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)

Dipyridamole is one of several agents that may be infused intravenously to nonivasively evaluate coronary perfusion without dynamic exercise. Among such agents it is the most investigated, and it is associated with the greatest clinical experience. Its mechanism of action utilizes intrinsic adenosine and does not require the induction of ischemia. Rather, the method tests the coronary flow reserve by dilating the precapillary and arteriolar capillary beds. Vessels with a limited coronary flow reserve demonstrate reduced responsiveness with relative flow reduction and a resultant defect on perfusion scintigraphy. Side effects are common and generally benign, but deaths have been reported and they generally relate to severe hypotension, prolonged dense ischemia and resultant infarction, or bronchospasm. Severe complications are rare and can be avoided by the prompt administration of aminophylline, the dipyridample antedote. Diagnostic accuracy for the identification of coronary disease appears similar to that for exercise perfusion scintigraphy. It should be applied to patients with known or suspected coronary disease who require coronary evaluation, but who cannot exercise adequately for diagnostic or prognostic purposes. In such patients, the method is useful for the preoperative assessment of risk at peripheral vascular and other major noncardiac surgery. It may be of value as well in the assessment of the otherwise uncomplicated patient postinfarction. Not yet established is its application to the patient with unstable angina or in the acute setting, after coronary reperfusion. Similarly, its comparison with direct adenosine infusion or with pharmacological agents whose mechanism rests entirely on ischemia induction, as does dobutamine, has until now been limited. Unlike its use with perfusion scintigraphy, the application of dipyridamole with echocardiography and other functional ischemic indicators is totally dependent on the induction of ischemia. This is likely less frequent than the induction of nonischemic perfusion heterogeneity. The agent is now commonly available and will make a significant beneficial impact on patient evaluation and management.
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PMID:Dipyridamole perfusion scintigraphy. 183 35

Our current understanding of the pathophysiology of angina and myocardial ischemia includes both anatomic and dynamic mechanisms. The relative contribution made by hemodynamically important atherosclerotic obstruction and dynamic coronary artery obstruction, either by arterial spasm or arteriolar constriction, to the pathophysiology of ischemia in any given patient should be delineated. This information appears to be useful in identifying patients likely to achieve major benefit from vasodilators on the one hand or beta-adrenergic blocking agents on the other. A number of agents are now available within these two pharmacologic classes. There are some differences in action of these various agents that require thorough familiarity of effects of these drugs so that their action can be optimized. Practically speaking, the large majority of patients with an angina syndrome will respond to nitrates. Nitrates are extremely safe and cheap; thus, their use for relief or prevention of the acute ischemic episode remains the initial treatment of choice. When symptoms are more than mild to moderate in severity, or unacceptably controlled in frequency using nitrates alone, other pharmacologic measures are needed (Fig. 2). In patients with a predominant symptom of effort angina, suggesting that a hemodynamically important atherosclerotic-type obstruction is responsible for the syndrome, beta-adrenergic blocking drugs can be very helpful. If effort angina remains unacceptably controlled or adverse effects occur, a calcium-channel antagonist may be added or substituted. These latter agents do not exacerbate bronchospasm or peripheral vascular disease, and they offer a distinct advantage over beta-adrenergic blocking agents in patients with angina who have such disorders. Where the predominant symptom is rest angina, or the patient has other evidence suggesting coronary spasm or arteriolar vasoconstriction, a calcium-channel antagonist may result in a very favorable response. This therapy should be extended not only to patients in whom coronary spasm occurs spontaneously but to those in whom it can be provoked by stimuli such as effort or cold. When spasm is superimposed upon hemodynamically important atherosclerotic obstruction, the favorable response does not seem to be as great as that seen when spasm exists alone. In these cases, coronary bypass surgery, plexectomy , and other nonpharmacologic approaches may have to be added to the pharmacologic regimen.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Comprehensive drug management of angina pectoris. 614 88

Many patients undergoing investigation for coronary artery disease are unable to exercise adequately due to physical or psychological reasons. Thallium-201 imaging using dipyridamole or adenosine may then be a suitable method of assessing myocardial perfusion. In patients with asthma, these drugs are contraindicated because of the risk of provoking bronchospasm. This study assesses the safety of dobutamine for thallium-201 myocardial perfusion imaging in patients with asthma who were unable to perform adequate exercise. Dobutamine was infused at rates < or = 40 micrograms/kg/min in 30 asthmatic patients for thallium-201 emission tomography. The severity of the airway reactivity ranged from mild to severe (bronchodilator treatment ranging from inhaled beta 2 agonists alone to maximal therapy including oral steroids). Coronary angiography was performed in 20 patients. Minor side effects of dobutamine were frequent, but did not limit the infusion rate. There were no episodes of bronchospasm, but tolerable dyspnea occurred in 8 patients who had reversible ischemia; this rapidly resolved with termination of the infusion. There were no serious cardiac complications, but chest pain occurred in 67% of patients. Thallium-201 images were abnormal in 10 of 11 patients with coronary artery disease (sensitivity 91%) and normal in 7 of 9 with normal coronary arteries (specificity 79%). Dobutamine thallium-201 myocardial perfusion tomography is a safe procedure in patients with asthma.
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PMID:Safety of dobutamine stress for thallium-201 myocardial perfusion tomography in patients with asthma. 849 79

