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)

Digitalis and diuretics constitute conventional therapy of congestive heart failure, but systemic vasodilators offer an innovative approach in acute and chronic heart failure of decreasing increased left ventricular systolic wall tension (ventricular afterload) by reducing aortic impedance and/or by reducing cardiac venous return. Thus, vasodilators increase cardiac output (CO) by diminishing peripheral vascular resistance (PVR) and/or decrease increased left ventricular end-diastolic pressure (LVEDP) (ventricular preload) by diminishing venous tone. Concomitantly, there is reduction of myocardial oxygen demand, thereby reliably reducing angina pectoris in coronary disease, and potentially limiting infarct size and ischemia provided systemic arterial pressure remains normal. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (decrease LVEDP); nitroprusside, phentolamine and prazosin produce balanced arterial and venous dilation (decrease LVEDP and increase CO) provided left ventricular filling pressure is maintained at the upper limit of normal; whereas hydralazine predominantly effects arteriolar dilation (increases CO). With depressed CO plus highly increased LVEDP and increased PVR, nitrates also induce some increase of CO by reducing PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. The 30-minute venodilator action of sublingual nitroglycerin is extended for 4 to 6 hours by cutaneous nitroglycerin ointment, by sublingual and oral isosorbide dintrate, and by oral pentaerythritol tetranitrate and sustained-release nitroglycerin capsules. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (relieve pulmonary congestion); hydralazine (improves fatigue); prazosin alone, combined nitrate-hydralazine combined prazosin-hydralazine (improve both dyspnea and fatigue).
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PMID:Afterload reduction and cardiac performance. Physiologic basis of systemic vasodilators as a new approach in treatment of congestive heart failure. 9 30

The purpose of this study was to investigate the effect of changes in developed tension on the ratio between O2 uptake and isometric developed tension in the in situ dog gastrocnemius-plantaris muscle group. O2 uptake and isometric developed tension of the muscle were measured during contractions at 1 twitch/s before and after fatigue with both single and twin impulses (6.5 V, 0.2-ms duration; the twins were separated by 10--20 ms). Twin impulses prior to fatigue raised developed tension to two times the tension developed with single impulses. Fatigue was obtained by stimulation at 10--20 impulses/s for 30--40 min. Twin impulses after fatigue returned developed tension to the level of single impulses before fatigue. O2 uptake and developed tension were also measured during the slower development of fatigue produced by continuous stimulation (3, 4, 5, and 6 impulses/s) as well as during "fatigue" induced by partial neuromuscular block with curare or ischemia. In all cases, there was no change in the O2 uptake per unit of tension developed, indicating a constant coupling between O2 uptake and developed tension.
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PMID:O2 uptake and developed tension during and after fatigue, curare block, and ischemia. 21 84

A constant-flow, cross-perfused, vascularly isolated gracilis muscle preparation was used to examine the hypothesis that locally produced and released products of ischemic muscle metabolism are responsible for the vascular decompensation (vasodilation) reported to occur in late oligemic hypotension. Well-oxygenated donor arterial blood perfused recipient gacilis muscles at a constant flow rate of 5.2 +/- 0.5 ml/100 gm/min while the recipient animals were subjected to a modified Wigger's hemorrhage protocol. Arterial and venous blood gases taken across the gracilis muscle at regular intervals during the experiments verified adequate tissue perfusion. Of the thirteen studies reported, only ten shocked recipient dogs progressed to irreversible shock postreinfusion. This series was identified as the "recipient-irreversibly shocked group." The remaining three shocked animals recovered from the shock protocol and were labeled "recipient-reversibly shocked series." The initial response to blood loss in both groups was intense vasconstriction, with the greatest initial constriction occurring in the irreversibly shocked series. The three animals that survived the protocol were able to sustain this compensatory effort, but the ten that ultimately progressed into irreversible shock postreinfusion invariably demonstrated a significant loss of vascular tone during late oligemia (conductance rose from 43% to 63% of control). Thus evidence is presented which indicates decompensation during adequate tissue perfusion, or absence of ischemia. A strong correlation was also shown to exist between sustained compensatory vasoconstriction in the gracilis muscle, and survival. The suggestion is made that part of the loss of vascular tone may be related to prejunctional inhibition of adrenergic transmission or alpha-receptor fatigue, with a minor role being played by the vasodepressor products of local tissue ischemia.
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PMID:Correlation between skeletal muscle vascular decompensation and survival: roles of tissue ischemia and innervation. 45 92

