Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to assess the incidence of silent myocardial ischaemia, 190 consecutive patients with cerebral ischaemia and without symptoms or electrocardiographic signs of ischaemic heart disease, underwent a maximal exercise treadmill test. Patients with a positive exercise test were submitted to exercise thallium myocardial scintigraphy. Results were compared with those obtained in a control group of 113 healthy subjects submitted to the same study protocol. An adequate exercise test was obtained in 140 patients with cerebral ischaemia. The exercise test was positive in 36 cases (26%). The end points were exhaustion in 24 patients, ST segment depression greater than or equal to 3 mm in seven and systolic blood pressure greater than or equal to 240 mmHg in five. The exercise thallium myocardial scintigraphy was normal in three and abnormal in 33: reversible perfusion defects were detected in 26 cases and fixed defects in seven. In the control group, matched for age and sex, the exercise test was positive in only seven cases (6%; P less than 0.01); the exercise myocardial scintigraphy was normal in five and abnormal in two subjects. In conclusion, in a remarkable proportion of middle-aged patients with cerebral ischaemia, silent myocardial ischaemia can be detected by means of noninvasive cardiologic investigations.
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PMID:Incidence of silent myocardial ischaemia in patients with cerebral ischaemia. 326 46

In patients with cerebral transient ischemic attacks or stroke myocardial infarction is the leading long-term cause of death. Despite the importance of coronary artery disease, patients with cerebrovascular insufficiency are seldom evaluated for the detection of ischemic heart disease and usually the cardiological evaluation is limited to the patients with angina or previous myocardial infarction. In order to identify asymptomatic coronary artery disease 74 consecutive patients with cerebral ischemia, and without symptoms or electrocardiographic signs of ischemic heart disease, underwent a maximal exercise treadmill test according to the Bruce protocol. An exercise Thallium myocardial scintigraphy was performed in patients with positive exercise test. A control group of 74 asymptomatic subjects underwent the same study protocol. The study population (Group I) included 57 men and 17 women; the age ranged from 22 to 72 years (mean age 54 years). An adequate exercise test was obtained in 67 patients. Exercise test was positive (ST-segment depression greater than or equal to 1.5 mm) in 19 cases (28%). The end points were exhaustion in 15 patients, ST-segment depression greater than 3 mm in 2 and systolic blood pressure greater than 240 mmHg in 2. The exercise Thallium myocardial scintigraphy was normal in 2 and abnormal in 17: reversible perfusion defects were detected in 12 cases and fixed defects in 5. In the control group (Group II), comparable for age and sex, exercise test was positive in 4 cases (5%; p less than 0.01 percentage of positive exercise tests in Group I vs Group II); the exercise myocardial scintigraphy was normal in 1 and abnormal in 3 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Early identification of ischemic cardiopathy in patients with cerebrovascular insufficiency.A prospective study with exertion test and perfusion myocardial scintigraphy]. 373 22

The cerebral metabolic responses to perinatal hypoglycemia (blood glucose less than or equal to 1 mmol/l) combined with asphyxia were studied in paralyzed, lightly anesthetized newborn dogs. No major differences in heart rate, blood pressure or arterial acid-base balance between control and hypoglycemic animals occurred either prior to or during asphyxia. The electroencephalogram, unaltered by hypoglycermia alone, became isoelectric at the same intervals in both groups following respiratory arrest. Intravenous carbon black infusion at 5 min of asphyxia demonstrated no relationship between blood glucose level and cerebral perfusion (p > 0.05), whereas a positive correlation did exist between systemic blood pressure and cerebral perfusion (p < 0.01). During asphyxia, anaerobic glycolysis in brain was less enhanced in hypoglycemic dogs, resulting in a more rapid exhaustion of high-energy phosphate reserves (phosphocreatine, ATP and ADP). Thus, the cerebral metabolic responses to asphyxia superimposed upon hypoglycemia were the direct consequence of insufficient cerebral glucose stores coupled with deficient circulating glucose to brain. These metabolic disturbances were no more the result of cerebral ischemia than that which occurs during asphyxia alone. The findings also suggest that systemic physiological monitoring may be an inadequate means of appraising cerebral homeostasis during combined hypoglycemia ad hypoxia.
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PMID:Cerebral metabolism during hypoglycemia dn asphyxia in newborn dogs. 689 22

