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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
J Mol Cell Cardiol 1990 Jan
PMID:Na+ accumulation increases Ca2+ overload and impairs function in anoxic rat heart. 215 54

Primary pulmonary hypertension is an enigmatic disease found predominantly in young women, but it also affects a significant number of middle-aged and elderly males and females. Its onset, characterized by progressively worsening dyspnea, fatigue, and chest pain, is insidious. Three distinct histopathologic subtypes have been identified, and the natural history of the disease process has been well-defined. Pharmacologic treatment options have, in general, been disappointing, and it appears that heart-lung transplantation will be applied only to a small minority of young patients with primary pulmonary hypertension in the near future. We review the histopathology, evaluation, treatment, and prognosis of primary pulmonary hypertension.
Clin Cardiol 1990 Jun
PMID:Primary pulmonary hypertension in adults. 218 65

We conducted a study on the clinical and angiographic characteristics of 140 patients with unstable angina. Average age of 57, male/female ratio 4 to 1. The most frequent risk factors: tobacco smoking (73%) and arterial hypertension (42%). They had old infarct (57%), and unstable angina at rest (37%). We did early submaximal stress test to 31% of them; in 38.6% test was stopped due to angina, 25% for fatigue. 91% had ischemic changes, there weren't any severe complications. Regarding significant coronary obstruction: 20% had one vessel, 26% two, 50% three and left trunk 4%. Normal ventriculogram 43%. Eight patients died; the causes were: disease of the trunk (37.5%) and "active" angina (87.5%), 25% during catheterization . All survivors responded to medical treatment. 54 patients were not candidates for surgical treatment, among them 70.3% were released in class I (NYHA). At follow up 90% were in class I-II, 12% had unstable angina recurrence, 3% had acute infarct. In the pathogenesis of unstable angina intervene fixed atherosclerosis, obstructive lesions, repetitive spasms and non-occlusive thrombosis, this physiopathologic behavior is responsible for the stages of ischemic activity. Treatment should be directed to maintain the balance between the distribution and the demand of O2, and also treating spasm and thrombosis.
Arch Inst Cardiol Mex
PMID:[Unstable angina: clinical and angiographic characteristics of 140 cases]. 224 1

The extent to which lipolysis is attenuated during prolonged submaximal exercise during beta blockade was determined in 12 normotensive endurance-trained and 12 hypertensive sedentary men using nonselective drugs with and without intrinsic sympathomimetic activity (ISA). Initially, subjects performed a graded treadmill test to determine maximal oxygen uptake (VO2max). This was followed by 2-hour walks at 25 and 45% of the subject's VO2max under each of 3 treatments: pindolol (ISA), propranolol (non-ISA) and placebo. The distribution of medication was randomized and double blinded. Blood samples taken at rest and every 30 minutes during the 2-hour walks were analyzed to determine the concentrations of free fatty acids (FFA) and glycerol. On the basis of the respective changes in FFA, glycerols and the respiratory exchange ratio, beta-adrenergic blockade did not attenuate lipolysis in the untrained hypertensive subjects when compared with the placebo administration. However, beta blockade did demonstrate a tendency to attenuate lipolysis in the trained, normotensive subjects when compared with results after placebo administration. This was particularly evident at 30 minutes of exercise, when both glycerol and FFA concentrations were not increased above resting values under both conditions of beta blockade. No differences between pindolol and propranolol were observed. Therefore, a beta-blocking agent with ISA properties appears to have no clear benefit with respect to lipid metabolism during low and moderate intensity exercise. Furthermore, these data demonstrate that beta blockade does not inhibit exercise-induced lipolysis at low and moderate intensities of exercise as formerly believed, and is unlikely to be the cause of fatigue normally observed during work in patient populations taking beta-blocking medication.
Am J Cardiol 1990 Dec 01
PMID:Changes in plasma free fatty acids and glycerols during prolonged exercise in trained and hypertensive persons taking propranolol and pindolol. 224 64

