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PubMed1992

Extracranial carotid arterial disease: a prognostic factor for atherothrombotic brain infarction and cerebral transient ischemic attack.

A prospective study investigated the prevalence of extracranial carotid arterial disease by carotid duplex ultrasonography, and evaluated its correlation with the incidence of atherothrombotic brain infarction or cerebral transient ischemic attack in 949 patients, mean age 82 +/- 8 years. The mean follow-up period was 45 months. Of 949 patients, 37 (4%) had 80%-100% extracranial carotid disease (mean follow-up, 24 +/- 15 months), 113 (12%) had 40%-80% extracranial carotid disease (40 +/- 19 months follow-up), and 799 (84%) had 0%-40% extracranial carotid disease (47 +/- 14 months follow-up). The average annual incidence of atherothrombotic brain infarction was 37% in patients with 80%-100% extracranial carotid disease, 9% in patients with 40%-80% extracranial carotid disease, and 4% in patients with 0%-40% extracranial carotid disease. The average annual incidence of transient ischemic attack was 3% in patients with 80%-100% extracranial carotid disease, 2% in patients with 40%-80% extracranial carotid disease, and 1% in patients with 0%-40% extracranial carotid disease. The Cox proportional hazard model showed that among the variables evaluated, the severity of extracranial carotid disease correlated with the highest relative risk of developing atherothrombotic brain infarction (2.5x higher relative risk) or transient ischemic attack (2.8x higher relative risk). Patients with an earlier atherothrombotic brain infarction had a 2.1x higher probability of developing atherothrombotic brain infarction and a 1.9x higher chance of developing transient ischemic attack than those without an earlier atherothrombotic brain infarction. Age was a prognostic variable for new atherothrombotic brain infarction, and male sex was a prognostic variable for new transient ischemic attack.

Aged↗
PubMed2000

Activation of thrombosis and fibrinolysis following brain infarction.

To clarify the sequence of alterations in the thrombotic and fibrinolytic systems after acute brain infarction, we prospectively examined sequential changes in coagulatory markers in 38 patients suffering from cardioembolic infarcts (CEI), 41 patients with atherothrombotic infarcts (ATI), 58 patients with lacunar infarcts (LI), and 32 age-matched controls. The plasma level of thrombin-antithrombin III complex (TAT), fibrinopeptide A (FpA), D-dimer, fibrin degradation products-E (FDP-E), fibrinogen, alpha2-plasmin inhibitor-plasmin complex (PIC), and percent activity of antithrombin III (AT-III) were measured within 48 h, at 1 week, and at 3 weeks after the stroke onset. Significantly elevated levels of TAT and FpA, which are both markers of thrombin formation, were observed in CEI patients, and these elevated levels were associated with increasing D-dimer levels for 3 weeks (P<0.0001). D-Dimer in CEI patients was significantly elevated compared to control, LI and ATI levels within 48 h (P<0.001). Percent activity of AT-III was significantly decreased in CEI patients for 3 weeks compared to this activity in controls, LI and ATI (P<0.001). TAT and FpA also increased significantly within 48 h in ATI subjects and declined thereafter. A significant elevation of FDP-E (P<0.001) and D-dimer (P<0.05, P<0.01) was detected in parallel with increasing fibrinogen for 3 weeks. However, there was no significant depletion of percent activity of AT-III in ATI. In LI subjects, no significant elevation of TAT, D-dimer or FDP-E were observed within 1 week. PIC increased significantly in three subtypes of brain infarcts, but did not differ significantly among the three subtypes for 3 weeks. An accurate assessment of sequential alterations in thrombotic and fibrinolytic markers in the acute stage of brain infarct should contribute to the clinical diagnosis of brain infarct subtype. Alterations in these markers in response to activation of the coagulatory system are attributable to the different pathogenesis of ischemic stroke.

Aged↗
PubMedDate not supplied

[Gasometric studies and lactic acid determinations in arterial blood and cerebrospinal fluid in brain infarction].

