Effect of hyperglycemia on brain pH levels in areas of focal incomplete cerebral ischemia in monkeys

1986 ◽  
Vol 65 (5) ◽  
pp. 693-696 ◽  
Author(s):  
W. Richard Marsh ◽  
Robert E. Anderson ◽  
Thoralf M. Sundt
Keyword(s):  
Adverse Effect ◽  
Cerebral Ischemia ◽  
Cell Damage ◽  
Treated Group ◽  
Squirrel Monkeys ◽  
Control Group ◽  
Content Type ◽  
Brain Ph ◽  
Fine Print ◽  
Incomplete Ischemia

✓ The adverse effect of a minimal cerebral blood flow (CBF) in models of global ischemia has been noted by many investigators. One factor believed important in this situation is the level of blood glucose, since a continued supply of this metabolite results in increased tissue lactate, decreased brain pH, and increased cell damage. The authors have extended these observations to a model of focal incomplete ischemia. Brain pH was measured in fasted squirrel monkeys in regions of focal incomplete ischemia after transorbital occlusion of the middle cerebral artery (MCA). In both control and hyperglycemic animals, CBF was reduced to less than 30% of baseline. At 3 hours after MCA occlusion, brain pH in the control group was 6.66 ± 0.68 as compared to 6.27 ± 0.26 in the glucose-treated group. This difference was statistically significant by Student's unpaired t-test (p < 0.05). Thus, hyperglycemia results in decreased tissue pH in regions of focal incomplete cerebral ischemia in monkeys.

Decompressive craniectomy in a rat model of “malignant” cerebral hemispheric stroke: experimental support for an aggressive therapeutic approach

1996 ◽  
Vol 85 (5) ◽  
pp. 853-859 ◽  
Author(s):  
Arnd Doerfler ◽  
Michael Forsting ◽  
Wolfgang Reith ◽  
Christian Staff ◽  
Sabine Heiland ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Decompressive Craniectomy ◽  
Control Group ◽  
Acute Ischemia ◽  
Vessel Occlusion ◽  
Content Type ◽  
Time Points ◽  
Infarction Size ◽  
Mca Occlusion ◽  
Fine Print

✓ Acute ischemia in the complete territory of the carotid artery may lead to massive cerebral edema with raised intracranial pressure and progression to coma and death due to uncal, cingulate, or tonsillar herniation. Although clinical data suggest that patients benefit from undergoing decompressive surgery for acute ischemia, little data about the effect of this procedure on experimental ischemia are available. In this article the authors present results of an experimental study on the effects of decompressive craniectomy performed at various time points after endovascular middle cerebral artery (MCA) occlusion in rats. Focal cerebral ischemia was induced in 68 rats using an endovascular occlusion technique focused on the MCA. Decompressive cranioectomy was performed in 48 animals (in groups of 12 rats each) 4, 12, 24, or 36 hours after vessel occlusion. Twenty animals (control group) were not treated by decompressive craniectomy. The authors used the infarct volume and neurological performance at Day 7 as study endpoints. Although the mortality rate in the untreated group was 35%, none of the animals treated by decompressive craniectomy died (mortality 0%). Neurological behavior was significantly better in all animals treated by decompressive craniectomy, regardless of whether they were treated early or late. Neurological behavior and infarction size were significantly better in animals treated very early by decompressive craniectomy (4 hours) after endovascular MCA occlusion (p < 0.01); surgery performed at later time points did not significantly reduce infarction size. The results suggest that use of decompressive craniectomy in treating cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. By performing decompressive craniectomy neurosurgeons will play a major role in the management of stroke patients.

Results of applying ADCON-L gel after lumbar discectomy: the German ADCON-L study

2001 ◽  
Vol 95 (2) ◽  
pp. 179-189 ◽  
Author(s):  
Hans-Peter Richter ◽  
Erich Kast ◽  
Rainer Tomczak ◽  
Werner Besenfelder ◽  
Wilhelm Gaus
Keyword(s):  
Lumbar Disc ◽  
Animal Experiments ◽  
Treated Group ◽  
Secondary Outcome ◽  
Control Group ◽  
Large Sample Size ◽  
Therapeutic Success ◽  
Content Type ◽  
The Mean ◽  
Fine Print

