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

The development of muscle fatigue due to exhaustive exercise is associated with impaired sarcoplasmic reticulum (SR) Ca-transport activity. This study tested the hypothesis that SR failure is a consistent feature of cardiac and skeletal muscle fatigue owing to relative functional overload regardless of the method of induction: excessive stimulation, diminished performance capacity, or excessive excitation-contraction coupling. The Ca-transport activity was determined using three unique models of muscle fatigue: chronic and rapid ventricular pacing in dogs; metabolic inhibition caused by global cardiac ischemia in swine; and the hypermetabolic syndrome of porcine malignant hyperthermia (MH). Both pacing- and ischemia-induced fatigue resulted in reduction of SR Ca-transport ATPase activity: from 275 +/- 58 to 159 +/- 57 nmol.min-1.mg-1 (mU/mg) and from 577 +/- 82 to 177 +/- 133 mU/mg, respectively. Both pacing-induced fatigue and halothane-induced MH resulted in reduction of Ca-sequestration activity of muscle homogenates from 5.95 +/- 2.4 to 3.11 +/- 0.67 nM/s at 300 nM Ca and 38.7 +/- 10.5 to 16.3 +/- 8.0 nM/s at 1500 nM Ca, respectively (all p less than 0.01). The isolated SR Ca-ATPase activity correlated with Ca-sequestration activity of myocardial homogenates (r = 0.76; p less than 0.005). Different models were used to study the relationship of Ca-transport activity with relaxation function, degree of acidosis, and ionized Ca concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac and muscle fatigue due to relative functional overload induced by excessive stimulation, hypersensitive excitation-contraction coupling, or diminished performance capacity correlates with sarcoplasmic reticulum failure. 205 42

Maintenance of low coronary flow (1 ml/min) during 40 or 70 min of anoxia maintained function and prevented Ca2+ overload during reoxygenation in isolated rat hearts. In comparison, recovery from 40 min of global ischemia resulted in only 20% of preischemic function and an increase in end-diastolic pressure (LVEDP) to 39 mmHg. Reperfusion Ca2+ uptake rose from 0.6 to 10.2 mumol/g dry tissue. Intracellular Na+ (Nai+) increased from 13 to 61 mumol/g dry tissue after 40 min of global ischemia, but was unchanged in hearts with low flow anoxia. When glucose and pyruvate were omitted from buffer used for anoxic perfusion, recovery was only 15% of preanoxic values, LVEDP rose to 32 mmHg, and reperfusion Ca2+ uptake was 7.2 mumol/g dry. In addition, Nai+ increased (47.4 mumol/g dry tissue) and ATP was depleted (1.0 mumol/g dry tissue) in the absence of substrate. In anoxic hearts supplied substrate, Nai+ stayed low (12 mumol/g dry tissue) and ATP was preserved (11.6 mumol/g dry tissue). Addition of ouabain (100 or 200 microM) and provision of zero-K+ buffer increased Nai+ and resulted in impaired functional recovery, increased LVEDP, and greater reperfusion Ca2+ uptake. These interventions also decreased energy availability in anoxic hearts. To distinguish between effects of Na+ accumulation and ATP depletion, monensin, a Na+ ionophore, was added during low flow anoxia. Monensin increased Nai+, decreased functional recovery and increased reperfusion Ca2+ uptake in a dose-dependent manner (1-10 microM) without changing ATP content. These results suggested that reduction of Nai+ accumulation by maintenance of Na+, K+ pump activity was the major mechanism of the beneficial effects of low coronary flow on reperfusion injury.
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PMID:Na+ accumulation increases Ca2+ overload and impairs function in anoxic rat heart. 215 54

L-Glutamate and related excitatory amino acids (EAA) are firmly established as major excitatory synaptic transmitter substances in the vertebrate central nervous system. Questions which have been addressed include: How many receptors are there for the EAAs?; What ion channels and/or 'second-messenger' systems are regulated by these receptors?; What are the roles of EAAs in higher neural functions?; Are they involved in neurological disorders? EAA receptors appear not only to mediate normal synaptic transmission along excitatory pathways but also to participate in the modification of synaptic connections during development. However, overaction of receptors can also mediate neuronal degeneration and even cell death. NMDA receptor antagonists markedly attenuate neuronal necrosis. Therefore, it appears that ischemia- and hypoglycemia-associated brain damage results not from a lack of energy substrates but rather via the mediation of NMDA receptors and 'excitotoxic' mechanisms. The action of ketamine anesthesia is closely associated with a block of the NMDA receptor. Ketamine binds to a site within the lumen of the NMDA-activated channel and can become trapped there when the channel closes. Current evidence indicated that NMDA receptor antagonists will be of value for the treatment of delayed neuronal death. NMDA receptor will lead to understanding the mechanisms underlying learning and memory, the control of neuronal excitability and neuronal death.
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PMID:[Synaptic mechanisms of excitatory amino acids and NMDA receptor mediated brain excitability]. 217 10

