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)

Excessive tiredness is one of the most prevalent premonitory symptoms of myocardial infarction and sudden cardiac death. This state is labelled as vital exhaustion and consists of three components: fatigue, increased irritability, and demoralization. Vital exhaustion has been found to be an independent risk-indicator of myocardial infarction in one prospective study and several case-control studies. It is as yet unclear whether the association between vital exhaustion and future myocardial infarction can be explained by confounding of (subclinical) coronary artery disease. Therefore, the present study investigates the predictive value of vital exhaustion for the occurrence of new cardiac events after percutaneous transluminal coronary angioplasty (PTCA), while explicitly controlling for the severity of coronary artery disease. Patients with a successful PTCA were followed during 1.5 years. A new cardiac event was defined as present if one of the following end points occurred: cardiac death, myocardial infarction, coronary bypass surgery, repeat-PTCA, increase of coronary atherosclerosis, or new anginal complaints with documented ischemia. Vital exhaustion was assessed using the Maastricht Questionnaire two weeks after hospital discharge. Participants of the present study were 127 patients (mean age 55.6 +/- 9.1; 105 men, 22 women). Fifteen (35%) of the 43 exhausted patients experienced a new cardiac event, whereas 14 (17%) of the 84 not exhausted patients had a new cardiac event (OR = 2.7; CI = 1.1-6.3; p = .02). Multiple logistic regression analysis revealed that vital exhaustion continued to be of predictive value when other significant risk factors for new cardiac events were controlled for (i.e., severity of coronary artery disease and hypercholesterolemia).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vital exhaustion predicts new cardiac events after successful coronary angioplasty. 797 9

Forty-nine skeletally mature patients who had either a non-union or a malunion of a fracture of the tibia or the femur had correction of the deformity and acute axial lengthening of the fractured bone. Distraction was provided by the short AO/ASIF fracture distractor applied directly to the site of the osteotomy or non-union. At an average of sixty-three months (range, twenty-six to 105 months), the average increase in the tibial and femoral length was 1.7 and 3.2 centimeters, respectively. There were no compartment syndromes or ischemia secondary to any of the procedures. One patient had a transient sensory-nerve loss. Fatigue fractures were seen in two tibial plates, two femoral plates, and one femoral intramedullary nail used for osteosynthesis. A non-union developed after four other femoral intramedullary nailing procedures. One infection developed after lengthening of a tibia. Restoration of normal length by acute lengthening and internal fixation was achieved in twenty-seven patients. One patient had overlengthening of one centimeter. Fifteen patients had residual shortening of approximately one centimeter, three had shortening of more than one to 2.5 centimeters, and three patients had more than 2.5 centimeters of shortening. The patients in this series had acute restoration of limb length after traumatic shortening with a low prevalence of complications of neurovascular compromise. Three of the thirty tibial lengthenings and seven of the nineteen femoral lengthenings had to be followed by at least one additional procedure to obtain union.
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PMID:Acute lengthening of shortened lower extremities after malunion or non-union of a fracture. 812 43

