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.

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.

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.

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.

Effects of nimodipine on the production of thromboxane A2 following total global cerebral ischemia

1988 ◽  
Vol 69 (3) ◽  
pp. 416-420 ◽  
Author(s):  
W. Scott Haddon ◽  
Donald S. Prough ◽  
Daniel Kong ◽  
Patricia Petrozza
Keyword(s):  
Cerebral Ischemia ◽  
Channel Blocker ◽  
Statistical Significance ◽  
Thromboxane A2 ◽  
Treated Group ◽  
Global Cerebral Ischemia ◽  
Intravenous Bolus ◽  
Content Type ◽  
To Receive ◽  
Fine Print

✓ To clarify the contribution of vasoconstrictor prostaglandins to the hypoperfusion state typically following total global cerebral ischemia, 14 mongrel dogs were subjected to 11 minutes of global cerebral ischemia. They were then randomly assigned to receive either no treatment or an intravenous bolus of the calcium channel blocker nimodipine, 10 µg/kg, 15 minutes after ischemia followed by a continuous infusion of nimodipine, 1.0 µg/kg/min. Thromboxane (Tx) A2 production, as measured by cerebral venous levels of TxB2 (the stable metabolite of TxA2) increased similarly in the two groups. In contrast to previous studies, mean postischemic cerebral blood flow did not increase sufficiently in the nimodipine-treated group to achieve statistical significance. These data suggest that the improved neurological outcome associated with nimodipine treatment following global cerebral ischemia does not relate to reduced levels of the prostaglandin precursor arachidonate.

Hemorrhagic dilation of the fourth ventricle: an ominous predictor

1994 ◽  
Vol 80 (5) ◽  
pp. 805-809 ◽  
Author(s):  
Scott A. Shapiro ◽  
Robert L. Campbell ◽  
Thomas Scully
Keyword(s):  
Functional Recovery ◽  
Fourth Ventricle ◽  
Outcome Predictor ◽  
Ventricular Dilation ◽  
Content Type ◽  
Chi Squared ◽  
Aggressive Care ◽  
Gcs Score ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ Very little is known about the effect of computerized tomography (CT)-documented fourth intraventricular hemorrhage (IVH). An analysis of 50 patients with CT-documented fourth IVH treated between 1987 and 1992 is presented. The various etiologies included intraparenchymal hemorrhage with secondary fourth IVH (19 cases), spontaneous subarachnoid hemorrhage (18 cases), spontaneous IVH (seven cases), and trauma (six cases). Overall, 28 patients (56%) had hemorrhagic dilation of the fourth ventricle and all 28 suffered brain death, despite aggressive therapy in 79% of cases. Twenty-two patients (44%) had fourth IVH without dilation; of these, nine (41%) died and 13 (59%) experienced functional survival, despite aggressive care in 90% of cases. The survival rate was significantly worse for patients with dilation of the fourth ventricle (p < 0.01, chi-squared test). Of the 28 patients with fourth IVH associated with dilation, 25 (89%) had diffuse clot, involving the lateral and third ventricles as well, and three (11%) had isolated fourth IVH. Of the 22 patients with fourth IVH and no dilation, 13 (59%) had diffuse IVH (eight of these died and five had functional recovery) and nine (41%) had isolated fourth IVH (one died and eight had functional recovery). Diffuse ventricular clot was associated with an increased mortality rate for patients with fourth IVH and no dilation (p < 0.05). Of the 28 patients with fourth IVH associated with dilation, 24 (86%) presented with a Glasgow Coma Scale (GCS) score of 3 or 4, one with a GCS score of 6, and three with a GCS score of 13 to 15; all 28 died. For the 22 patients with fourth IVH and no dilation, nine presented with a GCS score of 3 to 5 (eight died and one had functional recovery), three had a GCS score of 6 to 8 (all three had functional survival), two had a GCS score of 9 to 12 (both had functional survival), and eight had a GCS score of 13 to 15 (one died and seven had functional survival). There was a greater chance of higher GCS scores in patients with fourth IVH and no hemorrhagic dilation (p < 0.01). Logistic regression multivariate analysis showed hemorrhagic fourth ventricular dilation to be the most significant outcome predictor (p = 0.0001), followed by GCS score (p = 0.007) and the presence of diffuse IVH (p = 0.0279).

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.

Energy-requiring cell functions in the ischemic brain

1982 ◽  
Vol 56 (4) ◽  
pp. 482-497 ◽  
Author(s):  
Jens Astrup
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Specific Inhibition ◽  
Ischemic Brain ◽  
Content Type ◽  
Cell Functions ◽  
The Brain ◽  
Fine Print

✓ The energy-requiring cell functions in the brain are described. The role of specific inhibition of these functions, and their critical low-supply levels of blood flow and oxygen are reviewed in relation to clinical management of focal and complete global cerebral ischemia.