Object. Failed-back syndrome is still an unsolved problem. Use of ADCON-L gel, already commercially available, has been proven to reduce postoperative scarring in animal experiments. The authors of two controlled clinical studies have also shown positive results when applying the gel. They did not, however, establish patient-oriented endpoints. The authors report a study of ADCON-L in which they focus on patient-oriented endpoints. Methods. Patients with lumbar disc herniation were randomized to an ADCON-L—treated or control group. Therapeutic success was evaluated using the validated Hannover Questionnaire on Activities of Daily Living (FFbH) 6 months after surgery. The study took place between November 14, 1996, and April 20, 1998, in eight neurosurgical centers in Germany. A total of 398 patients was recruited; 41 patients dropped out during follow up. The mean functional FFbH score (100 points = all activities are possible without problem; 0 points = no activity is possible) was 78.5 points in the ADCON-L—treated group compared with 80 points in the control group. Furthermore, in terms of secondary outcome variables, the ADCON-L group did not have an advantage over the control group. Only the mean magnetic resonance imaging score showed a slight advantage of ADCON-L over the control group. Conclusions. The authors found no positive effect of treatment with ADCON-L gel in patients in whom one-level lumbar microdiscectomy was performed. Because of its rather large sample size and its homogeneity, the study had sufficient power to detect even small differences between the two groups.

Natural hypothermia immediately after transient global cerebral ischemia induced by spontaneous subarachnoid hemorrhage

2003 ◽  
Vol 98 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Kiyoshi Takagi ◽  
Yoshiaki Tsuchiya ◽  
Kimiko Okinaga ◽  
Masafumi Hirata ◽  
Tadayoshi Nakagomi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Body Temperature ◽  
Global Cerebral Ischemia ◽  
Control Group ◽  
Mean Body Temperature ◽  
Content Type ◽  
Transient Global Cerebral Ischemia ◽  
Gcs Score ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

Object. Spontaneous subarachnoid hemorrhage (SAH) has an aspect of graded transient global cerebral ischemia. The purpose of the present study was the documentation of sequential changes in body temperature immediately after SAH-induced transient global cerebral ischemia in humans. Methods. Patients admitted within 12 hours after the initial onset of SAH were examined retrospectively (426 patients). Patients with unruptured cerebral aneurysms served as a control group (73 patients). Body temperature measured at the axilla on admission was analyzed. The grade of SAH was established according to the Glasgow Coma Scale (GCS): Grade I, GCS Score 15; Grade II, GCS Score 11 to 14; Grade III, GCS Score 8 to 10; Grade IV, GCS Score 4 to 7; and Grade V, GCS Score 3. The mean body temperature of patients in the control group was 36.49 ± 0.45°C (mean ± standard deviation). The mean body temperature of patients in the SAH group who had been admitted within 4 hours of onset for Grades I to V were significantly different (p < 0.001, analysis of variance [ANOVA]): 36.26 ± 0.7°C, 59 patients; 35.98 ± 0.85°C, 73 patients; 35.52 ± 0.79°C, 25 patients; 35.9 ± 1.09°C, 108 patients; and 35.56 ± 1.14°C, 73 patients, respectively. These values were significantly lower than those in control volunteers, except for patients with Grade I SAH. The reduction in body temperature was unrelated to the location of the cerebral aneurysm and was not the product of circadian rhythm. The temperatures of patients in the SAH group who were admitted beyond 4 hours after onset for each grade were significantly different (p < 0.01, ANOVA): 36.8 ± 0.91°C, 36 patients; 36.74 ± 0.68°C, 31 patients; 36.73 ± 0.38°C, three patients; 37.41 ± 1.37°C, 17 patients; and 38.9°C, one patient, respectively. These values were significantly higher than those in patients admitted within 4 hours of SAH onset for all grades except Grade V, and significantly higher than control values in patients with Grades I and IV SAH. Conclusions. These results indicate that body temperature falls and then rises immediately after the SAH-induced transient global cerebral ischemia without cardiac arrest in humans. The reduction in temperature may be a natural cerebral protection mechanism that is activated shortly after ischemic insult.

