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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial infarction is linked to atherosclerosis, yet the sequence leading from silent coronary atherosclerosis to acute myocardial infarction has remained unclear. Here we show that hypercholesterolemic apolipoprotein E-/- low density lipoprotein receptor-/- mice develop not only coronary atherosclerosis but also myocardial infarction. Exposure of mice to mental stress or hypoxia led to acute ischemia, which, in a large proportion of the mice, was followed by electrocardiographic changes, leakage of troponin T, and loss of dehydrogenase from the myocardium, all indicative of acute myocardial infarction. Apoptotic death of cardiomyocytes was followed by inflammation and fibrosis in the heart. All these pathological changes could be prevented by a blocker of the endothelin type A receptor. Thus, stress elicits myocardial infarction through endothelin receptor signaling in coronary atherosclerosis caused by hypercholesterolemia.
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PMID:Myocardial infarction mediated by endothelin receptor signaling in hypercholesterolemic mice. 1035 14

The concordance rate of monozygotic twins showed that the occurrence of ulcerative colitis required both internal and environmental conditions. Genetic studies revealed that IBD1 locus on chromosome 16 and IBD2 locus on chromosome 12 showed highly suspicious susceptibility for inflammatory bowel disease. The other possible internal factors include antineutrophil cytoplasmic antibodies and mucin abnormality. Many environmental factors have been reported to cause relapse. These are viral and bacterial infection, medicine such as antibiotics, non-steroidal anti-inflammatory drugs and aminosalicylates, colonic ischemia, post-examination state, psychological stress, winter season, travel and overwork.
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PMID:[Influencing factors on occurrence and relapse in ulcerative colitis]. 1057 4

This study assesses the prognostic value of mental stress-induced ischemic left ventricular wall motion abnormalities and hemodynamic responses in patients with stable coronary artery disease (CAD). Seventy-nine patients (76 men and 3 women) with prior positive exercise test results were exposed to mental arithmetic and a simulated public speech stress in 2 prior studies. Ischemic wall motion abnormalities were monitored using echocardiography or radionuclide ventriculography (RNV). During mental stress testing, new or worsened ischemic wall motion abnormalities to mental stress and exercise were ascertained, as were peak changes in blood pressure and heart rate to mental stress. The occurrence of subsequent cardiac events (including cardiac death, nonfatal myocardial infarction, or revascularization procedures) was ascertained. New cardiac events were observed in 28 of 79 patients (35%) after a median follow-up duration of 3.5 years (range 2.7 to 7.3). Survival analysis indicated that 20 of 45 patients with mental stress ischemia (44%) experienced new cardiac events more frequently than those without mental stress ischemia (8 of 34; 23%; p = 0.048). Type of cardiac event did not differ between mental stress-positive and stress-negative patients. After controlling for baseline blood pressure and study group status (echocardiography vs RNV), there was a significantly higher relative risk of subsequent events for patients with high versus low peak stress-induced diastolic blood pressure responses (RR = 2.4, confidence interval 1.1 to 5.2; p = 0.03). These results demonstrate that ischemic and hemodynamic measures obtained from mental stress testing may be useful in assessing prognosis in CAD patients with prior positive exercise test results.
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PMID:Prognostic value of mental stress testing in coronary artery disease. 1061 93

