Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was performed to investigate the role of leukocyte accumulation in human cerebral infarction and its association with neurological functional outcome. A total of 42 patients diagnosed as acute ischemic stroke (22 embolism, 17 thrombosis, 3 TIA) were examined. Leukocyte accumulation was studied using indium-111-labeled leukocyte brain single-photon emission computed tomography (SPECT). Volume of brain infarction was evaluated by CT and/or MRI. The data were compared with the cerebral blood flow (CBF) imaging. Immediately after CBF study by SPECT using either technetium-99m hexamethylpropyleneamine oxine (Tc-99m-HMPAO) or technetium-99m ethyl-cysteinate dimer (ECD), In-111-labeled autologous leukocytes were injected intravenously. Brain scan for leukocytes was performed after 48 hours. The European Stroke Scale was used for neurological assessment. Thirteen patients with cerebral embolism and three patients with cerebral thrombosis showed intensive accumulation of leukocytes in the region of low flow. Leukocyte's accumulation was not seen in patients with TIA. The accumulation of leukocytes was more noticeable in the central zone of the ischemia. Patients who showed negative leukocyte accumulation revealed clinically mild functional outcome and the size of infarction on CT and/or MRI was small. The regional accumulation of leukocytes was seen in all the patients with hemorrhagic infarction, but the degree of hemorrhage on CT did not have significant influence on the amount of leukocyte accumulation. Abnormal accumulation of leukocytes was associated with reduced CBF during the acute embolic stroke. The present clinical study revealed that leukocyte accumulation correlated with the poor neurological functional outcome in patients with acute embolic stroke. The present study confirms that leukocytes contribute to the ischemic tissue damage of the brain and demonstrates a clinical evidence that the regional accumulation of leukocytes has a deleterious effect on the brain following ischemia.
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PMID:[In-111-labeled leukocyte brain SPECT imaging in acute ischemic stroke in man]. 914 67

Two patients with a cerebral embolism were evaluated by using both 99mTc-ethyl cysteinate dimer (ECD, or Bicisate) and 99mTc-hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed tomography (SPECT). In one patient, 99mTc-ECD SPECT images revealed hypoactivity in a reflow hyperemic area where an infarct was seen later on CT scans. In another patient, a reperfused area showed hyperactivity on 99mTc-ECD SPECT without any abnormality on follow-up CT. 99mTc-ECD represents a potential agent with which to evaluate cerebral tissue viability in early reperfusion after ischemia.
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PMID:99mTc-bicisate and 99mTc-HMPAO SPECT imaging in early spontaneous reperfusion of cerebral embolism. 1031 73

Cerebral infarct due to embolic stroke without recanalization was examined by cerebral blood flow (CBF) SPECT in the early acute stage, and the possibility of predicting the size it will reach in the later stages was evaluated. Twenty patients (67 +/- 13 years) were examined by CBF SPECT with 99mTc-ECD 4.5 +/- 3.1 hours after the onset of cardiogenic cerebral embolism. The ratio of the anteroposterior length of the cerebral hemisphere to that of the severe ischemic region, which was defined as an area of clear-cut severe reduction in CBF as observed by SPECT, was calculated. One week after the onset, the cerebral infarct was measured in the same manner by CT, and the relationship between the two measurements was evaluated. The CBF in the region of severe ischemia and the surrounding region was determined by the Patlak plot method, and the affected/non-affected (A/NA) ratio was calculated. In severe ischemic regions the CBF ranged from 1.7 ml/100 g/min to 20 ml/100 g/min (mean, 11 +/- 5 ml/100 g/min), whereas the A/NA ratio ranged from 4% to 45% (mean, 26 +/- 11%). On the other hand, the CBF in the surrounding regions ranged from 20 ml/100 g/min to 52 ml/100 g/min (mean, 34 +/- 8 ml/100 g/min) whereas the A/NA ratio ranged from 52% to 104% (mean, 77 +/- 11%). The coefficient of correlation between the infarct size predicted by SPECT and that measured by CT was r = 0.986, and the correlation equation was Y = 1.047X - 2.969. CBF SPECT performed in the early acute stage can be used to predict the size of cerebral infarct.
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PMID:Prediction of cerebral infarct sizes by cerebral blood flow SPECT performed in the early acute stage. 1051 Aug 74