The effects of the beta-adernergic blocking drug acebutolol were studied in 23 patients with angina pectoris and angiographically documented coronary artery disease. Patients were evaluated clinically, by graded treadmill testing and by 24-hour Holter monitoring in the control state, after 2 weeks treatment with placebo, and after 2 weeks treatment with 600 mg. and then 1,200 mg. of acebutolol. Acebutolol (in a daily dose of 600 mg.) was an effective antianginal drug: the number of clinical attacks of angina pectoris (p less than 0.001) and the consumption of sublingual nitrate decreased (p less than 0.01), there was a significant increase in the treadmill effort tolerance as measured by the time to appearance of ischemic ECG changes (p less than 0.001) and the total work performed (p less than 0.001), and there was also a significant decrease in ischemic ST segment depression on 24-hour Holter monitoring. Treatment with 1,200 mg. acebutolol was associated with a further decrease in heart rate and a further improvement in effort tolerance on treadmill testing (p less than 0.05). On the large dose of the drug, however, there was no further clinical improvement, and no further improvement on 24-hour ECG monitoring; several patients complained of weakness and fatigue. Graded treadmill testing was an excellent objective method for assessing physical effort tolerance and its improvement after treatment with the beta-blocking drug. Twenty-four-hour Holter monitoring was a useful and complementary test, especially in patients who stopped exercising on the treadmill because of fatigue or weakness, and especially for assessing the efficacy of beta-blockade in controlling emotionally induced tachycardia and ischemia in the patient's own daily environment.
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PMID:Evaluation of the beta-blocking drug acebutolol in angina pectoris. 49 6

When exercise testing 159 patients with prior myocardial infarction, we identified 39 who were limited by fatigue. This group was all in sinus rhythm; none were taking drugs likely to impair the chronotropic response of the heart; none experienced chest pain or developed ischemic ECG changes. In 18 of this group, maximal heart rate achieved with exercise was 2SD or more below the age predicted value, and their heart rate response to exercise was reduced compared to that of the other 21 whose maximal exercise heart rates were within 2SD of age predicted values. A subgroup of 8 subjects with reduced exercise heart rates was studied before and after vagal blockade. In the 4 subjects whose infarction was inferior, the reduction in heart rate response was more profound and persisted after vagal blockade, suggesting either reduced pacemaker responsivness, due to ischemia or infarction, or autonomic imbalance as possible mechanisms. All 8 showed alinear increases in ventilation at higher power outputs and mean blood lactate postexercise was 7.5 mM/I without vagal blockade. Our findings suggest that a reduced heart rate response to exercise, already shown to imply added coronary risk, may be subdivided aetiologically and possibly prognostically. The use of a "Target Heart Rate" in such patients offers no safety margin, and maximal exercise capacity will be grossly over-estimated if extrapolated from the submaximal heart rate response. A cardiovascular limitation to exercise may be detected by an alinear increase in ventilation.
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PMID:Reduced heart rate response to exercise in ischemic heart disease: the fallacy of the target heart rate in exercise testing. 52 31

The effect of 1.5 to 2.5 h tourniquet ischemia on energy metabolism of the quadriceps muscle was studied using percutaneous needle biopsy technique in sixteen patients operated on for an inveterated knee injury. During occlusion there was a moderate decrease in ATP with an increase in ADP and AMP. This change resulted in a decreased energy charge potential. At the same time phosphorylcreatine (PC) decreased markedly while creatine (Cr) increased giving a constant total creatine (TCr). An accumulation of lactate during occlusion with values up to 80 mmol/kg d.m. (dry muscle) was seen. A 15% reduction in glycogen was calculated. After release of the tourniquet the active phosphate concentration and the energy charge potential returned to basal levels within 5 min and most of the metabolites in the glycolytic sequence were also normalized. Muscle lactate content was normal after 30 min of intact circulation. The results suggest that longterm tourniquet ischemia induces marked changes in energy metabolism in skeletal muscle, but that the changes are rapidly and completely reversible with restoration of blood flow.
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PMID:The effect of long-term arterial occlusion on energy metabolism of the human quadriceps muscle. 52 75

