Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data from the records of 142 patients for carotid endarterectomy at Chugoku Rosai General Hospital between 1983 and 1995, were evaluated concerning perioperative risk factors and anesthetic management. As a preoperative anesthetic risk, the incidence of hypertension was the commonest (76%), and there was a significant incidence of ischemic heart disease (18%). Fentanyl and isoflurane have been used for anesthesia recently and the patients were closely observed and cared in the intensive care unit postoperatively. In order to prevent cerebral ischemia during the occlusion of the internal carotid artery, we measured somatosensory evoked potential as well as jugular venous oxygen saturation, and used near infrared spectophotometry. As a result, postoperative mortality and morbidity were 0% and 2%, respectively. The candidates for CEA have potentially high perioperative risks, and it is important to evaluate the coexisting diseases and to select proper anesthetic technic and monitors.
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PMID:[Perioperative risk factors and anesthetic management of patients for carotid endarterectomy]. 918 70

Polyvalent intravenous immunoglobulin (IVIg) is considered to be standard therapy for a variety of autoimmune and idiopathic disorders. Several reports have emphasized the temporal association between administration of IVIg and thrombotic events. Recent experience with a patient who suffered a large myocardial infarction shortly after receiving IVIg led the authors to review the clinical and basic literature on administration of IVIg as a possible precipitant for myocardial infarction. Although the existence of an association between IVIg administration and myocardial ischemia has not been demonstrated in clinical trials, a body of clinical experience has begun to accumulate that is suggestive of an association between IVIg administration and cardiac and cerebral ischemia in older individuals or individuals with a known history of ischemic disease. Basic research demonstrating that IVIg administration may increase blood viscosity suggests that such an association is plausible.
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PMID:Intravenous immunoglobulin, blood viscosity and myocardial infarction. 928 45

The endothelins (ETs) are regulatory peptides, distributed in many organ systems and with potent physiological effects. ETs represent the most powerful vasoconstrictive substances known today. They also act as growth factors and seem to be involved in fetal development. Much data support a pathophysiological role for ETs, especially in diseases of the vascular system, such as hypertension, preeclampsia, ischemic heart disease, subarachnoidal haemorrhage, and cerebral ischemia. The development of drugs affecting ET-receptors and the biosynthesis of ETs presently attract great interest for the establishment of new treatments of diseases in which ETs are involved. Hopefully, the elaboration of more specific ET-receptor ligands will fulfill some of these expectations.
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PMID:Endothelins--vasoactive peptides and growth factors. 950 6

Thermoregulation is impaired during anesthesia for cardiac surgery. Redistribution of body heat and heat loss to the environment result in mild hypothermia before cardiopulmonary bypass. Maintenance of normothermia, rather than hypothermia, may facilitate early tracheal extubation. Hypothermia alters the distribution and decreases the metabolism of most drugs, including anesthetic drugs and muscle relaxants, thus prolonging recovery. Postoperative shivering increases metabolic rate and potentially leads to myocardial ischemia; prevention is therefore critical to the success of early tracheal extubation after cardiac surgery. Coagulopathies, increased incidence of surgical wound infection, and perioperative cardiac morbidity are other potential risk factors identified in noncardiac patients. Hypothermia, however, does have potential benefits to the patient, including protection from cerebral ischemia and hypoxemia. Mild core hypothermia (approximately 34 degrees C) may represent the optimal balance between risks and benefits for fast-track patients.
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PMID:The implications of hypothermia for early tracheal extubation following cardiac surgery. 991 65