Low-dose aspirin prophylaxis and risk of intracranial hemorrhage in patients older than 60 years of age with mild or moderate head injury: a prospective study

2003 ◽  
Vol 99 (4) ◽  
pp. 661-665 ◽  
Author(s):  
Sergey Spektor ◽  
Samuel Agus ◽  
Vladimir Merkin ◽  
Shlomo Constantini
Keyword(s):  
Head Injury ◽  
Intracranial Hemorrhage ◽  
Ct Scanning ◽  
Treated Group ◽  
Control Group ◽  
Content Type ◽  
Significant Difference ◽  
Traumatic Intracranial Hemorrhage ◽  
Gcs Score ◽  
Fine Print

Object. The goal of this paper was to investigate a possible relationship between the consumption of low-dose aspirin (LDA) and traumatic intracranial hemorrhage in an attempt to determine whether older patients receiving prophylactic LDA require special treatment following an incidence of mild-to-moderate head trauma. Methods. Two hundred thirty-one patients older than 60 years of age, who arrived at the emergency department with a mild or moderate head injury (Glasgow Coma Scale [GCS] Scores 13–15 and 9–12, respectively), were included in the study. One hundred ten patients were receiving prophylactic LDA (100 mg/day) and these formed the aspirin-treated group. One hundred twenty-one patients were receiving no aspirin, and these formed the control group. There was no statistically significant difference between the two groups with respect to age, sex, mechanism of trauma, or GCS score on arrival at the emergency department. Most of the patients sustained the head injury from falls (88.2% of patients in the aspirin-treated group and 85.1% of patients in the control group), and had external signs of head trauma such as bruising or scalp laceration (80.9% of patients in the aspirin-treated group and 86.8% of patients in the control group). All patients underwent similar neurological examinations and computerized tomography (CT) scanning of the head. The CT scans revealed evidence of traumatic intracranial hemorrhage in 27 (24.5%) patients in the aspirin-treated group and in 31 patients (25.6%) in the control group. Surgical intervention was required for five patients in each group (4.5% of patients in the aspirin-treated group and 4.1% of patients in the control group). A surprising number of the patients who arrived with GCS Score 15 were found to have traumatic intracranial hemorrhage, as revealed by CT scanning (11.5% of patients in the aspirin-treated group and 16.5% of patients in the control group). Surgery, however, was not necessary for any of these patients. Conclusions. There was no statistically significant difference in the frequency or types of traumatic intracranial hemorrhage between patients who had received aspirin prophylaxis and those who had not. The authors conclude that LDA does not increase surgically relevant parenchymal or meningeal bleeding following moderate and minor head injury in patients older than 60 years of age.

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.

Antibiotic prophylaxis in neurosurgery

1984 ◽  
Vol 60 (4) ◽  
pp. 724-726 ◽  
Author(s):  
James Geraghty ◽  
Micheal Feely
Keyword(s):  
Antibiotic Prophylaxis ◽  
Randomized Trial ◽  
Infection Rate ◽  
Treated Group ◽  
Prophylactic Antibiotics ◽  
Control Group ◽  
Wound Infections ◽  
Content Type ◽  
Fine Print

✓ A randomized trial was performed to support the contention that prophylactic antibiotics can reduce the incidence of postoperative neurosurgical wound infections. The regime outlined by Malis was followed. Vancomycin and gentamicin were administered systemically just prior to surgery and streptomycin was added to the irrigating solution. Patients were randomly assigned to two groups: control and treated. The infection rate in the control group was 3.5% and in the treated group 0.5%.

Effect of nimodipine on intracellular brain pH, cortical blood flow, and EEG in experimental focal cerebral ischemia

1986 ◽  
Vol 64 (4) ◽  
pp. 617-626 ◽  
Author(s):  
Fredric B. Meyer ◽  
Robert E. Anderson ◽  
Tony L. Yaksh ◽  
Thoralf M. Sundt
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Adjunctive Treatment ◽  
Control Group ◽  
Cortical Blood Flow ◽  
Content Type ◽  
Mca Occlusion ◽  
Brain Ph ◽  
Major Branch

✓ Intracellular brain pH, cortical blood flow, and electroencephalograms (EEG's) were recorded in severely and moderately ischemic regions in 10 control and 10 nimodipine-treated rabbits prior to and following major branch occlusion of the middle cerebral artery (MCA). Preocclusion cortical blood flow was 51 ml/100 gm/min and intracellular brain pH was 7.01 in both the control and the treated animals. After MCA occlusion, the severely ischemic regions in the control group showed initial and 4-hour postocclusion flows of 12.7 and 5.2 ml/100 gm/min with a brain pH of 6.64 and 6.08, respectively. In animals given nimodipine after MCA occlusion, blood flow increased from 10.5 to 18.8 ml/100 gm/min, with an associated elevation in intracellular brain pH from 6.57 to 6.91. Comparable findings were observed in areas of moderate ischemia. Improvements in cortical blood flow, intracellular brain pH, and EEG attenuations produced by nimodipine were all statistically significant. Inspection of the cortex revealed reversal of cortical pallor and small-vessel spasm following treatment with nimodipine. It is hypothesized that nimodipine exerts its effects through reversal of ischemia-induced secondary vasoconstriction, and that this drug may be an important adjunctive treatment for patients with focal cerebral ischemia.