In choosing a pharmacologic agent for stress testing, the clinician must keep a number of things in mind, such as the diagnostic utility of the agent or in what situations a vasodilator or catecholamine will be the better choice. Although all stress agents produce similar diagnostic accuracy for CAD, vasodilators have a higher cardiac uptake than catecholamines, and the addition of exercise improves the heart/background contrast ratios. With regard to physiologic comparisons, exercise or dobutamine will double coronary perfusion compared with baseline flow, but vasodilators produce a threefold or fourfold increase. The clinician should also keep in mind that adenosine will produce the shortest duration of hyperemia, whereas dobutamine and arbutamine produce a longer effect, and dipyridamole has the longest duration. If electrophysiologic considerations are important, exercise and catecholamines accelerate sinoatrial and atrioventricular conduction and are not typically associated with heart block. In contrast, adenosine can cause transient atrioventricular block, but this rarely occurs with dipyridamole. Clinical factors also must be considered. Although clinical utility of pharmacologic stress agents in the first 24 hours after infarction has not been demonstrated, the prognostic utility of vasodilators in the subsequent 2- to 4-day period has been shown. With patients with pulmonary disease (asthma) who do not have wheezing, dipyridamole can be used, but dobutamine or arbutamine should be used in patients with recent respiratory failure or bronchospasm before testing. In patients with left bundle branch block, vasodilators are the preferred stress agents rather than synthetic catecholamines or dynamic exercise. In the first crossover thallium imaging, there was good overall agreement in segmental perfusion comparing adenosine and dipyridamole, but there was a tendency for adenosine to detect more ischemia. The clinical significance (if any) for these findings has yet to be determined.
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PMID:Comparison of pharmacologic stress agents. 898 83

Propranolol has been shown to be effective for as long as 5 days in massively burned children to reduce heart rate and cardiac work. This article describes the use of propranolol given for 10 days to burned children to test whether the drug remains effective and safe in reducing heart rate and cardiac work for longer periods. We prospectively studied 22 children, 1 to 10 years of age with burns covering > or = 40% of their total body surface area. These children were treated with 0.5 to 1.0 mg/kg propranolol given orally or intravenously every 8 hours for 10 days. In both septic and nonseptic patients, propranolol significantly decreased their daily average heart rate (between 10% and 13%, p < 0.05) and rate-pressure product (between 10% and 16%, p < 0.05) compared with their 24-hour mean before propranolol treatment. No significant change in mean arterial blood pressure, or plasma urea nitrogen creatinine or glucose levels could be shown. No hypotension, hypothermia, azotemia, hyperglycemia or hypoglycemia, arrhythmia, bronchospasm, or peripheral ischemia was noted during or after treatment. Whereas propranolol lowered heart rate more per milligram per kilogram body weight when given intravenously, both routes were safe and effective. From these data, we conclude that propranolol can be given to decrease the work of the heart safely and effectively for > or = 10 days.
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PMID:Prolonged use of propranolol safely decreases cardiac work in burned children. 916 45

Optimal management of dyspnea in terminal cancer patients requires an understanding of the responsible pathophysiological mechanisms. This prospective study assessed visual analogue scales (VAS) of shortness of breath (SOB) and anxiety, bedside spirometry, maximum inspiratory pressure (MIP), chest radiography, arterial blood gases, hemoglobin, and electrocardiogram, if indicated, in 100 terminally ill cancer patients. Forty-nine percent of the patients had lung cancer. The median VAS scores for SOB and anxiety were 53 mm and 29 mm, respectively. Spirometry was abnormal in 93% of patients, with 5% having obstructive, 41% restrictive, and 47% mixed patterns. The median MIP was 16 cm H2O. Sixty-five percent of the patients had parenchymal or pleural involvement on chest radiograph. Twenty-nine percent had evidence of cardiac ischemia, recent or current myocardial infarction or atrial fibrillation. Patients had a median of five different abnormalities that could have contributed to their shortness of breath. Only anxiety (p = 0.001), a history of smoking (p = 0.02), and pCO2 levels were statistically significantly correlated with SOB VAS scores. The potentially correctable causes of dyspnea included hypoxia (40%), anemia (20%), and bronchospasm (52%). The finding of very low MIPs suggests severe respiratory muscle weakness may contribute significantly to dyspnea in this patient population. Further studies are needed to confirm this finding and characterize the underlying pathophysiology.
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PMID:Dyspnea in the advanced cancer patient. 1058 52