In 54 cases of brain infarction and 17 control cases the gasometric parameters and lactic acid level were determined in arterial blood and cerebrospinal fluid. Metabolic acidosis was demonstrated in the arterial blood and cerebrospinal fluid. Respiratory acidosis compensated partly metabolic acidosis. Changes in the cerebrospinal fluid were more frequent and more pronounced, especially in cases with fatal outcome. Deep disturbances of acid-base balance complicated with hypoxia may have prosnostic significance while moderate rise in lactic acid level is without this significance.

Aged↗
PubMed2001

Carotid plaque echogenicity and types of silent CT-brain infarcts. Is there an association in patients with asymptomatic carotid stenosis?

BACKGROUND: The aim of this study was to identify the differences in echogenicity and the degree of stenosis of asymptomatic carotid plaques associated with different types of ipsilateral silent CT-brain infarcts. METHODS: Some 273 asymptomatic carotid plaques (218 patients) causing 50 to 99% stenosis were studied with high-resolution ultrasound. B-mode images were digitised and normalised by assigning certain grey values to blood and adventitia. The grey scale median (GSM) of the plaque in the normalised image was used to quantify echogenicity. Every patient had a CT-brain scan which an independent neuroradiologist read. The presence of 1) non-lacunar and 2) lacunar silent CT-brain infarcts ipsilateral to the carotid plaque was noted. RESULTS: The mean GSM of plaques associated with non-lacunar silent CT-brain infarcts was 19.6, of plaques associated with lacunar infarcts was 35.5 and of those associated with no infarcts was 32 (p=0.008, ANOVA). The mean degree of stenosis was 79%, 72% and 73% respectively (p = 0.1, ANOVA). Plaque echogenicity (p = 0.007) and not the degree of stenosis (p = 0.07) predicted the presence of non-lacunar silent CT-brain infarcts (logistic regression). CONCLUSIONS: Carotid bifurcation plaques, which are associated with non-lacunar silent CT-brain infarcts, are significantly more hypoechoic than those associated with lacunar or no infarcts. Plaques associated with lacunar silent infarcts and no infarcts have the same echogenicity and degree of stenosis. These findings suggest an embologenic mechanism of non-lacunar silent CT-brain infarcts that may have prognostic implications in patients with asymptomatic carotid stenosis. Prospective studies of asymptomatic carotid stenosis should assess the significance of 1) plaque echogenicity and 2) the presence of different types of silent CT-brain infarcts and atheroembolic stroke.

Adult↗
PubMed1994

Correlation between angiogenesis and basic fibroblast growth factor expression in experimental brain infarct.

BACKGROUND AND PURPOSE: Cerebral endothelial cells are quiescent under normal conditions; they are stimulated to proliferate around an infarct, although the mechanism is unclear. In the present study we explored the relation between angiogenesis and the expression of basic fibroblast growth factor (bFGF) by participating cells in brain infarct. METHODS: Brain infarct was created in rats by ligation of a branch of the left middle cerebral artery followed by permanent occlusion of the left common carotid artery and temporary occlusion of the right common carotid artery. The brains were removed after 1 to 14 days and studied with histological and immunohistochemical methods. Bromodeoxyuridine (BRdU) was used as an S-phase marker for the proliferative cells. RESULTS: Enhanced bFGF immunoreactivity was observed in neurons adjacent to the infarct after 1 day, and the change subsequently spread to distant neurons in the ipsilateral hemisphere. After 2 days blood vessels and glial cells around the infarct began to incorporate BRdU. During the first week new capillaries accompanied by macrophages extended into the infarct. The macrophages, endothelial cells, and reactive astrocytes expressed mild to moderate bFGF immunoreactivity. CONCLUSIONS: The spatial and temporal correlation between bFGF expression and angiogenesis in conjunction with the well-known biological properties of bFGF suggest that bFGF produced by neurons, macrophages, and glial cells may participate in angiogenesis in brain infarct.