Maintenance of cerebral perfusion pressure is a prerequisite for the prevention of cerebral ischemia. Physiological fluctuations in systemic perfusion pressure are compensated by cerebrovascular autoregulation. Cerebral hypoperfusion could result from (1) systemic hemodynamic failure (eg, distal to severe arterial stenosis), overcharging the vasoregulatory capacity; (2) dysfunction and exhaustion of cerebrovascular autoregulation; or (3) both. Ultrasound offers an excellent temporal resolution, is noninvasive, and is easily applicable for follow-up investigations. Despite its poor spatial resolution, transcranial Doppler sonography has been used for determination of cerebral perfusion reserve studies measuring cerebral blood flow velocity (CBFV) during hypercapnia or application of vasoactive agents (eg, acetazolamide). This approach evaluates vasomotor regulation in patients with hemodynamic compromise distal to severe stenosis or occlusion of the brain supplying arteries. Monitoring CBFV during tilt table examinations directly measures cerebral autoregulation. In patients with systemic orthostatic hypotension, maintainance or failure of cerebrovascular compensation and, even more importantly, cerebrovascular dysautoregulation, despite normal systemic blood pressure regulation, may be demonstrated. Vasoneuronal coupling is reflected by CBFV variations during appropriate neuronal stimulation. Neuronal dysfunction is associated with CBFV abnormalities as exemplified by preconditions of focal cerebral dysfunction in the posterior cerebral artery (PCA) in migraineurs with aura, where massive alteration of vasoneuronal coupling and ischemia is threatening during spreading depression. A highly significant asymmetric gain of vasoneuronal coupling in the interictal state may act as a trigger mechanism in these patients. Testing for vasoneuronal coupling within the middle cerebral artery (MCA) territory is more difficult due to the poor spatial resolution with various neuronal stimuli (eg, motorsensory or cognitive paradigms), only eliciting local neuronal areas underrepresented in the MCA CBFV global changes. However, motor stimulation evoked CBFV may be used to indicate dysintegration of vasoneuronal coupling in the course of acute cerebral ischemia with sensorimotor hemiparesis and, moreover, seems to be of prognostic value regarding the motor deficit.
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PMID:Cerebrovascular regulation and vasoneuronal coupling. 769

The paper describes the sequence of events typical in the pathogenesis of germinal layer hemorrhage (GLH): An initial, often prenatal, severe asphyxic event, leading to abolishment of autoregulation of cerebral perfusion, and, most likely, to hypoxic-ischemic lesions in the endothelium of the large capillaries of the germinal matrix. The hypoxia is accompanied by exhaustion of myocardial energy reserves with circulatory failure, hypotension and aggravation of cerebral ischemia. In the period immediately after birth, circulation failure proceeds with cardiac insufficiency, hypotension, cerebral ischemia, and possibly venous hypertension. Following resuscitation, arterial blood pressure gradually increases (type 3) with increased strain on the damaged germinal matrix capillary walls in the absence of autoregulation. This effect is further aggravated by arterial blood pressure increments of type 1 and 2 leading to GLH, possibly with increments of venous pressure as a contributing factor.
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PMID:On the pathogenesis of germinal layer hemorrhage in the neonate. 831 97

All the advancements in the understanding of the molecular and cellular processes leading to the great investments in developing neuroprotection against cerebral ischemic/hypoxic damage cannot obscure the simple fact that exhaustion of energy supplies is still at the basis of this disorder. Much has been investigated and postulated over the years about the quick collapse of energy metabolism that follows oxygen and glucose deprivation in the brain. Anaerobic glycolysis, recognized as a pathway of paramount importance in keeping energy supplies, although, at bare minimum, has also presented a dilemma-a significant increase in lactate production during ischemia/hypoxia (IH). The dogma of lactate as a useless end product of anaerobic glycolysis and its postulated role as a detrimental player in the demise of the ischemic cell has persisted for the past quarter of a century. This persistence is due to, at least in part, the well-documented phenomenon termed "the glucose paradox of cerebral ischemia," the unexplained aggravation of postischemic neuronal damage by preischemic hyperglycemia. Recent studies have questioned the deleterious effect of lactic acid, while others even have offered the possibility that this monocarboxylate serves as an aerobic energy substrate during recovery from IH. Reviewed here are studies published over the past few years along with some key older papers on the topic of energy metabolism and recovery of neural tissue from IH. New insights gained from both in vitro and in vivo studies on energy metabolism of the ischemic/hypoxic brain should improve our understanding of this key metabolic process and the chances of protecting this organ from the consequences of energy deprivation.
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PMID:Energy metabolism, stress hormones and neural recovery from cerebral ischemia/hypoxia. 1191 66

Uric acid (UA) is the end product of purine catabolism in humans and is a powerful antioxidant whose generation is increased under ischemic conditions. However, both clinical and experimental studies reveal a gradual exhaustion of the antioxidant capacity after transient cerebral ischemia, and the magnitude of this consumption seems to be correlated with the extent of brain tissue injury, growth of the infarction, severity of neurological impairment in the acute phase, and long-term functional outcome. Growing evidence supports the neuroprotective effect of UA administration after brain ischemia. In experimental conditions, the administration of UA is neuroprotective both in mechanical models of brain ischemia (transient or permanent intraluminal occlusion of the middle cerebral artery) and in thromboembolic models of autologous clot injection. The administration of UA is feasible and safe in healthy volunteers. In acute stroke patients treated with recombinant tissue plasminogen activator (rt-PA), co-administration of UA has proven to reduce lipid peroxidation and to prevent the fall in UA blood levels that occur very early after stroke onset. Currently, a multicentric Phase III clinical trial is testing whether the administration of UA increases the clinical benefits of rt-PA, which represents the only approved therapy in patients with acute ischemic stroke. This review summarizes the available information justifying such a novel therapeutic approach in this devastating clinical condition.
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PMID:Uric acid administration in patients with acute stroke: a novel approach to neuroprotection. 1827 11

