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)

Sixty-five patients with ST elevation were retrospectively studied in order to evaluate the clinical significance and underlying mechanisms of ST-segment elevation during exercise. Of these, 50 patients had previous myocardial infarction (Group I) and 15 patients did not (Group II). Exercise thallium-201 imaging was performed on 30 patients, resting gated blood pool imaging was performed on 33 patients, and 23 underwent cardiac catheterization for clinical indications. When the two groups were compared, patients in Group I had more frequent multivessel disease (9/13 vs. 3/10, p less than 0.05), anterior infarctions (33/50 vs. 4/10, p less than 0.02), while Group II patients had more frequent single-vessel disease (7/10 vs. 4/13, p less than 0.05). For Group I patients, the most common reason for termination of exercise was fatigue and/or dyspnea (35/50 vs. 0/15, p less than 0.05), with an irreversible defect noted in both stress and delayed views on thallium imaging (20/24 vs. 1/6, p less than 0.05). In Group II, the most common reason for termination was angina (15/15 vs. 2/50, p less than 0.001), with reversible thallium defects noted more frequently (4/6 vs. 3/24, p less than 0.01). Thus, we conclude that in patients with Q waves, left ventricular dysfunction rather than ischemia is the mechanism for ST elevation. In these patients angina is rare, but fatigue, dyspnea, multivessel disease, and fixed thallium defects are common. In patients with non-Q-wave exertional ST elevation, ischemia is the rule, manifested by frequent chest pain and reversible thallium defects.
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PMID:The role of ischemia and ventricular asynergy in the genesis of exercise-induced ST elevation. 335 73

Surgical instruments should be designed to optimize control and interact with tissues or other objects while avoiding surgeon fatigue, muscle spasms, tissue ischemia, and injuries. Several well-established ergonomic criteria can be used in the design of instruments. Analysis of some commonly used bone biting instruments reveal how they violate these criteria. The thoughtful redesign of instruments using these principles is recommended.
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PMID:Ergonomic considerations in the design of neurosurgery instruments. 340 42

Twenty male college students served as subjects for a study which investigated how artificially-induced ischemia, with and without muscular fatigue, affects the: 1) input/output (IEMG/Force) relationship, and 2) power density spectrum of EMG signals during submaximal static contractions. In the first experiment, subjects maintained constant-force (60% MVC) static handgrip contractions for 55 sec. Following exercise, EMG mean power frequency (MPF) was significantly (P less than 0.05) reduced and EMG amplitude (rmsEMG) was significantly (P less than 0.05) increased. With circulation intact during 5 min recovery, MPF and rmsEMG values returned to pre-exercise levels. With ischemic recovery, MPF remained significantly (P less than 0.05) lower than pre-exercise values, while rmsEMG returned to approximately normal levels. In the second experiment, subjects performed either 3 sec ramp (90 N/sec) or constant-force (40% MVC) contractions immediately before, during the final 3 sec of, and 1, 3, 5 and 10 min after a 10 min tourniquet application. No statistically significant differences (P greater than 0.05) in the IEMG/Force slope coefficients, IEMG/Force ratios or MPF were observed for subjects performing either static ramp or constant-force contractions following temporary ischemia. Results suggest that reduced blood flow may contribute to fatigue-induced EMG changes. However, in the absence of motor activity, ischemia is an insufficient stimulus to cause either increased amplitude or frequency shift of the EMG signal during static contractions.
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PMID:Effects of ischemia on myo-electrical signal characteristics during rest and recovery from static work. 343 27

The relationship between muscle fibre conduction velocity (MFCV) and the power spectrum of surface EMGs in 3 human volunteers was studied during isometric contractions at 40% maximum voluntary contraction. In addition, the recovery of these two parameters was measured during short lasting contractions at the same force level every 30 s. The recovery phase was also studied during ischaemia, thereby preventing the recovery of MFCV. The mean MFCV was calculated by the cross-correlation method. The measurements were facilitated by a real-time estimation of the cross-correlation and the MFCV and by a graphic display of the digitised signal. During contraction a nearly linear relation was found between MFCV and the median frequency of the power spectrum (MPF). During recovery this relationship was lost in one subject: MPF restored much faster then MFCV. During recovery under ischemia MFCV did not recover, but MPF recovered partially in all subjects. It is concluded that the shift of the power spectrum to lower frequencies during fatigue cannot be explained by changes in MFCV alone. Central mechanisms also influence the power spectrum and studying the recovery of local muscle fatigue during ischemia may separate these influences from that of MFCV on the power spectrum during fatigue.
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PMID:Relationship between average muscle fibre conduction velocity and EMG power spectra during isometric contraction, recovery and applied ischemia. 356 28

