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)

The role of epinephrine in eliciting myocardial ischemia was examined in patients with coronary artery disease. Objective signs of ischemia and factors increasing myocardial oxygen consumption were compared during epinephrine infusion and supine bicycle exercise. Both epinephrine and exercise produced myocardial ischemia as evidenced by ST segment depression and angina. However, the mechanisms of myocardial ischemia induced by epinephrine were significantly different from those of exercise. Exercise-induced myocardial ischemia was marked predominantly by increased heart rate and rate-pressure product with a minor contribution of end-diastolic volume, while epinephrine-induced ischemia was characterized by a marked increase in contractility and a less pronounced increase in heart rate and rate-pressure product. These findings indicate that ischemia produced by epinephrine, as may occur during states of emotional distress, has a mechanism distinct from that due to physical exertion.
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PMID:Mechanisms of myocardial ischemia induced by epinephrine: comparison with exercise-induced ischemia. 341 71

It has been demonstrated in rat experiments that total ischemia of the liver leads to disorders of the metabolism of xenobiotics and endogenous substrates. Upset hexenal metabolism manifests in the prolongation of the hexenal-induced sleep and hexenal concentration elevation in blood plasma for 18 days of the postischemic period. Following exposure to ischemia liver microsomes show a decrease in the rate of amidopyrine, aniline and hydrocortisone hydroxylation. Hydrocortisone metabolism returns to normal by day 14, that of amidopyrine by day 21 of the postischemic period. Aniline metabolism gets disturbed to a greater degree, remaining 33.4% lower by day 21. It has been shown that the inducibility of microsomal monooxygenases is substantially restricted by days 7 and 14 of the postischemic period.
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PMID:[Characteristics of the ischemic disorders of xenobiotic metabolism in the liver of rats in the early and late stages of recovery]. 673 4

The role of emotional distress (e.g., anger, depression, and anxiety) in anginal chest discomfort (ACD) may have been underestimated. The authors review the empirical studies in this area, which are inconsistent with the standard theory on the ischemia-angina relationship; summarize the substantial evidence indicating a strong and consistent cross-sectional/prospective epidemiological association of emotional distress and ischemia/ACD; review the distress-targeted, interventional evidence confirming a causal relationship (i.e., reduced chest discomfort and health system utilization), thus confirming clinical utility of such interventions; and explore the possible mechanisms that might account for the relationship between emotional distress and chest discomfort. Substantial clinical benefit may be achieved by aggressively detecting and treating emotional distress in ACD patients.
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PMID:What's "unstable" in unstable angina? 1512 42

Common, noncentral nervous system medical conditions linked with cognitive impairment in adults and the elderly include: acute respiratory distress syndrome; cancer; chronic kidney disease; chronic obstructive pulmonary disease; coronary heart disease; hypertension; obesity (bariatric surgical candidates); obstructive sleep apnea; and type 2 diabetes. Cross-condition comparison of the nature and frequency of cognitive impairment is difficult as these conditions often coexist, and there exists no consensus as to the definition of cognitive impairment, nor the optimal number and type of neuropsychological tests required for evaluation. There is as yet no clear evidence for condition-specific profiles of cognitive impairment. Rather, a generalized profile consisting of subclinical levels of impairment in attention, processing speed, executive, and memory functions from bilateral frontal-subcortical ischemia fits across all conditions. This profile: occurs only in subgroups of patients; is inconsistently related to measures of illness severity; is unrelated to patient self-report or level of functional independence; is exacerbated by very high levels of emotional distress; and is reversible in some cases but can also progress to frank neurological disease (dementia) in others, especially the elderly, when multiple conditions coexist, and/or when medical condition severity progresses.
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PMID:Cognitive impairment in common, noncentral nervous system medical conditions of adults and the elderly. 2121 18

Raynaud's Syndrome is a frequent manifestation of digital ischemia which occurs or is aggravated upon exposure to cold temperatures or emotional distress. Primary Raynaud is a benign disease which predominantly affects younger women and is transient without serious sequelae. In contrast, secondary Raynaud is usually one of the manifestations of systemic disease and is, in addition to symptoms of the basic disease, associated with ischemic lesions. The diagnosis of primary Raynaud is mostly based on the clinical presentation. In secondary Raynaud, additional investigating techniques including imaging investigations and laboratory tests for the detection of underline disease are needed. Treatment is based on lifestyle modification, which includes smoking cessation, avoiding low outside temperatures, avoiding the use of vibrating tools and limiting repeated hand actions. Drug treatment consists of calcium-channel blockers, nitroglycerine ointments, prostacyclins and various new drugs such as endothelin receptor antagonists, phosphodiesterase inhibitors and serotonin receptor antagonists. Most of these drugs are effective in less than 50% of treated patients and do not completely abolish vasospastic attacks, but reduce the severity and frequency of attacks. The prostacyclin derivate iloprost is the most promising drug in the management of secondary Raynaud's disease. Other therapeutic procedures including chemical or surgical sympathectomy are obsolete and without any long-term positive effects.
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PMID:Raynaud's Syndrome: a neglected disease. 2567 14

Raynaud phenomenon (RP) is a transient digital ischemia that occurs after exposure to cold temperature or emotional distress. It presents with a triphasic course: the initial white phase is followed by cyanotic discoloration and, subsequently, erythema. The attacks may be associated with pain, paresthesia, and complicate with nonhealing ulceration often leading to amputation. To date, there are no clear-cut therapeutic guidelines and many medications are used off-label. Encouraging results were reported with the use of botulinum neurotoxin-A (BoNT-A). However, there is still ongoing debate regarding indications, contraindications, best injection technique, and mechanism of action. The aim of this study was to address these issues by providing an up-to-date and detailed overview of the use of BoNT-A in RP.A PubMed database search was conducted. The available studies and techniques were evaluated and compared.The search yielded a total of 29 studies. Ten papers, published between 2004 and 2014, were considered relevant. A total of 128 patients underwent BoNT-A injections. Seventy-five percent to 100 % of the patients reported pain reduction after treatment. Healing of ulcers was reported in 75% to 100% of the affected patients. The most common complication was temporary hand weakness, with an average incidence of 14.1%. Injections targeting the neurovascular bundle at or slightly proximal to the A1 pulley were the most commonly performed.Botulinum neurotoxin-A injection proved to be a valid approach in both primary and secondary RP. The available evidence shows the achievement of both symptomatic and functional improvements in this debilitating condition. However, the patient should be adequately informed about the risk of transient hand weakness.
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PMID:The Role of Botulinum Toxin A in the Treatment of Raynaud Phenomenon. 2680 52