Effects of sleep deprivation on neural cardiovascular control may have important clinical implications. We tested the hypothesis that sleep deprivation increases heart rate, blood pressure, and sympathetic activity and potentiates their responses to stressful stimuli. We studied 8 healthy subjects (aged 40+/-5 years, 6 men and 2 women). Blood pressure, heart rate, forearm vascular resistance, and muscle sympathetic nerve activity were measured at rest and during 4 stressors (sustained handgrip, maximal forearm ischemia, mental stress, and cold pressor test). Measurements were obtained twice, once after normal sleep and once after a night of sleep deprivation. All measurements were obtained in a blinded, randomized manner. In comparison with normal sleep, sleep deprivation resulted in an increase in blood pressure (normal sleep versus sleep deprivation=82+/-8 versus 86+/-7 mm Hg, mean+/-SEM, P=0.012) and a decrease in muscle sympathetic nerve activity (normal sleep versus sleep deprivation=28+/-6 versus 22+/-6 bursts/min, P=0.017). Heart rate, forearm vascular resistance, and plasma catecholamines were not significantly changed by sleep deprivation, nor did sleep deprivation affect autonomic and hemodynamic responses to stressful stimuli. Sleep deprivation results in increased resting blood pressure, decreased muscle sympathetic nerve activity, and no change in heart rate. Thus, the pressor response to sleep deprivation is not mediated by muscle sympathetic vasoconstriction or tachycardia.
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PMID:Effects of sleep deprivation on neural circulatory control. 1081 83

This paper describes the influence of stress on learning and memory. The mice receiving inescapable electroshock fail to perform the active conditioned avoidance response of lever-pressing. This is called learned helplessness, which is ameliorated by treatment with antidepressants including one of the selective serotonin reuptake inhibitors (SSRIs). It is of particular interest that posttraumatic stress disease (PTSD) accompanied by memory impairment could be improved by treatment with SSRIs. The different kinds of stress including ischemia, footshock, psychological stress, and forced swimming influence learning and memory as indexed by spontaneous alternation performance as well as passive avoidance learning. In addition, a variety of stresses influence the activity of hormones and neurotransmitters like monoamines, neuropeptides, and excitatory amino acids resulting in changes in learning and memory. Finally, the accumulation of data is necessary to clarify the exact mechanism of stress on learning and memory.
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PMID:[Influence of stress on learning and memory]. 1121 55

Sympathetic overactivity is a common feature of certain cardiovascular diseases. An acute activation of the sympathetic nervous system can provoke angina pectoris attacks through the increase of myocardial oxygen demand, frequently associated to coronary arterial constriction. It can also promote cardiac arrhythmias leading, in some cases, to cardiac sudden death. The aim of the present study was to evaluate the cardiovascular effects of a single oral dose of baclofen or ifenprodil (two drugs modulating central glutamatergic relays) at rest and during three laboratory stressors (a cold pressor test, a mental arithmetic stress test and an exercise test on a cycloergometer), in human healthy volunteers. Ifenprodil increased resting heart rate and did not reduce the cardiovascular response to any test. In contrast, baclofen reduced the tachycardic response to mental stress test and so limited the increase of myocardial oxygen demand during the test. Nevertheless, this drug was not able to affect the cardiovascular response to exercise. Finally, we have shown in this study that baclofen exhibits a profile of a central sympathomodulator without cardiodepression. Its activity towards mental stress induced cardiovascular responses leads us to proposing this compound for testing after a chronic treatment, in patients with silent myocardial ischemia and mental stress test induced ischemia.
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PMID:Effects of centrally-acting glutamatergic modulators on cardiovascular responses to stress in humans. 1143 32

The relationship between stressful life events and the onset of disease is well documented. However, the role of psychological stress as a risk factor for life-threatening cerebrovascular insults such as stroke remains unspecified, but could explain individual variation in stroke outcome. To discover the mechanisms through which psychological stress may alter stroke outcome, we modeled the effects of chronic social intimidation and stress on ischemia-induced bcl-2 expression and early neuronal cell loss resulting from cerebral artery occlusion in mice (C57BL/6). The bcl-2 protooncogene promotes cell survival and protects against apoptosis and cellular necrosis in numerous neurodegenerative disorders, including stroke. In our study, male mice were chronically exposed to aggressive social stimuli before induction of a controlled, mild ischemic insult. Stressed mice expressed approximately 70% less bcl-2 mRNA than unstressed mice after ischemia. In addition, social stress greatly exacerbated infarct in wild-type mice but not in transgenic mice that constitutively express increased neuronal bcl-2. Despite similar postischemic concentrations of corticosterone, the major stress hormone in mice, high corticosterone concentrations were significantly correlated with larger infarcts in wild-type mice but not bcl-2 transgenic mice. Thus, enhanced bcl-2 expression offsets the potentially deleterious consequences of high postischemic plasma corticosterone concentrations. Taken together, these data demonstrate that stressful prestroke social milieu strongly compromises an endogenous molecular mechanism of neuroprotection in injured brain and offer a new behavioral target for stroke therapy.
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PMID:Social stress exacerbates stroke outcome by suppressing Bcl-2 expression. 1155 85

