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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The goal of the current study was to determine whether treatment of hypertension reduces cerebral infarction after occlusion of the middle cerebral artery in stroke-prone spontaneously hypertensive rats (SHRSPs). Three-month-old SHRSPs received untreated drinking water or drinking water containing cilazapril, an angiotensin converting enzyme inhibitor, or hydralazine and hydrochlorothiazide. After 3 months of treatment, the left middle cerebral artery was occluded and neurological deficit was evaluated. Infarct volume was measured 3 days after occlusion using computer imaging techniques from brain slices. Cilazapril and hydralazine with hydrochlorothiazide were equally effective in reducing systolic blood pressure in SHRSPs. One day after occlusion of the middle cerebral artery, neurological deficit was decreased by both cilazapril and hydralazine with hydrochlorothiazide compared with untreated SHRSPs, and the deficit 3 days after occlusion was decreased significantly only by cilazapril. Infarct volume was 178 +/- 7 mm3 (mean +/- SEM) in untreated SHRSPs, and it was significantly reduced to 117 +/- 15 mm3 by hydralazine with hydrochlorothiazide and to 101 +/- 17 mm3 by cilazapril. Infarct volume in Wistar-Kyoto rats was 27 +/- 16 mm3. Thus, reduction in arterial pressure by hydralazine with hydrochlorothiazide or an angiotensin converting enzyme inhibitor is protective against focal cerebral ischemia in SHRSPs.
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PMID:Effect of antihypertensive treatment on focal cerebral infarction. 153 16

We administered hyperbaric oxygen or air in a double-blind prospective protocol to 39 patients with ischemic cerebral infarction. We interrupted the study when we noticed what appeared to be a trend favoring the air-treated patients, whose neurological deficits were less severe (mean +/- SEM score on graded neurological examination: air, 25.6 +/- 4.9; oxygen, 34.5 +/- 7.5) and whose infarcts were smaller (air, 29.0 +/- 12.2 cm3; oxygen, 49.2 +/- 11.7 cm3) at 4 months. The trend, we decided, was probably an artifact of the randomization process. Nevertheless, we chose not to resume the trial because the treatment was difficult to administer by schedule (for various reasons the treatment protocol was broken in 15 of the 39 patients), was poorly tolerated (eight of the 39 patients refused to continue treatments), and did not produce dramatic improvement.
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PMID:A pilot study of hyperbaric oxygen in the treatment of human stroke. 192 56

Tissue plasminogen activator is an endogenous fibrin-specific serine protease with potent thrombolytic activity. We investigated the efficacy of tissue plasminogen activator in reducing cerebral infarct size after thromboembolic stroke in a rabbit model. Seventeen rabbits were randomized to receive either tissue plasminogen activator (2.5 mg/kg, n = 6) or vehicle control (n = 11). We controlled mean arterial pressure, hematocrit, and arterial blood gases before and after the intracarotid embolization of an autologous clot. Cerebral blood flow (cm3/100 g/min) (mean +/- SEM) was immediately reduced from 55.2 +/- 7.7 to 8.5 +/- 2.5 in the control group and from 61.8 +/- 14.8 to 10.0 +/- 3.5 in the treated group after embolization. Cerebral blood flow recovered significantly within 60 minutes of thrombolytic therapy and attained a value of 59.6 +/- 10.0 cm3/100 g/min 4 hours after embolization, whereas cerebral blood flow in control animals demonstrated only a minimal recovery to 15.3 +/- 8.9 cm3/100 g/min. Cerebral infarct size (percent of hemisphere) was reduced from 34.4 +/- 5.6% in control animals to 8.8 +/- 5.6% in treated animals (mean +/- SEM, p less than 0.01). These results suggest that tissue plasminogen activator may be efficacious in restoring cerebral blood flow and thus limiting infarct size in acute thromboembolic stroke.
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PMID:Tissue plasminogen activator reduces brain injury in a rabbit model of thromboembolic stroke. 212 36

Although patients with acute type A aortic dissection are best managed by emergency surgical intervention, preoperative stroke is known to be an independent predictor of late mortality and is considered by some to be a contraindication to operation because of the risk of precipitating hemorrhagic cerebral infarction and poor long-term outcome. In a series of 272 consecutive, unselected patients with aortic dissection undergoing surgical treatment during a 25-year span (1963-1987), 128 (47 +/- 3% [+/- 70% confidence level (CL)]) had an acute type A dissection. A total of seven patients with acute type A dissection (2.6 +/- 1% of all patients, 5.5 +/- 2% of the acute type A cohort) developed a new stroke preoperatively. Thirteen (4.8 +/- 1%) patients had a diminished or absent carotid pulse, only four (31 +/- 13%) of whom sustained a stroke. One patient died in the immediate postoperative period due to severe brain injury, yielding an operative mortality rate of 14 +/- 14%. Two patients had persistent neurological deficits and died within 4 months of operation; the actuarial survival estimate at 1 year was 57 +/- 19% (mean +/- SEM). One patient recovered function of one upper extremity (preoperative left hemiparesis compounded by paraplegia) but died 6 years later. The remaining three long-term survivors (43 +/- 19%) had major resolution of their neurological deficits and are clinically well 2-8 years postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Surgical management of acute aortic dissection complicated by stroke. 276 34