Animals↗
PubMedDate not supplied

High-b-value diffusion-weighted MR imaging of suspected brain infarction.

BACKGROUND AND PURPOSE: Recent technological advances in MR instrumentation allow acquisition of whole-brain diffusion-weighted MR scans to be obtained with b values greater than 1,000. Our purpose was to determine whether high-b-value diffusion-weighted MR imaging improved contrast and detection of signal changes in acute and chronic brain infarction. METHODS: We prospectively evaluated the MR scans of 30 subjects with a history of possible brain infarction on a 1.5-T MR imager with 40 mT/meter gradients (slew rate 150 T/m/s) by use of the following single-shot echo-planar diffusion-weighted MR sequences: 1) 7,999/ 71.4/1 (TR/TE/excitations, b = 1,000; 2) 999/ 88.1/3, b = 2,500; and 3) 7,999/ 92.1/4, b = 3,000. Diffusion-weighted MR imaging was performed in three orthogonal directions during all sequences. All subjects were scanned with fast fluid-attenuated inversion recovery (FLAIR) (10,006/145/2,200/1 [TR/TE/TI/excitations]) and fast spin-echo T2-weighted (3,650/95/3 [TR/TE/excitations], echo train length, 8). The diagnosis of brain infarction was established by clinical criteria. RESULTS: Twenty women and 10 men with a mean age of 67.7 years were enrolled in the study. One subject was excluded owing to poor image quality. Twelve of 29 subjects had a clinical diagnosis of acute infarction. All 12 had lesions that were hyperintense on diffusion-weighted images at all three b values; five were cortical and seven subcortical. There was increased contrast of all lesions on high-b-value scans (b = 2,500 and 3,000). Lesions that were hypointense on diffusion-weighted images were identified and evaluated at the three different b values. At b = 1,000, there were 19 hypointense lesions, whereas at b = 2,500 and 3,000 there were 48 and 55 lesions, respectively. On FLAIR and T2-weighted images, these low-signal lesions were predominantly chronic, subcortical, ischemic lesions and lacunar infarcts, but four chronic cortical infarcts, one porencephalic cyst, and one primary brain tumor were also found. Low-signal lesions were also noted to have increased contrast on high-b-value diffusion-weighted scans. CONCLUSION: High-b-value diffusion-weighted MR imaging (b = 2,500 or b = 3,000) had no impact on diagnosis of acute infarction. High-b-value diffusion-weighted MR imaging (b = 2,500) combined with diffusion-weighted MR imaging at b = 1,000 improves tissue characterization by increasing the spectrum of observed imaging abnormalities in patients with suspected brain infarction.

Aged↗
PubMed1987

Associations between brain infarction, diabetes and alcoholism: observations from the Gothenburg population cohort study.

The relationship of brain infarction to diabetes and alcoholism was studied in a 10-year follow-up of a defined general population (n = 159,200) of native, urban Swedes. Confounding bias due to high age and lower socioeconomic conditions was reduced with a new epidemiological technique which was used instead of conventional mathematical multivariate procedures. We observed 6-13-fold and 4-6-fold excess rates of subjects with brain infarction among diabetics (P less than 0.001) and alcoholics (P less than 0.001), respectively. In addition, diabetes and alcoholism were often found to be associated. The distribution of these diseases varied with the topography of the city and demography of the population. Hence, in future studies into the pathogenesis of brain infarction, study samples should be made homogeneous not only from a clinical, but also from an epidemiological point of view. We conclude that diabetes, alcoholism and both in combination, associate with brain infarction.

Adult↗
PubMed2000

[Therapeutic hemodynamic effects of external counterpulsation on elderly patients with brain infarction during convalescence].