Vascular lesions of the shoulder may be misinterpreted as one of the more familiar shoulder abnormalities by a treating physician. We are reporting on 13 athletes who were found to have symptoms related to compression of the subclavian or axillary artery or their tributaries. Nine were amateur or professional baseball pitchers. Severe arm fatigue or finger ischemia, secondary to embolization, were presenting symptoms. Arm fatigue was noted in all pitchers. After complete history and physical examination, including auscultation for bruits in functional positions, all athletes were evaluated by noninvasive tests (Doppler and Duplex scanning). Arteriography was performed with positional testing, recreating overhead activity, and complete radiographic visualization of the dye to the digital arteries. Two patients were found to have subclavian artery aneurysm. The remaining athletes were found to have compression of the subclavian artery beneath the anterior scalene muscle (five patients), the axillary artery beneath the pectoralis minor (two patients), both arterial segments (two patients), and one was found to have arterial compromise at the level of the humeral head. Branch artery compression was also noted. One pitcher occluded the posterior circumflex humeral artery with embolization to the digit. The two patients with subclavian aneurysms underwent saphenous vein bypass with cervical rib resection. All of the other athletes except one underwent resection of a 2 to 3 cm segment of the anterior scalene muscle or pectoralis minor muscles. All returned to their previous level of activity except one patient who developed impingement type symptoms and required acromioplasty. He is currently undergoing rehabilitation. Proper recognition of vascular compromise in the upper extremity of athletes is essential to avoid the catastropic complications of arterial thrombosis.
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PMID:Arterial abnormalities of the shoulder in athletes. 225 94

In view of possible adverse consequences resulting from being turned to the prone position on the Stryker frame, the critical care nurse should be alert for evidence of brainstem ischemia and subsequent cardiac arrhythmias and should take steps to minimize respiratory fatigue in the spinal cord patient. In addition, the nurse should be cognizant of the necessity of maintaining a properly aligned cervical spine to prevent complications secondary to hyperextension.
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PMID:Cardiac complications of the Stryker frame. 240 Nov 61

The protective effect of calcium antagonists on ischemic heart has been attributed to decreased energy expenditure. We administered one of the newer calcium antagonists, DL-bepridil (0.1-10 microM), to Langendorff rat hearts 10 or 15 min before ischemia (flow reduction approximately 80%). Vasodilation during normoxia was already observed with 0.3 microM DL-bepridil (flow increase 34%, p less than 0.005). This concentration decreased normoxic contractility and ischemic purine release, a marker for ATP breakdown. In the absence of bepridil, purine release of hearts that were made ischemic was 8.5-fold higher than that of normoxic control hearts. With 1 microM bepridil, the ischemic purine efflux was suppressed by 55% (p less than 0.05), with negative inotropy (p greater than 0.05) during normoxia. At 3 and 10 microM, bepridil decreased normoxic contractility by 40 and 75%, respectively (p less than 0.001), concomitant with a decrease in ischemic purine release by 80 and 76%, respectively (p less than 0.01). At the end of ischemia, myocardial ATP and creatine phosphate had decreased by 22 and 55%, respectively (p less than 0.05), and ADP, AMP, and creatine had increased 1.5-3.5-fold (p less than 0.05). Bepridil (3 microM) normalized the adenine nucleotide values; creatine and creatine phosphate approached control levels. The dose-dependent protection of the ischemic heart by bepridil appears to arise from its negative inotropic action during normoxia.
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PMID:Protection by bepridil against myocardial ATP-catabolism is probably due to negative inotropy. 244 Nov 54