The role of the adenosine A3 receptor continues to baffle, and, despite an increasing number of studies, the currently available data add to, rather than alleviate, the existing confusion. The reported effects of adenosine A3 receptor stimulation appear to depend on the pattern of drug administration (acute vs. chronic), dose, and type of the target tissue. Thus, while acute exposure to A3 receptor agonists protects against myocardial ischemia, it is severely damaging when these agents are given shortly prior to cerebral ischemia. Mast cells degranulate when their A3 receptors are stimulated. Degranulation of neutrophils is, on the other hand, impaired. While reduced production of reactive nitrogen species has been reported following activation of A3 receptors in collagen-induced arthritis, the process appears to be enhanced in cerebral ischemia. Indeed, immunocytochemical studies indicate that both pre- and postischemic treatment with A3 receptor antagonist dramatically reduces nitric oxide synthase in the affected hippocampus. Even more surprisingly, low doses of A3 receptor agonists seem to enhance astrocyte proliferation, while high doses induce their apoptosis. This review concentrates on the studies of cerebral A3 receptors and, based on the available evidence, discusses the possibility of adenosine A3 receptor serving as an integral element of the endogenous cerebral neuroprotective complex consisting of adenosine and its receptors.
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PMID:Stimulation of adenosine A3 receptors in cerebral ischemia. Neuronal death, recovery, or both? 1066 16

Tumor necrosis factor-alpha (TNF-alpha) level, tissue-typed plasminogen activator(t-PA) activity and PA inhibitor (PAI) activity were determined in three groups: (1) 25 NIDDM patients with silent myocardial ischemia (SMI) or silent cerebral ischemia (SCI); (2) 18NIDDM patients without SMI or SCI; (3) 20 age-matched normal controls. Diagnosis of SMI or SCI was based on the finding of ischemic evidence by SPECT of myocardiotomograph or cerebrotomograph. All patients ECG and blood pressure were normal, and they had no history of clinical symptoms and signs of MI or CI. The result showed that the TNF-alpha level and PAI activity in the ischemia group were the highest and the t-PA activity in the ischemia group was the lowest, as compared with those in the other two groups respectively. It suggests that in NIDDM patients who have high TNF-alpha, high PAI activity, low t-PA, and even no symptoms and signs of MI or CI, anticoagulant therapy might be useful to prevent the progression of diabetic macroangiopathies.
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PMID:[Changes of serum TNF-alpha level, t-PA activivty and PAI activity in patients with silent myocardial ischemia or silent cerebral ischemia]. 1068 70

Heart and brain vascular diseases are the leading causes of mortality in the world. Cardiac complications can frequently occur during the development of cerebral ischemia. The aim of this study was to establish the possible changes in fractions of creatinine-phosphokinase as the sensitive laboratory index of parenchymal lesion of brain parenchyma and the presence/absence of risk factors for ischemic brain and heart disease. The study comprised 80 patients with acute ischemic brain disease (AIBD), without the history of previous coronary disease. Blood samples were taken in all patients within the first 48 hours from AIBD onset aiming to determine a total (muscular MM) and heart fraction of creatinine-phosphokinase (MB), and brain parenchyma ischemia was confirmed by CT or MR scan of the head. A detailed history of the risk factors for ischemic brain disease (IBD) and ischemic heart disease was taken from all patients with AIBD, and the profile of glycemia and lipid status were determined, and blood pressure was measured 6 times a day. Independent variables in statistical analysis were: age, degree of severity and the side of neurologic event, size of ischemic lesion and maximal values of systolic and dyastolic pressure. Dependent variables were the values of fractions of creatinine-phosphokinase (CPK). Control group (n = 40) comprised patients with neurologic diseases of non-vascular origin. All parameters as well as their interrelations were statistically analyzed. The results revealed significant correlation of the increased levels of CPK of MM and MB fraction with the size and place of ischemic lesion in the right cerebral hemisphere, which was highly significant for MB fraction in the total group of patients with AIBD, and for MM fraction, only for cases of more severe IBD. Highly significant increased values of those fractions were also observed compared to the control group of patients.
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PMID:The significance of determination of the fraction of creatinine-phosphokinase in patients with acute ischemic brain disease. 1093 26