The therapeutic hemodynamic effects of external counterpulsation(ECP) and medical routine therapy in elderly patients with brain infarction during convalescence were investigated by Transcranial Doppler (TCD). The results showed that hemodynamic parametres(Vp, Vm, DVp, DVm) and asymmetry of MCA in elderly patients with brain infarction who were treated with ECP have improved significantly(P < 0.001), but that of MCA in elderly patients with brain infarction who were treated with medical routine therapy have not significantly improved. Therapeutic hemodynamic effects of ECP on elderly patients with brain infarction were much better than that of medical routine therapy(P < 0.001).

Aged↗
PubMed1997

Lifestyle-associated risk factors for acute brain infarction among persons of working age.

BACKGROUND AND PURPOSE: This study was designed to identify whether cigarette smoking, alcohol drinking, obesity, and use of oral contraceptives are independent risk factors for brain infarction among persons of working age. METHODS: Health habits and previous diseases of 506 patients (366 men and 140 women aged 16 to 60 years) with acute first-ever symptomatic brain infarction were compared with those of 345 hospitalized control patients (219 men and 126 women) who did not differ from case subjects in respect to day of onset of symptoms or acuteness of disease onset. With the use of stepwise logistic regression, the variables for which the simultaneous risks of acute brain infarction were tested by sex were age, amount of alcohol consumed within 24 hours and 1 week before the illness, heavy drinking, smoking status, current smoking, cardiac disease, hypertension, diabetes, hyperlipemia, migraine, body mass index, and, in women, current use of oral contraceptives. RESULTS: Intake of > 40 g ethanol within the 24 hours preceding the onset of illness increased the risk for acute brain infarction both among men (P < .001) and women (P < .01) independently from other risk factors. Other significant independent risk factors for brain infarction among men were hypertension (P < .001), cardiac disease (P < .01), current smoking (P < .01), diabetes (P < .05), and history of migraine (P < .05) and among women, current use of oral contraceptives (P < .01) and current smoking (P < .05). CONCLUSIONS: Recent heavy drinking of alcohol, hypertension, cardiac disease, current smoking, diabetes, and history of migraine among men, and recent heavy drinking of alcohol, current use of oral contraceptives, and current smoking among women, seem to be independent risk factors for acute brain infarction.

Adolescent↗
PubMed1990

Molecular biology of atherothrombotic brain infarction.

Because reduced high density lipoproteins may contribute to atherothrombotic brain infarction, we performed molecular biologic and metabolic studies to characterize high density lipoprotein metabolism with respect to its role in reverse cholesterol transport, to clone the high density lipoprotein receptor, and to determine gene polymorphism for apolipoprotein A-I, the major protein of high density lipoprotein, because altered structure may impair reverse cholesterol transport. For high density lipoprotein metabolism measurements, high density lipoprotein 3 was isolated, purified, and labeled with iodine-125. The radiolabeled high density lipoprotein 3 was reinjected, and daily blood samples were taken for 10 days. Synthesis rates and fractional catabolic rates were determined from the specific activities and daily decrements. Preliminary data indicate that stroke-prone individuals' fractional catabolic rates for high density lipoprotein 3 are twice those of normal individuals. Also, the conversion of high density lipoprotein 3 to high density lipoprotein 2 is reduced in these individuals, suggesting that high density lipoprotein may be abnormally processed in individuals prone to atherothrombic brain infarctions. We surveyed more than 100 patients with carotid stenosis using a 2.2-kb probe for the apolipoprotein A-I gene. A subset of these patients displays polymorphism with restriction enzymes SacI or PstI. These preliminary findings suggest that gene polymorphism for apolipoprotein A-I may provide a molecular clue of atherothrombic brain infarction.

Arteriosclerosis↗
PubMed1999

Evaluation of genetic risk factors for silent brain infarction.