In cerebral ischemia survival of neurons, astrocytes, oligodendrocytes and endothelial cells is threatened during energy deprivation and/or following re-supply of oxygen and glucose. After a brief summary of characteristics of different cells types, emphasizing the dependence of all on oxidative metabolism, the bioenergetics of focal and global ischemia is discussed, distinguishing between events during energy deprivation and subsequent recovery attempt after re-circulation. Gray and white matter ischemia are described separately, and distinctions are made between mature and immature brains. Next comes a description of bioenergetics in individual cell types in culture during oxygen/glucose deprivation or exposure to metabolic inhibitors and following re-establishment of normal aerated conditions. Due to their expression of NMDA and non-NMDA receptors neurons and oligodendrocytes are exquisitely sensitive to excitotoxicity by glutamate, which reaches high extracellular concentrations in ischemic brain for several reasons, including failing astrocytic uptake. Excitotoxicity kills brain cells by energetic exhaustion (due to Na(+) extrusion after channel-mediated entry) combined with mitochondrial Ca(2+)-mediated injury and formation of reactive oxygen species. Many (but not all) astrocytes survive energy deprivation for extended periods, but after return to aerated conditions they are vulnerable to mitochondrial damage by cytoplasmic/mitochondrial Ca(2+) overload and to NAD(+) deficiency. Ca(2+) overload is established by reversal of Na(+)/Ca(2+) exchangers following Na(+) accumulation during Na(+)-K(+)-Cl(-) cotransporter stimulation or pH regulation, compensating for excessive acid production. NAD(+) deficiency inhibits glycolysis and eventually oxidative metabolism, secondary to poly(ADP-ribose)polymerase (PARP) activity following DNA damage. Hyperglycemia can be beneficial for neurons but increases astrocytic death due to enhanced acidosis.
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PMID:Bioenergetics of cerebral ischemia: a cellular perspective. 1863 6

Matrix metalloproteinase-9 (MMP-9) plays a deleterious role in cell death after global cerebral ischemia. Preconditioning with hyperbaric oxygen (HBO-PC) reduces neuronal damage in the post-ischemic brain; however, its effect on ischemia-induced increase in MMP-9 activity and expression remains unexplored.We investigated effects of HBO-PC on alterations in MMP-9 activity/tissue expression accompanying neuronal death after transient global cerebral ischemia.Male SD rats (300-350 g), were allocated either to non-ischemic (naive control or sham-operated) or ischemic (four-vessel occlusion, 4VO; 10 min) groups that were HBO-preconditioned (2.5 ATA, 1 h daily for 5 days; the last session 24 h before ischemia) or not. Neurobehavioral deficits were assessed prior to collection of brain tissue for gel zymography (MMP-9) and histology (MMP-9 immunofluorescence, TUNEL) at 0 (without ischemia), 6, 24, 72 h and 7 days after 4VO.Both, MMP-9 levels and cell death increased in the hippocampus at 72 h after 4VO. HBO-PC suppressed postischemic MMP-9 activity and CA1 cell damage, and improved functional performance. The increase in MMP-9 immunoreactivity in the brain was also detected after HBO-PC alone. HBO-PC suppresses MMP-9 activity and expression in the postischemic hippocampus. The mechanism of HBO preconditioning may depend on the induction of MMP-9 in the preischemic phase and may be in part mediated by exhaustion of MMP-9 stores in cerebral tissues.
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PMID:Reduced matrix metalloproteinase-9 activity and cell death after global ischemia in the brain preconditioned with hyperbaric oxygen. 1981 19

We report the case of a patient who suffered a serious subarachnoid hemorrhage with a cardialaffection and development of an inverted Tako-Tsubo-cardiomyopathy. To avoid apparent cerebral ischemia due to severe cerebral vasospasm after exhaustion of conservative therapeutic options a temporarily endovascular therapy with continuous intra-arterial application of Nimodipine was necessary. In the overall protracted and complicated course the special challenge were the therapeutic efforts to avoid apparent cerebral ischemia in context to the significant cardial affection.
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PMID:[Case report: Aneurysmatic subarachnoid hemorrhage -- complicated course due to coincidental manifestation of an inverted Tako-Tsubo-cardiomyopathy]. 2513


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