The mechanical effects of ischemic contracture may be important in the development of irreversible cellular damage as it increases mechanical stress on sarcolemmal membranes and restricts endocardial perfusion. To assess the relative importance of these mechanical effects compared with decreased energy supply in the development of irreversible injury, the effects of inhibiting ischemic contracture with 2,3-butanedione monoxime (BDM), an agent that disrupts excitation-contraction coupling, were delineated in isovolumically contracting isolated rabbit hearts. Administration of 20 mmol/L BDM in 12 hearts subjected to 60 minutes of low-flow ischemia prevented ischemic contracture (left ventricular end-diastolic pressure [LVEDP], 12 +/- 3 compared with 48 +/- 14 mm Hg in 20 control hearts; P < .001), reduced membrane damage (creatine kinase [CK] release, -54% compared with control hearts; P < .05), and enhanced functional recovery during reperfusion (left ventricular developed pressure [LVDP], 86 +/- 10% of baseline compared with 56 +/- 23% in control hearts; P < .01). These observations were not related to increased intracavitary pressure and its effects on flow distribution, since venting the left ventricle in additional hearts did not result in improved function during reperfusion. Although it would be tempting to conclude that BDM protected ischemic myocardium by preventing ischemic contracture, administration of BDM was also associated with reduced depletion of ATP during ischemia, perhaps related to diminished energy demand. To distinguish between the relative importance of inhibiting contracture from provision of adequate energy, the period of ischemia was extended to 120 minutes. BDM still prevented ischemic contracture (LVEDP, 10 +/- 6 mm Hg) and preserved ATP stores, but it did not prevent membrane damage (CK release, 483 +/- 254 U/g dry weight) or contractile failure during reperfusion (LVDP, 68 +/- 7% of baseline). In contrast, increasing the rate of anaerobic glycolysis during ischemia by doubling glucose and insulin in the presence of BDM markedly decreased membrane damage (CK release, 114 +/- 72 U/g dry weight; P < .05) and contractile failure during reperfusion (LVDP, 88 +/- 7% recovery of baseline; P < .01). These results suggest that insufficient energy production is primarily responsible for myocardial ischemic damage, whereas mechanical effects of ischemic contracture appear to play only a minor role.
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PMID:The relative importance of myocardial energy metabolism compared with ischemic contracture in the determination of ischemic injury in isolated perfused rabbit hearts. 815 29

The objective of this study was to determine the pumping capability of dynamic cardiomyoplasty during induced ventricular fibrillation. In this acute study of 6 dogs, the pumping capability of the unconditioned left latissimus dorsi (LD) muscle (141 to 292 gm), wrapped around both ventricles, was investigated during induced ventricular fibrillation. Left-ventricular and femoral artery pressure, the ECG and aortic root flow velocity were monitored. Prior to inducing ventricular fibrillation, the ability of the unconditioned LD muscle to augment stroke volume (SV), was quantified as the area under the aortic flow-velocity record. The ventricles were then fibrillated and, after 10 sec, rhythmic 250 msec trains (1/sec) of stimuli (40/sec) were delivered to the thoracodorsal nerve to contract the LD muscle tetanically. In no case could dynamic cardiomyoplasty produce the same SV as when the ventricles were beating normally. In one animal, the SV attained two percent of the normal SV by 5 contractions; in another, the SV reached one percent by 25 contractions. In the remaining animals, the SV varied around 20% of the prefibrillation SV. By 90 contractions, the stroke volume was 10% of the prefibrillation value. The progressive decrease in SV was likely a consequence of LD muscle ischemia and fatigue, since the latissimus dorsi muscle provided low blood flow during the period of fibrillation.
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PMID:Stroke volume with dynamic cardiomyoplasty during ventricular fibrillation in the acute dog. 820 83

The pathogenetic mechanisms of chronic muscle pain are not known, but may be related to incomplete recovery between bouts of work. During monotonous repetitive static muscle contraction, fatigue develops gradually, parallel to an increase in oxidative metabolism combined with a change in Ca(2+)-homeostasis in a few muscle fibres. Ischemia or high lactate probably do not contribute to fatigue in this state. We review some recent results on muscle fatigue during a low force static work situation and also discuss the significance of K+ released from muscle as an important extracellular messenger.
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PMID:[Can processes connected to muscular activity explain development of chronic pain?]. 820 18

Recent studies have shown a lack of an increase in muscle sympathetic nerve activity (MSNA) during leg exercise. Experiments using isometric knee extension (IKE) have shown a biphasic response in MSNA with a decrease during the 1st min and a return of MSNA to control levels during the 2nd min of IKE. Moreover, MSNA was not augmented during postexercise muscle ischemia (PEMI) of the exercising leg, suggesting that the muscle metaboreflex may have not been engaged in these experiments. The purpose of the present study was 1) to examine MSNA during IKE performed to fatigue to determine whether MSNA could be increased with leg exercise and 2) to determine whether increases in MSNA during fatiguing IKE were associated with an augmented MSNA response during PEMI. IKE was initially performed to fatigue at 30% of maximal voluntary contraction in the sitting position (n = 7; trial 1). IKE elicited a marked increase in mean arterial pressure and heart rate (P < 0.01). Total MSNA (burst frequency x mean burst amplitude; units) in the contralateral leg increased 96 +/- 40% (P < 0.01) above control levels during the final 30 s of IKE (207 +/- 23 s). Subjects (n = 8) then performed IKE to fatigue followed by PEMI (trial 2). MSNA in the contralateral leg increased 107 +/- 50% (P < 0.01) above control levels during the final 30 s of IKE (169 +/- 12 s) and remained significantly elevated during PEMI (83 +/- 40% above control), indicating that the muscle metaboreflex was engaged during fatiguing IKE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmentation of muscle sympathetic nerve activity during fatiguing isometric leg exercise. 837 68