Adenosine regulates many physiological functions through specific cell membrane receptors. On the basis of pharmacological studies and molecular cloning, four different adenosine receptors have been identified and classified as A(1), A(2A), A(2B), and A(3). These adenosine receptors are members of the G-protein-coupled receptor family. While adenosine A(1) and A(2A) receptor subtypes have been pharmacologically characterized through the use of selective ligands, the A(3) adenosine receptor subtype is presently under study in order to better understand its physio-pathological functions. Activation of adenosine A(3) receptors has been shown to stimulate phospholipase C and D and to inhibit adenylate cyclase. Activation of A(3) adenosine receptors also causes the release of inflammatory mediators such as histamine from mast cells. These mediators are responsible for processes such as inflammation and hypotension. It has also been suggested that the A(3) receptor plays an important role in brain ischemia, immunosuppression, and bronchospasm in several animal models. Based on these results, highly selective A(3) adenosine receptor agonists and/or antagonists have been indicated as potential drugs for the treatment of asthma and inflammation, while highly selective agonists have been shown to possess cardioprotective effects. The updated material related to this field of research has been rationalized and arranged in order to offer an overview of the topic.
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PMID:A(3) adenosine receptor ligands: history and perspectives. 1072 24

Mechanical ventilation can worsen morbidity and mortality by causing ventilator-associated lung injury, especially where adverse ventilatory strategies are employed. Adverse strategies commonly involve hyperventilation, which frequently results in hypocapnia. Although hypocapnia is associated with significant lung alterations (e.g., bronchospasm, airway edema), the effects on alveolar-capillary permeability are unknown. We investigated whether hypocapnia could cause lung injury independent of altering ventilatory strategy. We hypothesized that hypocapnia would cause lung injury during prolonged ventilation, and would worsen injury following ischemia-reperfusion. We utilized the isolated buffer-perfused rabbit lung model. Pilot studies assessed a range of levels of hypocapnic alkalosis. Experimental preparations were randomized to control groups (FI(CO(2)) = 0.06) or groups with hypocapnia (FI(CO(2)) = 0.01). Following prolonged ventilation, pulmonary artery pressure, airway pressure, and lung weight were unchanged in the control group but were elevated in the group with hypocapnia; elevation in microvascular permeability was greater in the hypocapnia versus control groups. Injury following ischemia-reperfusion was significantly worse in the hypocapnia versus control groups. In a preliminary series, degree of lung injury was proportional to the degree of hypocapnic alkalosis. We conclude that in the current model (1) hypocapnic alkalosis is directly injurious to the lung and (2) hypocapnic alkalosis potentiates ischemia-reperfusion-induced acute lung injury.
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PMID:Injurious effects of hypocapnic alkalosis in the isolated lung. 1093 60

The purpose of this study was to describe the perceptions of nurse anesthesia students (NAS) who used a MedSim simulator (MedSim USA, Inc, Ft Lauderdale, Fla) as part of their educational training. A convenience sample of 12 NAS in their first year of clinical training was researched. The researcher analyzed data qualitatively from observations made during 4 different sessions. Session 1 introduced the students to the simulator. Session 2 involved each student performing an anesthetic induction. A minor incident such as hypotension, hypertension, bradycardia or tachycardia occurred in session 3, and a major incident such as cardiac ischemia, anaphylaxis, bronchospasm, or malignant hyperthermia occurred in session 4. Data collection involved observation by the primary investigator, journal entries by the anesthesia students, and focus group interviews with the students. Results of the study indicate that, although students experience feelings of apprehension, uneasiness, or fear during the sessions, they felt it was very educational. Disadvantages include the lack of reality, lack of knowledge on handling crisis events, possibility of fixation errors, and the presence of anxiety. Advantages include improved critical thinking and decision-making skills, increased confidence, and improved clinical preparation. Results can be used to assist instructors in improving the students' learning experiences and to teach more effectively.
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PMID:Nurse anesthesia students' perceptions of the anesthesia patient simulator: a qualitative study. 1207 70

The present study summarizes the biological effects elicit upon A(3) adenosine receptor (A(3)AR) activation in normal and tumor cells. Anti-inflamatory response is mediated upon A(3)AR activation in neutrophils, eosinophils and macrophages via direct effect on cell degranulation or the production of anti-inflamatory cytokines. In basophils, which highly express A(3)AR, degranulation and mediator release upon receptor activation lead to pro-inflammatory effects resulting in bronchospasm and asthma. In other normal cells such as cardiomyocytes, neuronal cells and bone marrow cells A(1)AR activation induces cytoprotective effects in vitro. In vivo, A(3)AR agonists act as cardio- and neuroprotective agents and attenuate ischemic damage. Furthermore, agonists to A(3)AR induce granulocyte colony stimulating factor (G-CSF) production and myeloprotective effect in chemotherapy treated mice. Interestingly, A(3)AR agonists inhibit tumor cell growth both in vitro and in vivo through a cytostatic effect mediated via the de-regulation of the Wnt signaling pathway. The variety of activities elicit by A(3)AR agonists suggest their potential use as therapeutic agents in inflammation, brain/cardiac ischemia and cancer. Antagonists to A(3)AR may be implemented to the therapy of asthma and additional allergic conditions.
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PMID:Pharmacology and therapeutic applications of A3 receptor subtype. 1257 Jul 62


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