BACKGROUND AND PURPOSE: Silent brain infarction (SBI) is often found with white matter hyperintensity. A recent genetic study on elderly twins indicated that the susceptibility to white matter hyperintensity was largely determined by genetic factors, implying the existence of genetic susceptibility for SBI as well. We therefore studied 3 genetic polymorphisms in SBI, the deletion/insertion polymorphism of angiotensin-converting enzyme (ACE) gene, the apolipoprotein(a) [apo(a)] size polymorphism, and the T677C polymorphism of methylenetetrahydrofolate reductase (MTHFR) gene, by a case-control study. METHODS: By MRI, 147 subjects with SBI and 214 without cerebral infarctions (control group) were selected from participants of a health examination of the brain. Seventy-four patients with symptomatic subcortical infarction (SSI) from the same area were also included in the study. In addition to the control group, 2 more reference populations were recruited. Typing of the apo(a) size polymorphism was done by Western blotting with the use of an anti-apo(a) antibody. Genotypes of ACE and MTHFR were determined by polymerase chain reaction amplification of the genomic DNA and subsequent restriction enzyme digestion. RESULTS: The ACE polymorphism was not associated with either SBI or SSI. In contrast, the small apo(a) was associated with both SSI and SBI. The MTHFR polymorphism was associated only with SSI. The association of MTHFR and apo(a) was greater in the younger subjects. CONCLUSIONS: Among the 3 genetic polymorphisms studied, only the apo(a) size polymorphism is a risk factor for SBI.

Aged↗
PubMed1998

[The relationship between angiotensin-converting enzyme gene polymorphism and brain infarction in Chinese hypertensives].

OBJECTIVE: To identify the insertion/deletion(I/D) polymorphism of angiotensin-converting enzyme(ACE) gene in Chinese hypertensives complicated with brain infarction. METHODS: ACE genotyping with polymerase chain reaction(PCR) was performed in 62 unrelated healthy controls, 55 hypertensives without cardio-cerebrovascular diseases and 44 hypertensives complicated with brain infarction (all controls had no hypertension family history, while the cases had hypertension family history). RESULTS: No significant differences could be detected between ACE gene I/D polymorphism and hypertension. However,the frequencies of DD genotype and deletion allele among hypertensives complicated with brain infarction (29.6% vs 56.8%) were higher than those among healthy controls (12.9% vs 38.7%, P<0.05 and P<0.01) and those among hypertensive without cardio-cerebrovascular diseases(12. 8% vs 40%, P<0.05 and P<0.02). CONCLUSION: A deletion polymorphism of ACE gene is probably an important hereditary factor of brain infarction's morbidity in Chinese hypertensives. The detection of ACE genotypes in hypertensives would improve the early diagnosis of brain infarction.

Adult↗
PubMed2005

Reduction in brain infarction by augmentation of central histaminergic activity in rats.

Inflammation is a factor in the aggravation of reperfusion injury after cerebral ischemia. Since histamine H(2) receptor stimulation suppresses inflammatory reactions, effects of the central histaminergic activation on brain infarction were examined in rats. Focal cerebral ischemia for 2 h was provoked by transient occlusion of the right middle cerebral artery, and the infarct size was determined by 2,3,5-triphenyltetrazolium chloride stain after 24 h. Effects of postischemic administration of thioperamide, an H(3) antagonist, and metoprine, an inhibitor of histamine-N-methyltransferase, were evaluated in rats treated with l-histidine, a precursor of histamine. Furthermore, effects of these agents on changes in the striatal histamine level were examined by a microdialysis procedure. Focal ischemia provoked marked damage in rats treated with l-histidine (1000 mg/kg) alone. Administration of l-histidine (1000 mg/kg) with either thioperamide (5 mg/kg) or metoprine (10 mg/kg) alleviated brain infarction. The size of brain infarction was 27% and 10% of that in animals treated solely with l-histidine, respectively. The combination treatment with thioperamide and metoprine decreased the size of brain infarction in rats given l-histidine (500 mg/kg), although protective effects were not clear without l-histidine. A marked increase in the histamine concentration was observed in the histidine plus metoprine group, the value being 363% of that in the saline-injected group after 2-3 h. The histamine concentrations in the histidine group and histidine plus thioperamide group were 188% and 248%, respectively. These findings indicate that facilitation of central histaminergic activity reduced the brain infarction.