GPI 6150 (1,11b-dihydro-[2H]benzopyrano[4,3,2-de]isoquinolin-3-one) is a novel inhibitor of poly(ADP-ribose) polymerase (PARP). It has demonstrated efficacy in rodent models of focal cerebral ischemia, traumatic brain injury, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine damage to dopaminergic neurons, regional myocardial ischemia, streptozotocin-induced diabetes, septic shock, and arthritis. Here we report the structure of GPI 6150, its enzymatic characteristics, and biochemical property in cytoprotection. As a competitive PARP inhibitor (K(i) = 60 nM), GPI 6150 protected the P388D1 cells against hydrogen peroxide cytotoxicity, by preventing PARP activation and the depletion of NAD(+), the substrate for PARP. To address the concerns of potential side effects of PARP inhibition, we tested GPI 6150 and found it had no effect on the repair and expression of a plasmid DNA damaged by N-methyl-N'-nitro-N-nitrosoguanidine. Neither did it affect dehydrogenases with NAD co-enzyme. GPI 6150 was much less potent to inhibit mono-ADP-ribosyltransferase. There was no selectivity for GPI 6150 between PARP isozymes. These attributes render GPI 6150 a useful tool to probe the functions of PARP.
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PMID:GPI 6150 prevents H(2)O(2) cytotoxicity by inhibiting poly(ADP-ribose) polymerase. 1109 54

Blood pressure (BP) elevations may correspond to different clinical situations. Hypertensives emergencies are situations that require immediate reduction in BP because of acute or rapidly progressing target organ damage: accelerated malignant hypertension, hypertensive encephalopathy, acute myocardial infarction, acute aortic dissection, acute left ventricular failure, and eclampsia. Hypertensive urgencies are those with marked elevated BP in which it is desirable to reduce BP progressively within few hours, such as severe hypertension, progressive target organ damage, perioperative hypertension. Cerebrovascular accidents have to be individualized. In most patients in the immediate post-stroke period, BP should not be lowered. Caution is advised in lowering BP in these patients because excessive falls may precipitate cerebral ischemia. In situations without symptoms or progressive target organ it is necessary to exclude proximate causes of elevated BP such as pain and elevated BP alone rarely requires antihypertensive treatment. Among parenteral antihypertensive (AH) drugs labetalol, nicardipine, urapidil, and nitroprussiate are generally used, and the choice of AH drug depends on the clinical situation. It is not required to normalize BP immediately but to reduce mean BP no more than 25%, then toward 160/100 mmHg as recommended by JNC VI, in order to avoid an impairment of renal, cerebral or coronary ischemia. Oral long-acting dihydropyridines are often subsequently administrated, except in myocardial ischemia. Therapeutic attitudes vary considerably according to the clinical situation: abstention, immediate decrease or progressive decrease in BP have to be decided.
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PMID:[Acute blood pressure elevations]. 1119 Feb 94

Abnormalities of coagulation and fibrinolysis may play an important role in the pathogenesis of ischaemic stroke and vascular dementia. We aimed to determine whether haemostatic function is altered in acute recent-onset or chronic ischaemic cerebrovascular disease. We studied consecutive patients with ischaemic stroke (n = 74) and vascular dementia (n = 42) compared with healthy controls (n = 40) in a case-control study. The ischaemic stroke group was assessed twice, 3-10 days after the acute stroke and at 1-3 months. Fibrinogen, fibrin D-dimer (marker of fibrin turnover) and von Willebrand factor (vWF) (marker of endothelial disturbance) were elevated acutely (P < 0.0001) and in the convalescent phase after ischaemic stroke (P < 0.0001, P < 0.0001, and P < 0.01 respectively, compared with controls). Similar results were seen in the vascular dementia group. Stepwise multivariate regression analyses showed that cerebrovascular disease correlated independently with fibrinogen (P < 0.001) and fibrin D-dimer levels (P < 0.001), while vWF correlated independently with electrocardiograph evidence of ischaemic heart disease (P = 0.004). Changes between acute and convalescent phases in ischaemic stroke were slightly inconsistent. However, in the acute stage there were tendencies for fibrinogen, D-dimer and vWF to be increased, and factor VIII was significantly higher. Abnormalities of haemostasis, including increased fibrin turnover and endothelial disturbance, are found in both acute and chronic cerebral ischaemia. Many of these patients have co-existent ischaemic heart disease and this may contribute to some of these changes. Acute ischaemic stroke is associated with transient changes in haemostatic factors; however, most abnormalities persist into the convalescent phase, and are also demonstrable in subjects with vascular dementia.
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PMID:Haemostasis in ischaemic stroke and vascular dementia. 1173 65


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