This study assesses the safety of and physiologic responses to maximal repetition, dynamic, resistive weight lifting at 40, 60, 80 and 100% of maximal voluntary contraction compared with aerobic exercise using a maximal treadmill exercise test. Twelve men with coronary artery disease exercised to fatigue at 4 stations (overhead press, biceps curl, quadriceps extension and supine press). The electrocardiogram was monitored continuously. Heart rate and systolic and diastolic blood pressures (by sphygmomanometer) were measured at rest and during peak exercise. No symptoms or electrocardiographic evidence of ischemia occurred with weight lifting, whereas 5 of 12 patients had ischemic ST-segment depression (> or = 1 mm) with the treadmill. No significant ectopy occurred with either activity. Mean peak heart rates with all lifts were less (range 74 to 92 beats . min-1; p < or = 0.05) than with the treadmill (157 beats . min-1). Peak systolic blood pressures were similar, whereas peak diastolic blood pressures were greater with all lifts (range 93 to 117 mm Hg; p < or = 0.05), except 100% maximal contraction biceps curl and quadriceps extension, than with the treadmill (79 mm Hg). Peak rate pressure product was greater with the treadmill than with all lifts (p < or = 0.05). Diastolic time interval from the electrocardiograph was shorter with the treadmill (0.154 second) than with all lifts (range 0.323 to 0.448 second; p < or = 0.05). Diastolic pressure-time index was greater with all lifts than with the treadmill (p < or = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Physiologic responses to weight lifting in coronary artery disease. 842 69

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67

The purpose of this study was to evaluate the effects of U74006F, a new antioxidant, on isometric contractile function after tourniquet-induced ischemia-reperfusion injury. Twenty-six NZW rabbits underwent either 2 or 4 hr of thigh tourniquet compression. Animals were randomized to receive U74006F or an equal volume of its citrate vehicle. When tibialis anterior function was tested 2 days later, there was no difference between treatment groups in peak tension, rate of force production, contraction time, half relaxation time, or resistance to fatigue. The use of U74006F failed to improve functional outcome in this model of ischemia-reperfusion injury.
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PMID:Effects of an antioxidant in a rabbit model of tourniquet-induced skeletal muscle ischemia-reperfusion injury. 859 19

The metabolic effects of partial ischemia on canine skeletal muscle were examined during 20 min of isometric contraction. A reduction in blood flow of approximately 75% resulted in an approximate 40% reduction in contractile function. Muscle lactate accumulation and phosphocreatine (PCr) hydrolysis were greater during ischemia, indicating a greater reliance on anaerobic ATP regeneration. Pyruvate dehydrogenase transformation to its active form (PDCa) during contraction was not affected by ischemia, such that PDCa did not appear to be a determinant of skeletal muscle fatigue. Acetylcarnitine concentration was greater during ischemic contraction and inversely correlated with PCr concentration (r = -0.79, P<0.01). Furthermore, acetylcarnitine accumulation and PCr degradation correlated with the degree of skeletal muscle fatigue (r = 0.56, P<0.05 and r = 0.70, P<0.01, respectively). Thus the greater the acetyl group oxidation, the lesser the contribution from anaerobic ATP provision and, subsequently, the smaller the degree of muscle fatigue observed. The metabolic characteristics of this model of ischemic muscle contraction are indistinguishable from the normal metabolic responses observed with increasing contractile intensity.
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PMID:Metabolic responses of canine gracilis muscle during contraction with partial ischemia. 863 84


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