During recent 8 years, combined procedures of valve surgery and coronary artery bypass grafting (CABG) were performed in fifty-five patients at Omiya Medical Center. AVR (31 cases), MVR (12 cases), MVP (8 cases), DVR (1 case), TVR (1 case), TAP (2 cases) were performed with the average of 2.0 bypass graftings in this series. Five patients died due to organ ischemia (3 cases), cerebral embolism and heart failure. Organ ischemia occurred in dialysis patients and the results of combined surgery in dialysis patients were unsatisfactory (3/5 cases, mortality rate is 60%). On the other hand, the results of combined surgery in non-dialysis patient is reasonable (2/50 cases, mortality rate is 4%). Before the combined surgery in dialysis patient, careful analysis of surgical risk including organ ischemia is needed and avoiding the prolonged perfusion time is important to achieve a successful surgical result.
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PMID:[Results of valve surgery combined with CABG]. 1093 79

Catastrophic neurologic events occur rarely postoperatively and must be diagnosed quickly. A 63-year-old woman who had undergone uneventful total hip arthroplasty experienced obtundation after admission to the postanesthesia care unit. Cranial magnetic resonance imaging revealed multiple lesions consistent with ischemia or infarction, and fat cerebral embolism was diagnosed. We describe the numerous complications that may occur in patients in the postanesthesia care unit and review the differential diagnosis of altered mental status in such patients. Paradoxical cerebral fat embolization must be considered in the differential diagnosis of altered mental status after pelvic or long bone fracture or lower extremity major joint replacement, and this condition may occur despite normal pulmonary function and no patent foramen ovale or right-to-left intracardiac shunt. Magnetic resonance imaging with T2-weighted sequences is the cranial imaging study of choice for early evaluation of patients with sudden multifocal neurologic deficits and suspected fat embolism syndrome.
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PMID:Cerebral embolization presenting as delayed, severe obtundation in the postanesthesia care unit after total hip arthroplasty. 1107 54

The most serious complication of neurovascular interventions is distal cerebral embolism. Diffusion-weighted MR imaging (DWI) appears to be the most sensitive technique for detecting early and small ischemic lesions. To evaluate the incidence and radiological features of embolic events associated with neuro-intervention, we applied DWI to screening for procedure-related ischemic lesions including silent embolisms. One hundred and thirty-seven patients who have received 154 neuro-interventional procedures were studied with DWI before and within 5 days after treatment. Imaging was performed, using single-shot echo-planar imaging with b value of 1000-1100 sec/mm2. DWI findings were classified into 5 groups by size and location of lesions: type 0 (n = 71), no lesions; I (n = 33), lesions in border-zone regions only; II (n = 9), lesions at perforator territories mainly; III (n = 29), small territorial lesions (< 5 mm); IV (n = 12), large territorial lesions (> or = 5 mm). DWI detected procedure-related lesions in 83 of 154 procedures (53.9%), 36 of which demonstrated new neurological symptoms during and/or after procedures. The parent artery occlusion for cerebral aneurysms had a higher incidence of symptomatic embolisms than other procedures. In 71 of 154 procedures (46.1%), DWI detected no lesions (type 0). Although type I was the most frequent pattern presented, it included few neurological symptoms. Type III often resulted in transient symptoms, and type II and IV tended to induce strokes. Because ischemic lesions detected by DWI were likely to arise in border-zone territories by parent artery occlusions, we considered that hypoperfusion as well as emboli were involved in the evolution of cerebral infarctions. Thus, DWI is a useful method to detect silent embolisms, and to determine the safety of neuro-intervention and the mechanism of embolic ischemia.
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PMID:[Embolic complications associated with neurovascular intervention: prospective evaluation by use of diffusion-weighted MR imaging]. 1180 6

4 cases of induced abortions during which anomalies appeared in the EKG are reported. A review of the French literature on the subject revealed 13 similar cases, in which the EKG anomalies usually consisted of subepicardiac ischemia or injury. There are 3 theories to explain the cause of these anomalies: they may be secondary to cerebral embolism, septic shock, air embolism of the right heart or coronary arteries. All the theories, however, remain unproven.
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PMID:[Electrocardiogram anomalies during induced abortions]. 1230 24