Rat slow-twitch muscle, in contrast to fast-twitch muscle, maintains its ATP content near normal during intense stimulation conditions that produce rapid fatigue. An extensive depletion of adenine nucleotide content by the deamination of AMP to IMP + NH3, typical of fast-twitch muscle, does not occur. We evaluated whether this response of slow-twitch muscle could be simply due to failure of synaptic transmission or related to cellular conditions influencing enzyme activity. Stimulation of soleus muscles in situ via the nerve or directly in the presence of curare at 120 tetani/min for 3 min resulted in extensive fatigue but normal ATP contents. Thus the lack of ATP depletion must be related to cellular events distal to neuromuscular transmission. Even nerve and direct muscle stimulation (with curare) during ischemia did not cause a large depletion of ATP or a large elevation of lactate content (12.0 +/- 0.7 mumol/g), even though the decline in tension was essentially complete. However, if the same tension decline during ischemia was prolonged by stimulating for 10 min at 12 tetani/min a large decrease in ATP (2.24 +/- 0.09 mumol/g) and increase in IMP (2.47 +/- 0.16 mumol/g) and lactate (30.4 +/- 2.0 mumol/g) content occurred. Thus adenine nucleotide deamination to IMP can occur in slow-twitch muscle during specific contraction conditions. The cellular events leading to the activation of AMP deaminase require an intense contraction condition and may be related to acidosis caused by a high lactate content.
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PMID:ATP depletion in slow-twitch red muscle of rat. 363 Dec 51

Treadmill exercise tests were carried out in 397 women, aged 20 to 69, who were selected at random from an unorganized population. Four types of response were identified: ischemia, reduced stress tolerance due to excessively elevated systolic arterial blood pressure or other causes; reduced stress tolerance due to premature muscular fatigue or dyspnea (in less than 9 minutes of exercise) and the adequate type. The parameters of adequate response to physical stress were established. The incidence of ischemic response was relatively small in women, as compared to men. Ischemic response was only seen in women between 50 and 69 years of age, making a 4.5% rate.
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PMID:[Characteristics of the adequate and pathological reactions to the standard treadmill test in a female population 20 to 69 years old]. 376 33

This investigation was undertaken in patients who had an acute myocardial infarction 12.6 +/- 0.4 months earlier to determine, using conventional methods, the nature of stroke volume changes during training regimens. Twenty-seven patients (mean age 52 +/- 2 years; rest ejection fraction 49 +/- 2%; New York Heart Association functional class I or II) and 9 normal, age-matched sedentary control subjects (mean age 50 +/- 1 years) exercised in the upright position on a bicycle ergometer. Stroke volume was measured by impedance cardiography at rest and after each workload. Ten patients (group A) had a stroke volume response similar to that of the normal sedentary subjects. In 8 patients (group B) the stroke volume increased initially, then decreased (more than 15%) at heart rates (HRs) greater than 100 to 105 beats/min. Nine patients (group C) had a flattened stroke volume response throughout exercise. Training HR determined by conventional methods corresponded to a maximal stroke volume in the normal subjects. Training HR in group A corresponded to a stroke volume that was maximal or near-maximal. Training HR in group B corresponded to a maximal or diminishing stroke volume. In group C, the training HR corresponded to a stroke volume no different from that at rest. Thus, training HR determined by conventional methods based solely on the chronotropic responses to exercise may place patients who have abnormal stroke volume responses to upright exercise in a situation during training sessions in which an inappropriately high HR, excessive fatigue or silent ischemia may develop.
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PMID:Importance of considering ventricular function when prescribing exercise after acute myocardial infarction. 377 45