Mental stress has long been implicated as a potential trigger of myocardial infarction and sudden cardiac death. This article reviews research conducted in the past two decades utilizing laboratory studies to investigate behaviorally-induced pathophysiological effects (including increased cardiac demand, decreased myocardial supply, and impaired dilation of coronary resistance vessels), in patients with coronary artery disease. The clinical significance of mental stress-induced ischemia is supported by findings of a predictive relationship of mental stress-induced ischemia for ambulatory ischemia and subsequent cardiac events. Mental stress-induced ventricular fibrillation, ventricular tachycardia, and T-wave alternans are also being explored as possible markers of arrhythmic vulnerability in human and animal models. T-wave alternans comparable to exercise can be induced by an anger-like state in an animal model, and with mental stress in patients with implantable cardioverter-defibrillators. Future directions for research on mental stress and cardiac events are suggested, including further studies of mechanisms of mental stress-induced arrhythmia and ischemia, additional studies of the prognostic significance of stress-induced ischemia and T-wave alternans, and use of pharmacological and psychosocial treatments for preventing stress-induced cardiac events.
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PMID:Mental stress as a trigger of acute cardiac events: the role of laboratory studies. 1183 35

Changes of temporomandibular joint (TMJ) under repeated +Gz stress were discussed. From the etiological point of view in TMJ, many papers in the fields of aviation medicine, microcirculation, maxillofacial surgery and bone surgery were reviewed. +Gz forces can cause inadequacy of blood of oxygen supply to TMJ area. This situation can be worsened by release of free radical agent and cellular factors, ischemia/reperfusion injury, and/or hemorrheologic changes. Furthermore, G-induced injury of cervical muscles and spine may break the maxillofacial muscle chain balance. In addition to the above factors, mental stress may do harm to TMJ. This paper introduced the researches on this area in an attempt to enlighten the concern about TMJ responses to increased +Gz acceleration forces.
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PMID:[Analysis of the changes of temporomandibular joint under repeated +Gz stress]. 1188 99

As well as pheochromocytoma, in which it has been established that an excess of circulating catecholamines is responsible for the development of catecholamine-induced acute myopathy, some rare cases have been reported of a similar cardiac incident following intense emotional stress. In this study, the case has been examined of a 56-year old female with no history of cardiovascular disorder who presented with intense, nitro-resistant prolonged chest pain mimicking an acute coronary syndrome immediately following a situation involving major psychological stress. The admission electrocardiogram revealed a sharp decrease in R-wave amplitude in the right chest leads associated with an extended QT interval, and secondarily with subepicardiac ischemia in the lower leads. However, a few days after admission the electrical signs and septo-apical akinesia that had initially been observed by echocardiography completely disappeared. The clinical examination ruled out a diagnosis of myocardial necrosis, acute myocarditis, or pheochromocytoma. Moreover, no direct evidence of coronary spasm was found. The outcome was positive, with complete reversibility of all clinical signs and no organic sequelae. It is considered that this was probably a case of catecholaminergic acute cardiomyopathy triggered by intense emotional stress, a rare occurrence that should nevertheless be systematically taken into account in cases with similar clinical signs.
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PMID:[Myocardial pseudo-infarction: "stress"-associated catecholamine-induced acute cardiomyopathy or coronary spasm?]. 1255 32


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