The introduction, more than twenty years ago, of beta-blockers in the treatment of arterial hypertension, represented a significant advance. With these medications, many hypertensive patients are effectively under control and malignant hypertension is practically inexistent. Today, the treatment of hypertension is markedly improved with the development of new, active medications, while the beta-blockers family has markedly evolved. The role of beta-blockers in the treatment of hypertension, must therefore be re-evaluated according to their properties as compared to those of other classes of antihypertensive medications. Indeed, there are standard contraindications to he use of beta-blockers, sometimes resulting in adverse reactions, either clinical (fatigue, sexual disorders, vasomotor syndromes)--much less frequent with the new molecules--or biological (especially serum lipid levels), the consequences of which remains ill-defined--some beta-blockers appear practically without any harmful effect. Actually, despite these drawbacks, usually minimal, there are numerous and strong arguments in favor of the use of beta-blockers in the treatment of hypertension: 1) their significant follow-up in the treatment of hypertension; this is a well-known argument; 2) their effectiveness in hypertension, as a single drug and single daily dose; 3) their cost, which is lower than that of new anti-hypertensive medications; 4) their cardio-protective role, demonstrated by experimental data (myocardial protection and anti-arrhythmic effect in experimental ischemia), and clinical data (improvement of left ventricular hypertrophy, control of blood pressure increase during exertion and stress, secondary prevention after myocardial infarction).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Role of beta-blockers in the treatment of arterial hypertension]. 256

Recent work has now clearly established that coronary arterial thrombosis is the direct cause of acute myocardial infarction. This thrombotic event occurs when a pre-existing atherosclerotic plaque ruptures or fissures, thereby exposing underlying thrombogenic material to the circulation. Platelets are thus activated and the clotting cascade is initiated. It is as yet unclear why a previously stable atherosclerotic plaque should fissure or rupture. However, suggested mechanisms include release of vasoactive substances from activated platelets, coronary arterial vasomotion, mechanical stress fatigue of the atherosclerotic plaque, and rupture of vasa vasorum within the atherosclerotic plaque. The resultant cessation of myocardial blood flow produces specific biochemical and physiological alterations secondary to myocardial ischemia. Intracellular acidosis, loss of high-energy phosphates, reduced sensitivity of contractile proteins to calcium, and accumulation of inorganic phosphate and lipid, all occur within the ischemic myocyte. Diastolic compliance is markedly reduced by ischemia followed by cessation of systolic contractile activity. Most of these alterations are reversible if ischemia is relieved promptly. Prolonged ischemia leads to delayed biochemical and physiological recovery and/or cell necrosis.
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PMID:The pathophysiology of acute myocardial infarction. 266 57

Despite its low energy cost, isometric contraction can result in the onset of local muscle fatigue. The onset of fatigue occurs more rapidly when the relative force exerted is greater than 15-20% of the maximum voluntary contraction (MVC) of the muscle considered, and when the contraction time is increased. The maximum maintenance time (limit-time) and the corresponding relative force are linked by a hyperbolic relation. Ischaemia promotes accumulation of acid metabolites produced during contraction, and hinders their elimination, thus constituting the main causal factor in the onset of local muscle fatigue. The introduction of rest periods of sufficient duration to ensure restoration of normal blood flow through the muscle is an effective way of delaying, or even preventing, the onset of muscle fatigue. Other factors may also be taken into account, such as the position in which the static work is performed, and the nature and number of muscles used simultaneously, etc. Numerous laboratory and field studies have allowed the development of various models that take into account the conditions relating to isometric contractions during static work.
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PMID:Fatigue induced by static work. 268 Apr 79

Exercise tolerance in patients with normal cardiac function can improve with an exercise program. Controversy exists whether this is also true for patients with congestive heart failure (CHF). The limiting symptoms in patients with CHF are shortness of breath and fatigue. Hemodynamic parameters do not correlate well with exercise capacity in patients with CHF. These symptoms may be more related to factors that cause fatigue during exercise than to hemodynamic parameters or even to changes in pulmonary capillary pressure. The factors that cause symptoms include an increased lactate production and metabolic and blood flow abnormalities in the skeletal muscle. Exercise training can improve vasodilation and oxidation capacity, thereby reducing lactate production. Exercise programs may improve exercise capacity in the majority of patients with CHF due to coronary artery disease or idiopathic cardiomyopathy. However, certain patients with ischemia and with anterior infarctions may experience a detrimental effect on their cardiac function. Further studies are needed to better enable recognition of these patients but until this is possible, good clinical judgement must suffice.
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PMID:Cardiac rehabilitation for heart failure patients. 268 76


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