The regulation of glycogen phosphorylase and glycogen breakdown in human skeletal muscle has been investigated using the needle biopsy technique. Preliminary studies showed that the activity of phosphorylase in vitro was dependent upon the concentration of inorganic phosphate (Pi) used in the assay system. The Km of phosphorylase a for Pi was found to be 26.2 mmol/l, and that of (a+b) (assayed in the presence of saturating AMP) was 6.8 mmol/l. Because of the difference in Km the apparent percentage of a to (a+b) activity varies with the Pi concentration used in the assay system. Phosphorylase a and (a+b) activities were therefore adjusted to saturating Pi concentrations. The ratio of the activities in this case is independent of the Pi concentration and constitutes a minimal estimate of the fraction of phosphorylase molecules in the a form. The fraction of phosphorylase in the a form in resting muscle was as a mean 22%. Despite nearly a quarter of the phosphorylase being in the a form glycogenolytic activity is extremely low. It is proposed that the concentration of Pi at the active site of the enzyme is low compared to the Km for this of either form of the enzyme, and is limiting to activity. A Pi concentration in resting muscle of 1-3 mmol/l was calculated. During epinephrine infusion at rest 90% of the phosphorylase was transformed to the a form but only a moderate increase in the glycogenolytic rate occurred. This rate approximated to 5-10% of the maximum rate of the enzyme (Vmaxa). During prolonged epinephrine infusion the glycogenolytic rate decreased despite the continuance of 90% or more of the phosphorylase in the a form. In contrast to epinephrine infusion prolonged ischemia resulted in a decrease in the mole fraction of phosphorylase a and simultaneously in an increase of the glycogenolytic rate. During isometric and dynamic exercise there was a rapid transformation of phosphorylase b to a paralleled by pronounced increase in the rate of glycogen breakdown. The increased rate of glycogenolysis during isometric exercise was close to the Vmax of phosphorylase a in vivo. When either form of exercise was continued to fatigue/exhaustion, a re-transformation of phosphorylase a to b was observed. During dynamic exercise cAMP in the muscle increased two fold. This increase was blocked by the prior administration of propranolol.+
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PMID:The regulation of glycogen phosphorylase and glycogen breakdown in human skeletal muscle. 613 34

Endorphins and endorphin receptors are believed to modulate pain perception. To investigate whether naloxone, a specific antagonist, could initiate anginal pain during exercise-induced myocardial ischemia in asymptomatic patients with angiographically defined coronary artery disease, a single-blind trial was conducted in 10 men with prior positive exercise electrocardiograms. Multistage treadmill exercise tests were performed twice within a week. On the second test, patients received naloxone, 2 mg intravenously, by a syringe infusion pump. Exercise was terminated because of fatigue in 6 patients and completion of the protocol in 4. No patient reported chest pain during exercise. Naloxone did not significantly alter exercise duration, heart rate, blood pressure and ST-segment changes compared with control testing. It is concluded that endorphins do not play a significant role in the recognition of anginal pain in patients who have asymptomatic exercise-induced ischemia.
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PMID:Naloxone and asymptomatic ischemia: failure to induce angina during exercise testing. 649 61

In five healthy males sustained isometric torques during elbow flexion, knee extension, and plantar flexion correlated positively with intramuscular tissue pressure (MTP) in the range 0-80% of the maximal voluntary contraction (MVC). During passive compression of the muscle at rest 133-Xenon muscle clearance stopped when MTP reached diastolic arterial pressure (DAP) indicating that the muscle vascular bed was occluded. However, during sustained contraction this relation between DAP, flow and MTP was not seen. In two cases 133-Xenon clearance from M. soleus did not stop in spite of an 80% maximal contraction and MTP stayed below DAP. In other cases MTP would reach as high as 240 mm Hg before clearance was zero. In the deeper parts of the muscles MTP during contraction was increased in relation to the more superficial parts. The means values for the % MVC that would stop MBF varied between 50 and 64% MVC for the investigated muscles. Mean rectified EMG (MEMG) showed a high correlation to MTP during sustained exhaustive contractions: When MEMG was kept constant MTP also remained constant while the exerted force decreased; when force was kept constant both MEMG and MTP increased in parallel. This demonstrated that muscle tissue compliance is decreasing during fatigue. Muscle ischemia occurring during sustained isometric contractions is partly due to the developed MTP, where especially the MTP around the veins in the deeper parts of the muscle can be considered of importance. However, ischemia is also affected by muscle fiber texture and anatomical distorsion of tissues.
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PMID:Skeletal muscle tension, flow, pressure, and EMG during sustained isometric contractions in humans. 668 38


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