hydrogen clearance method; the EEG was recorded continuously and a power spectrum analysis was performed. Cerebral ischemia was produced by occlusion of both common carotid arteries and induction of hypotension (approximately 50 mm Hg). The flat EEG reversibility was investigated for 3 hours after reperfusion. As parameters of brain development, the neuronal density and the time at which the S-100 protein appeared in the brain were examined. Normal CBF was highest in neonatal pigs and decreased with age. The critical CBF at a flat EEG was lowest in newborn pigs and was elevated with development of the brain. Tolerance against cerebral ischemia was greatest in newborn pigs.

Effect of mild hypothermia on uncontrollable intracranial hypertension after severe head injury

1993 ◽  
Vol 79 (3) ◽  
pp. 363-368 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Hisashi Sugimoto ◽  
Mamoru Taneda ◽  
Hiroyoshi Yoshida ◽  
Atsushi Iwai ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Hypertension ◽  
Mild Hypothermia ◽  
Controlled Study ◽  
Control Group ◽  
Content Type ◽  
Hypothermia Group ◽  
Oxygen Difference ◽  
Fine Print

✓ Recent experimental studies have demonstrated that mild hypothermia at about 34°C can be effective in the control of intracranial hypertension. A randomized controlled study of mild hypothermia was carried out in 33 severely head-injured patients. All patients fulfilled the following criteria: 1) persistent intracranial pressure (ICP) greater than 20 mm Hg despite fluid restriction, hyperventilation, and high-dose barbiturate therapy; 2) an ICP lower than the mean arterial blood pressure; and 3) a Glasgow Coma Scale score of 8 or less. The patients were divided into two groups: one received mild hypothermia (16 patients) and one served as a control group (17 patients). Mild hypothermia significantly reduced the ICP and increased the cerebral perfusion pressure. Eight patients (50%) in the hypothermia group and three (18%) in the control group survived (p < 0.05), while five (31%) in the hypothermia group and 12 (71%) in the control group died of uncontrollable intracranial hypertension (p < 0.05). In five patients in the hypothermia group, cerebral blood flow was measured by the hydrogen clearance method and arteriojugular venous oxygen difference was evaluated before and during mild hypothermia. Mild hypothermia significantly decreased the cerebral blood flow, arteriojugular venous oxygen difference, and cerebral metabolic rate of oxygen (p < 0.01). The results of this preliminary investigation suggest that mild hypothermia is a safe and effective method to control traumatic intracranial hypertension and to improve mortality and morbidity rates.

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