Role of a synthetic pyrimidine compound, MS-818, in reduction of infarct size and amelioration of sensorimotor dysfunction following permanent focal cerebral ischemia in rats

2002 ◽  
Vol 96 (6) ◽  
pp. 1072-1076 ◽  
Author(s):  
Tetsuryu Mitsuyama ◽  
Takakazu Kawamata ◽  
Fumitaka Yamane ◽  
Akira Awaya ◽  
Tomokatsu Hori
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Biological Activities ◽  
Infarct Volume ◽  
Saline Control ◽  
Control Group ◽  
Sprague Dawley ◽  
Triphenyltetrazolium Chloride ◽  
Content Type ◽  
Fine Print

Object. A synthetic heterocyclic pyrimidine compound, MS-818 (2-piperadino-6-methyl-5-oxo-5,6-dihydro-(7H) pyrrolo-[3,4-d] pyrimidine maleate) is reported to have a variety of biological activities including neurite outgrowth, astrocyte differentiation, suppression of neuronal apoptosis, regeneration of injured peripheral nerves, fracture repairs, angiogenesis, and superovulation. To be able to explicate the neurotrophic effects of MS-818, the authors evaluated its effect on the reduction of infarct volume and amelioration of sensorimotor dysfunction in a rat model of focal ischemia. Methods. Forty male Sprague—Dawley rats were subjected to right middle cerebral artery occlusion and assigned to one of four treatment groups (10 animals in each group). The MS-818 (1, 5, or 10 mg/kg) or phosphate-buffered saline (control group) was administered intraperitoneally at onset of ischemia and again 24 hours later. The rats were killed 48 hours after they underwent surgery to induce stroke, and infarct volume was determined using an image-analysis computer software program following staining with 2,3,5-triphenyltetrazolium chloride. Postischemic neurological deficit and body weight were also assessed. Conclusions. Significant reductions in infarct volume (total and cortical infarction) were found in all the MS-818—treated groups compared with the control group. Furthermore, MS-818 induced significant amelioration of sensorimotor dysfunction, as indicated by the results of forelimb and hindlimb placing tests. The present findings suggest that MS-818, which has a much smaller molecular weight than neurotrophic peptides, represents a new approach to the treatment of focal cerebral ischemia.

The effect of resuscitative moderate hypothermia following epidural brain compression on cerebral damage in a canineoutcome model

1993 ◽  
Vol 79 (2) ◽  
pp. 241-251 ◽  
Author(s):  
Shlomo Pomeranz ◽  
Peter Safar ◽  
Ann Radovsky ◽  
Samuel A. Tisherman ◽  
Henry Alexander ◽  
...  
Keyword(s):  
Intensive Care ◽  
Body Temperature ◽  
Brain Death ◽  
Control Group ◽  
Intraventricular Pressure ◽  
Content Type ◽  
Brain Compression ◽  
Normothermic Group ◽  
Fine Print ◽  
Hypothermic Group

✓ A canine model of temporary epidural cerebral compression and standardized intensive care was developed to evaluate the effect of resuscitative (postinsult) moderate systemic hypothermia. A balloon was inflated over the temporal region to maintain contralateral intraventricular pressure (IVP) at 62 mm Hg for 90 minutes. For a 66-hour period after initiation of brain compression, the intubated dogs received controlled ventilation and standard intensive care. From 66 to 90 hours postinjury, the extubated dogs were evaluated as to functional outcome. Morphological brain damage was evaluated at 90 hours or earlier if brain death occurred. Eight dogs in a control group were maintained at a body of temperature of 38°C. Eight treated dogs had core body temperature reduced by surface cooling starting 15 minutes after balloon inflation, first to 31°C for 5 hours and then to 35°C from 5 to 62 hours after insult. Intraventricular pressure increased to 20 mm Hg or greater in the control group at a mean of 2.9 hours (range 2 to 4 hours) following the insult, and in the hypothermic group at a mean of 14.8 hours (range 5 to 30 hours) — that is, during the time period when the body temperature was 35°C, not 31°C (p = 0.01). There was no difference in peak pressures between the two groups. Brain death occurred in four of the eight dogs in the normothermic group at 18, 24, 24, and 48 hours (mean ± standard deviation 28 ± 13 hours) and in three of the eight in the hypothermic group at 27, 42, and 45 hours (mean 38 ± 10 hours) (not significant). The animals surviving 90 hours (four in the normothermic and five in the hypothermic group) were neurologically near normal. The total mean macroscopically damaged brain volume was 2584 ± 1890 cu mm in the normothermic versus 765 ± 611 cu mm in the hypothermic group (p = 0.03). The mean necrotic volume was 741 ± 599 cu mm in the normothermic versus 263 ± 346 cu mm in the hypothermic group (p = 0.07). Microscopically, the damaged regions consisted of ischemic neurons, reactive glia, edema, vascular endothelial hypertrophy, and erythrocyte extravasation. It is concluded that, in this model, immediate postinsult hypothermia of 31°C (not 35°C) for 5 hours prevents a rise in IVP and significantly decreases cerebral tissue damage, but does not prevent brain herniation during rewarming.

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