Animals↗
PubMed1996

Platelets, alcohol consumption, and onset of brain infarction.

OBJECTIVES: Previous investigations have suggested that recurrent rebound thrombocytosis after alcohol misuse may be a factor in the pathogenesis of thromboembolic disease. Alcohol consumption, platelet count, and platelet function were examined among patients of working age with brain infarction. METHODS: Platelet count and risk factors for stroke were studied in 426 stroke patients and 157 control patients in hospital. The measures were platelet count obtained within four days after the stroke onset, in vitro adenosine diphosphate induced platelet aggregation, associated thromboxane B2 formation, and urinary excretion of 11-dehydrothromboxane B2. RESULTS: After adjustment for sex, age, cardiac disease, diabetes, and alcohol intake, hypertension (OR 3.4, 95% confidence interval (95% CI) 2.0-6.0) and current smoking (OR 2.1, 95% CI 1.4-3.3) were associated with an increased risk for brain infarction. Platelet count shortly after the onset of disease was higher in the stroke patients than in the controls (OR 1.05/10(10)/1 platelets; 95% CI 1.02-1.09). The patients with brain infarction who were heavy alcohol drinkers (n = 144) showed both thrombocytosis (OR 2.30, 95% CI 0.82-6.44) and thrombocytopenia (OR 3.20, 95% CI 1.19 to 8.59) more often at the onset of the stroke than the other patients with brain infarction. The thromboxane variables showed inconsistent associations with the onset of stroke. There was no consistent platelet abnormality among alcohol misusers at the onset of ischaemic brain infarction. CONCLUSIONS: Alcohol induced thrombocytopenia and rebound thrombocytosis were both often seen at the onset of brain infarction in patients who were heavy alcohol drinkers. Therefore, other mechanisms which could contribute to the high frequency of recurrences of ischaemic stroke among heavy drinkers should be investigated.

Adenosine Diphosphate↗
PubMed1995

Relationship between diffusion-weighted MR images, cerebral blood flow, and energy state in experimental brain infarction.

The regional evolution of brain infarction was studied in Wistar rats submitted to remotely controlled thread occlusion of the middle cerebral artery. Occlusion was performed in the magnet of an NMR tomography system to allow continuous recording of diffusion-weighted images. After 30 min (n = 6) or 2 h (n = 9), cerebral blood flow was measured by [14C] iodoantipyrine autoradiography while the regional distribution of ATP, glucose, lactate, and pH was imaged using pictorial bioluminescence and fluoroscopic methods. In diffusion-weighted images, the hemispheric lesion area (HLA) at the level of caudate-putamen amounted to 54.2 +/- 10.9% after 30 min and to 67.0 +/- 5.9% after 2 h vascular occlusion. These areas corresponded to the regions exhibiting tissue acidosis (60.8 +/- 9.3% and 70.4 +/- 4.5%), but were clearly larger than those in which ATP was depleted (22.3 +/- 20.8% and 49.6 +/- 12.9% after 30 min and 2 h, respectively). The threshold of blood flow for the increase of signal intensity in diffusion-weighted images increased between 30 min and 2 h occlusion from 34 to 41 ml/100 g per minute, the threshold of acidosis from 40 to 47 ml/100 g per minute, and the threshold for ATP depletion from 13 to 19 ml/100 g per minute. Our study demonstrates that diffusion-weighted imaging detects both the core and the penumbra of the evolving infarction but is not able to differentiate between the two parts. It further shows that the ischemic lesion grows during the initial 2 h of vascular occlusion, and that the size of the infarct core increases more rapidly than that of the penumbra.

Adenosine Triphosphate↗
PubMed1995

Is haemodynamical compromise a specific cause of border zone brain infarcts following cardiac surgery?