Following simultaneous ligation of the aorta and femoral artery in the cat, organelles accumulated in distal portions of the sciatic nerve and in lower portions of the tibial and peroneal nerves. The accumulations were located in the proximal and distal ends of the nerve infarction and delineated the borders of the necrotic area. Topographical analysis of the necrosis and organelle accumulations following ligation of these main arteries showed the larger nerve fascicles to be more sensitive to ischemia than the smaller ones. The center of a nerve fascicle was more sensitive than the periphery. The organelles accumulated in ischemic nerves during the first hours after arterial ligation, presumably as a result of lack of energy for fast axoplasmic transport. Later accumulations reflected mechanical block of axoplasmic transport due to focal necrosis of the nerve. The content of organelle accumulations was similar to that found in lesions resulting from transection except for the presence of 60 to 70 A filaments at the distal end of the infarction.
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PMID:Peripheral nerve ischemia: Part 2. Accumulation of organelles. 74 48

The sensitivity of myocardial perfusion imaging (MPI) using thallium-201 injected both at rest and during peak exercise was compared to simultaneously recorded 12 lead electrocardiography (ECG) for the detection of transient ischemia in 20 normal subjects and 63 patients with coronary artery disease (CAD). No significant perfusion defects or ECG changes were seen on either the rest or exercise studies in any of the normal subjects. Fifty-six percent of patients with CAD developed new perfusion defects with exercise compared to 38% who developed ischemic ST-segment depression (P less than 0.02). However, when chest pain and/or ST depression were considered indices of ischemia, the sensitivity of exercise testing and thallium-201 MPI was similar. The increased sensitivity of MPI compared to ST-segment depression on the ECG was due to patients with baseline ECG abnormalities and those who failed to achieve 85% of predicted maximum heart rate with exercise. Analysis of the exercise results according to the extent of coronary artery disease revealed a progressive increase in both positive ECGs and MPI with the number of vessels involved. In patients with single vessel disease the MPI was more sensitive than the ECG (P less than 0.02). The combination of the rest and exercise ECG, MPI and chest pain during exercise failed to identify 11% of patients with CAD. Exercise thallium-201 MPI is a useful adjunct to conventional exercise testing particularly when evaluating patients with abnormal resting ECGs, those who develop ventricular conduction defects of arrhythmias during exercise, and those who fail to achieve their predicted heart rate because of fatigue or breathlessness.
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PMID:Thallium-201 myocardial perfusion imaging at rest and during exercise. Comparative sensitivity to electrocardiography in coronary artery disease. 83 Feb 22

Variations of the soleus H-reflex were studied during voluntary isometric or anisometric contractions of the tibialis anterior in man. At the onset of isometric contractions there was a weak inhibition of the soleus H-reflex, which was not related to the force of the tibialis anterior contraction. 110 msec after the onset of the EMG activity, the inhibition became secondarily more marked and was then related to the force of the contraction. This secondary potentiation of the H-reflex inhibition is brought about by group I fibres activity, since it was markedly reduced during ischemia of the leg. It persisted during local muscular fatigue, this indicating that Ib fibres from tibialis anterior are not involved and that, by the process of elimination, group Ia fibres must be responsible for the supplementary secondary inhibition. It is concluded that the early inhibition is only due to suprasegmental activity, whereas during the secondary part of the inhibition there is a supplementary inhibitory action brought about by Ia fibres from tibialis anterior. The secondary potentiation of the inhibition is therefore likely to be produced via the gamma loop.
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PMID:Role of Ia afferents in the soleus motoneurones. Inhibition during a tibialis anterior voluntary contraction in man. 85 19

The author describes a family (48 year old mother and 15 year old son) with the muscular variant of glycogenosis-McArde's metabolic myopathy. The mother has been ill since 22 years old, the son--since 7. The disease had a slowly progressive development. The clinical picture was characterized by convulsions of the type of cramps following physical loadings on muscles of the body and extremities. Convulsions were accompanied by pain, an induration and enlargment of the muscles, muscle fatigue and increased significantly in an artifical ischemia of the extremities. A histochemical study of the muscle revealed a pathological accumulation of glycogen. The content of lactic and pyruvic acid in the blood after work in ischemic conditions did not change significantly. A study of the sugar curve in the blood with a loading with glucose and a parallel determination of insulin by a radioimmune method found hyperinsulinemia and a dysfunction of the pancreas.
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PMID:[McArdle's disease (a familial case)]. 106 64


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