scholarly journals Brain pH in Focal Cerebral Ischemia and the Protective Effects of Barbiturate Anesthesia

1983 ◽  
Vol 3 (4) ◽  
pp. 493-497 ◽  
Author(s):  
Robert E. Anderson ◽  
Thoralf M. Sundt
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Focal Ischemia ◽  
Squirrel Monkeys ◽  
Protective Effects ◽  
Halothane Anesthesia ◽  
Fluorescent Indicator ◽  
Normal Value ◽  
Brain Ph ◽  
Incomplete Ischemia

Intracellular brain pH was measured with a lipid-soluble, pH-sensitive fluorescent indicator in 16 squirrel monkeys. Eight of these were under halothane anesthesia and eight under barbiturate anesthesia. Measurements were taken before, during, and after focal incomplete ischemia. Brain pH following 3 h of cerebral focal ischemia changed from a normal value of 7.0 to 6.5 and 6.2 in animals studied under barbiturate and halothane anesthesia, respectively. Brain pH returned toward normal after flow was restored in animals under barbiturate anesthesia but continued to deteriorate in animals under halothane anesthesia.

Development of cyclooxygenase and lipoxygenase metabolites of arachidonic acid after transient cerebral ischemia

1986 ◽  
Vol 64 (1) ◽  
pp. 118-124 ◽  
Author(s):  
Robert J. Dempsey ◽  
Mark W. Roy ◽  
Kathleen Meyer ◽  
David E. Cowen ◽  
Hsin-Hsiung Tai
Keyword(s):  
Arachidonic Acid ◽  
Cerebral Ischemia ◽  
Transient Cerebral Ischemia ◽  
Control Group ◽  
Mongolian Gerbils ◽  
Transient Ischemia ◽  
Ischemic Lesion ◽  
Content Type ◽  
Local Generation ◽  
Fine Print

✓Vasoactive arachidonic acid metabolites are postulated to play a role in the pathogenesis of cerebral ischemia. In order to characterize the local generation of cyclooxygenase and lipoxygenase metabolites of arachidonic acid in transient ischemia with reperfusion, Mongolian gerbils were studied for regional cerebral blood flow (CBF), using the hydrogen clearance technique, and for cerebral levels of the thromboxane metabolite TXB2, and prostaglandins 6-keto-PGF1α and PGE2, as well as the leukotriene LTB4. The gerbils were anesthetized with pentobarbital, and half of the animals were pretreated with the cyclooxygenase inhibitor indomethacin. All received 10 or 20 minutes of dense forebrain ischemia followed by reperfusion of 10 minutes, 50 minutes, or 100 minutes. A separate control group received no ischemic lesion. Regional CBF decreased significantly from 23.7 ± 2.6 to 4.3 ± 1.7 cc/100 gm/min during ischemia (p < 0.01). Reperfusion resulted in initially normal flows (22.5 ± 5.1 cc/100 gm/min) followed by a progressive hypoperfusion (11.3 ± 2.7 cc/100 gm/min). All metabolites showed parallel significant (p < 0.05) increases after transient ischemia and reperfusion compared to baseline levels (values (in pg/mg protein) were: TXB2 45.5 ± 7.1 vs 23.3 ± 3.6; 6-keto-PGF1α 262.8 ± 47.9 vs 175.8 ± 26.8; PGE2 256.5 ± 35.6 vs 112.5 ± 11.2; and LTB4 37.8 ± 4.6 vs 24.6 ± 6). These levels were all significantly decreased (p < 0.05) by pretreatment with indomethacin except for the leukotriene LTB4, which was increased. Transient cerebral ischemia results in a reperfusion abnormality and the local generation of cyclooxygenase products, which are reduced by pretreatment with indomethacin; however, cyclooxygenase inhibition may result in increased substrate availability for the lipoxygenase system. Studies of such an interaction may lead to new understandings of the pharmacological modification of detrimental vascular changes after transient cerebral 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.

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