Both I-123 IMP scintigraphy and MRI have been suggested as sensitive detectors of changes shortly after acute cerebral infarction. We compared the uptake of N-isopropyl I-123 p-iodoamphetamine (IMP) and MR spectroscopy of the brain after internal carotid artery ligation. Thirteen gerbils were lightly anesthetized with ether. After neck dissection, an internal carotid artery was occluded. After 2.8 hours, 100 muCi I-123 IMP was injected intravenously into the 13 experimental animals plus three controls. Seven gerbils remained asymptomatic while six developed hemiparesis. At 3 hours after ligation, the animals were killed. The brains were bisected and T1 and T2 relaxation times were determined for the right and left hemispheres by MR spectroscopy immediately after dissection. I-123 IMP uptake was then determined in the samples. Interhemispheric differences in uptake for I-123 IMP were 0.1 +/- 1.7% (SEM) in the control, 33.5 +/- 10% in the asymptomatic and 54.6 +/- 9.7% in the symptomatic animals. Significant differences were seen with I-123 IMP in 6/7 asymptomatic and 6/6 symptomatic animals. In conclusion, I-123 is more sensitive than T1 or T2 relaxation times for the detection of cerebral perfusion abnormalities. Prolongation in T1 and T2 relaxation times correlates closely with increased brain tissue water content and the development of symptoms, indicators of structural brain damage and probable infarction.
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PMID:Comparison of I-123 IMP cerebral uptake and MR spectroscopy following experimental carotid occlusion. 404 77

Positron emission tomography was used to study the effect of supratentorial infarction on cerebellar metabolic rate for oxygen and cerebellar blood flow. In a control group of patients, the mean cerebellar metabolic rate for oxygen was 2.97 +/- 0.11 (standard error of the mean [SEM] ) ml-1 . min-1 . hg-1 and mean cerebellar blood flow was 41.1 +/- 1.5 ml . min-1 . hg-1. No significant right-left asymmetry in either cerebellar metabolic rate for oxygen or cerebellar blood flow was noted. Patients with frontal lobe infarction showed 16.8 +/- 1.8% (cerebellar metabolic rate for oxygen) and 19.6 +/- 2.1% (cerebellar blood flow) differences between cerebellar hemispheres, with the hemisphere contralateral to the cerebral infarction having the lower values. These differences were highly significant (p less than 0.001). In addition, cerebellar blood flow and cerebellar metabolic rate for oxygen were significantly decreased in the ipsilateral cerebellar hemisphere (metabolism: 2.13 +/- 0.19 ml . min-1 . hg-1; p less than 0.002; blood flow: 35.2 +/- 2.4 ml . min-1 . hg-1; p less than 0.05). Patients with parietooccipital infarction also showed a significant bilateral decrease in cerebellar metabolic rate for oxygen (2.43 +/- 0.11 ml . min-1 . hg-1) and cerebellar blood flow (34.6 +/- 2.5 ml . min-1 . hg-1) relative to control subjects, but no significant cerebellar asymmetry. Our findings demonstrate a general depression of cerebellar blood flow and metabolism from cerebral hemisphere infarction unrelated to the site of infarction as well as a specific depression occurring contralateral to infarction involving the frontal lobe. These are among the first quantitative data concerning regional cerebellar metabolic rates for oxygen and cerebellar blood flow in humans.
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PMID:Cerebellar blood flow and metabolism in cerebral hemisphere infarction. 660 10

Plasminogen activator inhibitor-1 (PAI-1) is a serpin proteinase inhibitor which regulates fibrinolysis and the proteinase cascade of tumour invasion. In this study, PAI-1 was identified in the cerebrospinal fluid (CSF) from patients without neurological disease and patients with various neurological disorders. The mean level of PAI-1 in the CSF of 28 patients without central nervous system (CNS) disease was 0.28 +/- 0.03 (SEM) ng/ml. CSF PAI-1 was significantly increased in the following diagnostic categories:dementia (Alzheimer's disease), cerebral infarction, CNS infection, alcohol withdrawal seizures and CNS neoplasia. In all these disorders, with the exception of CNS infection, PAI-1 was also increased as a fraction of total CSF protein. CSF PAI-1 was not increased in patients with hydrocephalus or idiopathic seizure disorders. Complementary plasma samples were available for 18 of the 128 CSF specimens studied. For these cases, there was no correlation between plasma PAI-1 and CSF PAI-1 levels. PAI-1 may represent a non-specific marker of disease in the central nervous system.
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PMID:Plasminogen activator inhibitor-1 in the cerebrospinal fluid as an index of neurological disease. 805 48