Cerebral infarction is induced by injecting 700-900 microspheres with a diameter of 50 microm into the right internal carotid artery of the rat. Approximately 82% of the rats with typical symptoms of stroke survived at fifteen hours after the injection of microspheres. Microsphere-induced cerebral embolism elicits the widespread formation of small emboli in the ipsilateral hemisphere and subsequent neuronal loss and/or the development of multiple infarct areas in the brain, particularly in the cortex, striatum, and hippocampus. Thus, this model is considered to mimic focal ischemia-induced human stroke or multi-infarct dementia. We have found that this model showed sustained decreases in cerebral blood flow and cerebral high-energy phosphates; accumulation of tissue lactate, glucose, and glycogen; changes in the activity of several enzymes in the tricarboxylic acid cycle; loss of mitochondrial phosphorylation activity; and decreases in neurotransmitters, acetylcholine, monoamines, and amino acids in the ipsilateral hemisphere. Accordingly, microsphere embolism is capable of inducing severe and sustained cerebral ischemia resulting in disturbances of the energy and neurotransmitter metabolism in the brain. Such ischemic damage leads to learning and memory dysfunction. This model provides useful information about the pathogenesis, prophylaxis, and therapeutics of cerebral ischemic diseases.
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PMID:[The model of stroke induced by microsphere embolism in rats]. 1283 38

Cerebral ischemia causes an irreversible and neurodegenerative disorder that may lead to progressive dementia and global cognitive deterioration. Since the overall process of ischemic brain injuries is extremely complex, treatment with endogenous multifunctional factors would be better choices for preventing complicated ischemic brain injuries. Hepatocyte growth factor, HGF, is a multifunctional cytokine originally identified and purified as a potent mitogen for hepatocyte. The activation of the c-Met/HGF receptor evokes diverse cellular responses, including mitogenic, morphogenic, angiogenic and anti-apoptotic activities in various types of cell. Previous studies showed that HGF and c-Met were expressed in various brain regions under normal conditions and that HGF enhanced the survival of hippocampal and cortical neurons during the aging of cells in culture. The protective effects of HGF on in vivo ischemic brain injuries and their mechanisms have not fully understood. To elucidate therapeutic potencies of HGF for ischemic brain injuries, we examined effects of HGF on ischemia-induced learning and memory dysfunction, neuronal cell death and endothelial cell damage by using the 4-vessel occlusion model and the microsphere embolism model in rats. Our findings suggested that treatment with HGF was capable of protecting hippocampal neurons against ischemia-induced cell death through the prevention of apoptosis-inducing factor translocation to the nucleus. Furthermore, we demonstrated that HGF had the ability to prevent tissue degeneration and improved learning and memory function after cerebral embolism, possibly through prevention of cerebral vessel injuries. As HGF has a potent cerebroprotective effect, it could be a prospective agent for the therapy against complicated ischemic brain diseases.
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PMID:[Ischemic brain injury and hepatocyte growth factor]. 1797 57

Cardiac surgery continues to be associated with significant adverse cerebral outcomes, ranging from stroke to cognitive decline. The underlying mechanism of the associated cerebral injury is incompletely understood but is believed to be primarily caused by cerebral embolism and hypoperfusion, exacerbated by ischemia/reperfusion injury. Extensive research has been undertaken in an attempt to minimize the incidence of perioperative cerebral injury, and both pharmacological and nonpharmacological strategies have been investigated. Although many agents demonstrated promise in preclinical studies, there is currently insufficient evidence from clinical trials to recommend the routine administration of any pharmacological agents for neuroprotection during cardiac surgery. The nonpharmacological strategies that can be recommended on the basis of evidence include transesophageal echocardiography and epiaortic ultrasound-guided assessment of the atheromatous ascending aorta with appropriate modification of cannulation, clamping or anastomotic technique and optimal temperature management. Large-scale randomized controlled trials are still required to address further the issues of optimal pH management, glycemic control, blood pressure management and hematocrit during cardiopulmonary bypass. Past, present and future directions in the field of neuroprotection in cardiac surgery will be discussed.
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PMID:Neuroprotection during cardiac surgery. 1840 40


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