We evaluated the hypothesis that if hypotension or hypoperfusion is a major cause of border zone brain infarction, infarcts following cardiac surgery will be likely to be located in the vascular border zone areas, whereas cerebral perfusion would be lower compared with non-border zone infarcts. Ten of 37 patients with brain infarction following cardiac surgery had an infarct in one of the vascular border zones on CT. Haemodynamical characteristics and clinical features did not differ between border zone infarcts and remaining infarct subgroups. We conclude that compared with stroke series brain infarcts following cardiac surgery are more frequently located in one of the vascular border zone areas, but peri-operative haemodynamic compromise alone does not sufficiently explain this difference. Other possible mechanisms, such as showers of (micro-)emboli, should also be considered.

Adult↗
PubMed1986

Four-year prognosis of patients under the age of 65 surviving their first ischaemic brain infarction.

A 4-year follow-up study was carried out on the prognosis of 54 patients (36 men and 18 women) who survived their first ischaemic brain infarction which had occurred under the age of 65. Twenty patients (15 men and 5 women) already had documented atherosclerotic vascular disease other than ischaemic brain infarction at the time of the hospital admission (atherosclerotic group). When both sexes were considered together, mortality during the 4-year follow-up was significantly higher in the atherosclerotic group than in the non-atherosclerotic group (6/20 versus 3/34; p less than 0.05) and this was due to an excess of cerebrovascular mortality (4/20 versus 0/34; p less than 0.05). The incidence of recurrent fatal or non-fatal ischaemic brain infarction was significantly higher in the atherosclerotic group than in the non-atherosclerotic group (8/20 versus 3/34; p less than 0.01). Among those patients who survived the 4-year follow-up period the incidence of new non-fatal atherosclerotic vascular events (cerebrovascular accident, myocardial infarction, other heart disease or intermittent claudication) was significantly higher in the atherosclerotic group than in the non-atherosclerotic group (8/14 versus 8/31; p less than 0.05). It is concluded, that the presence of atherosclerotic vascular disease at the time of first ischaemic brain infarction in patients under the age of 65 is associated with a significantly increased risk for recurrent ischaemic brain infarction or other new atherosclerotic vascular events.

Arteriosclerosis↗
PubMed2000

Evolution of brain infarction after transient focal cerebral ischemia in mice.

The evolution of brain infarction after transient focal cerebral ischemia was studied in mice using multiparametric imaging techniques. One-hour focal cerebral ischemia was induced by occluding the middle cerebral artery using the intraluminal filament technique. Cerebral protein synthesis (CPS) and the regional tissue content of adenosine triphosphate (ATP) were measured after recirculation times from 0 hours to 3 days. The observed changes were correlated with the expression of the mRNAs of hsp-70, c-fos, and junB, as well as the distribution of DNA double-strand breaks, visualized by TUNEL. At the end of 1 hour of ischemia, protein synthesis was suppressed in a larger tissue volume than ATP in accordance with the biochemical differentiation between core and penumbra. Hsp70 mRNA was selectively expressed in the cortical penumbra, whereas c-fos and junB mRNAs were increased both in the lateral part of the penumbra and in the ipsilateral cingulate cortex with normal metabolism. During reperfusion after withdrawal of the intraluminal filament, suppression of CPS persisted except in the most peripheral parts of the middle cerebral artery territory, in which it recovered between 6 hours and 3 days. ATP, in contrast, returned to normal levels within 1 hour but secondarily deteriorated from 3 hours on until, between 1 and 3 days, the ATP-depleted area merged with that of suppressed protein synthesis leading to delayed brain infarction. Hsp70 mRNA, but not c-fos and junB, was strongly expressed during reperfusion, peaking at 3 hours after reperfusion. TUNEL-positive cells were detected from 3 hours on, mainly in areas with secondary ATP depletion. These results stress the importance of an early recovery of CPS for the prevention of ischemic injury and suggest that TUNEL is an unspecific response of delayed brain infarction.

Adenosine Triphosphate↗