Gamma-glutamyl transferase (GGT) serum levels were measured in 42 female patients within 72 hours, and on day 10, after an ischaemic cerebral infarction (CI) and correlated with neurological impairment at admission and with mortality during hospitalization. Mean +/- SEM GGT serum value within 72 hours after CI was significantly higher compared to the mean +/- SEM value observed in control subjects (26.7 +/- 2.5 vs 16.5 +/- 1.2 U/L, P < 0.001) and it correlated with the severity of neurological status and with mortality. A positive correlation between GGT and creatine kinase (CK) serum levels was also observed (r = 0.47, P < 0.01). On day 10 after CI, normalization of serum GGT values was found. We conclude that GGT serum level increases in CI as a consequence of brain damage and that this increment may be considered as a clinical and prognostic unfavourable index of the disease.
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PMID:Clinical aspects of early increase in serum gamma-glutamyl transferase in cerebral infarction. 810 94

To develop a reliable canine model of cerebral infarction of moderate size, we compared infarctions caused by permanent occlusion of the following vessels in 42 dogs: 1) the middle cerebral artery (MCA), 2) the MCA and azygous anterior cerebral artery (ACA), 3) the MCA, azygous ACA, and posterior cerebral artery (PCA), and 4) sham-operated controls. The infarction volume was determined at 6 hours in half the animals and at 6 days in the others. Studies of somatosensory evoked potentials (SSEPs) and regional cerebral blood flow (rCBF) were performed before and after arterial occlusion, and good correlation was observed between the decrease in amplitude of the SSEPs and the decrease in rCBF observed after arterial occlusion. Only the groups in which the MCA and azygous ACA were occluded showed moderate infarctions of relatively consistent size. Analysis involving all groups revealed that the animals with SSEP amplitude preserved after vessel occlusion had only small infarctions; thus, preservation of SSEP amplitude after occlusion of the MCA and azygous ACA could in the future be used prospectively as a rejection criterion to improve the uniformity of infarction size. Conversely, animals with loss of SSEP amplitude after vessel occlusion had infarctions of moderate to large size; thus, loss of SSEP amplitude after MCA occlusion alone could in the future be used prospectively as a rejection criterion. When these rejection criteria were retrospectively applied to the groups in which both the MCA and azygous ACA were occluded, the resulting mean infarction volumes +/- 1 SEM) for the acute and chronic subgroups were 20.3 +/- 2.8% and 38.2 +/- 4.5% of the hemisphere, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of somatosensory evoked potential monitoring to produce a canine model of uniform, moderately severe stroke with permanent arterial occlusion. 832 1

Considerable evidence indicates that brain temperature during ischemia affects the extent and distribution of ischemic injury. However, only limited data have been presented concerning the influence of temperature on ischemic damage after reversible focal cerebral ischemia. Because focal ischemic events of this type resemble conditions observed in the clinic, studies were undertaken to examine the effects of mild and moderate hypothermia on the extent of cerebral infarction after focal neocortical ischemia. Under halothane anesthesia, the left middle cerebral artery and both carotid arteries were occluded reversibly for a period of 3 hours in adult Sprague-Dawley rats. The animals were killed 3 days later. Brain sections were stained with triphenyltetrazolium chloride and analyzed for infarction using a computerized image analysis system. Temporal muscle temperature and rectal temperature were monitored continuously. The following groups with different intraischemic temporal muscle temperatures were analyzed: 1) control, 35.8 to 36.2 degrees C; 2) mild hypothermia, 33.0 to 33.5 degrees C; and 3) moderate hypothermia, 27.5 to 29.2 degrees C. The volumes of infarction were 214.5 +/- 17.9, 166.5 +/- 6.8, and 108.2 +/- 5.9 mm3 (mean +/- SEM) for the control, mild hypothermia, and moderate hypothermia groups, respectively. These findings demonstrate that both mild and moderate hypothermia reduce the impact of temporary focal ischemia in Sprague-Dawley rats.
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PMID:Effects of intraischemic hypothermia on cerebral damage in a model of reversible focal ischemia. 832 2


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