In vivo nuclear magnetic resonance (NMR) spectroscopy was used to define several intracellular high energy phosphate variables of the gastrocnemius muscle of normal subjects during rest, graded plantar flexion exercise to exhaustion, and recovery. There were nine males and eight females with an average age of 34 +/- 8 years. At rest, pH averaged 7.09 +/- 0.03 and the energy cost index (ECI)--the ratio of inorganic phosphate to phosphocreatine--averaged 0.13 +/- 0.03. At peak exercise, the ECI increased markedly to 2.71 +/- 2.0 (P less than 0.001) and pH fell precipitately to 6.76 +/- 0.17 (P less than 0.001), indicating the high intensity of the exercise. Exercise endurance averaged 12 +/- 5 mins; it was not highly correlated with sex, age (r = 0.35), rest pH (r = 0.26), rest ECI (r = 0.38), peak exercise pH (r = 0.23) or peak exercise ECI (r = 0.38), nor exercise changes in pH (r = 0.17) and ECI (r = 0.28). At 23 mins post exercise all variables were similar to rest. Rest pH was the only variable different between males (7.10 +/- 0.03) and females (7.07 +/- 0.03) (P less than 0.05). Thus, dynamic exercise of large skeletal muscles in normal subjects was characterized by marked temporal changes in high energy phosphate profiles and very low pH at exhaustion. No single metabolic variable correlated highly with exercise endurance, suggesting that the intracellular pathophysiology of exhaustive muscle exercise and clinical fatigue may be multifactorial.
Can J Cardiol 1990 Nov
PMID:Metabolism of normal skeletal muscle during dynamic exercise to clinical fatigue: in vivo assessment by nuclear magnetic resonance spectroscopy. 227 74

Hemodynamic and metabolic changes were measured at rest and during exercise in 23 patients with chronic heart failure and in 6 control subjects. Exercise was limited by leg fatigue in both groups and capacity was 40% lower in the patients with failure. At rest, comparing patients with control subjects, heart rate and right atrial and pulmonary wedge pressure were higher; cardiac output, stroke volume and work indexes and ejection fraction were lower; mean arterial and right atrial pressure and systemic resistance were similar. During all phases of exercise in patients with heart failure, pulmonary wedge pressure and systemic vascular resistance were higher and pulmonary vascular resistance remained markedly elevated compared with values in control subjects. Cardiac output was lower in the patients with failure, but appeared to have the same physiologic distribution in both groups during exercise. Although arterial-femoral venous oxygen content difference was higher in patients with heart failure, this increase did not compensate for the reduced blood flow. Even though the maximal oxygen consumption was significantly reduced, femoral venous lactate and pH values were higher than values in control subjects, but femoral venous pH was similar in both groups at their respective levels of maximal exercise. Ejection fraction was lower in those with heart failure at rest and did not increase with exercise. Ventilation in relation to oxygen consumption was higher in patients with failure than in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1990 Apr
PMID:Hemodynamic and metabolic basis of impaired exercise tolerance in patients with severe left ventricular dysfunction. 231 88

A 37 year old man was referred to our institution because of a cardiac murmur, exertional dyspnea and fatigue, symptoms that began since 18 years of age. He reported a cardiac murmur since childhood, with no past history of rheumatic fever or infectious endocarditis. On clinic examination there was a systolic-diastolic murmur louder in the third and fourth left intercostal space, just at the sternal left border. The 2 D-echo revealed a small disruption in the aorto-septal continuity. Right heart catheterisation was performed, showing an increased pressure in the pulmonary artery and right ventricle; an increase in the oxygen saturation on the right heart chambers, suggested the presence of a left-to-right shunt, nevertheless the exact location of the defect was not possible to recognise. The study was complemented with Doppler color flow imaging that revealed a turbulent flow through the defect, with blood flowing from the aortic root into the right ventricular outflow tract. The diagnosis of ruptured aneurysm of sinus of Valsalva was made, being confirmed later by aortic angiography. A rare case is reported in which an aneurysm of the right coronary sinus ruptured into the right ventricle; we emphasize the important contribution of the Doppler color flow imaging to the correct diagnosis, technique rarely described in this type of complication.
Rev Port Cardiol 1990 Jan
PMID:[Ruptured aneurysm of the sinus of Valsalva into the right ventricle--apropos of a case]. 232 38

Eleven cases with 13, incidentally found coronary-pulmonary fistulous communications were discovered out of about 11,000 diagnostic coronary angiograms performed in different patients, over the period 1968 to 1989. These patients were followed-up for an average period of 4.4 years (range 2-11 years). The majority had a fistulous malformation originating from the proximal part of the left anterior descending artery and terminating in the pulmonary trunk. In three subjects, the right coronary artery participated in formation of the shunt. The fistulas consisted either of a convoluted mass of serpentive vessels, sometimes with aneurysmal formation, or of a solitary single vessel. Angina pectoris, atypical chest pain and fatigue were the most common symptoms. All patients were treated conservatively except one, who underwent ligation of the fistula and coronary arterial bypass grafting. Two subjects are still free of symptoms. No death occurred. None of the patients developed subacute bacterial endocarditis, acute myocardial infarction or left ventricular failure during the period of follow-up of more than four years. Three individuals, prior to the follow-up period, had suffered myocardial infarction contralateral to the shunt. They had no recurrence.
Int J Cardiol 1990 May
PMID:Coronary-pulmonary fistula: long-term follow-up in operated and non-operated patients. 236 8

Key safety parameters of sotalol were examined in 1,288 patients entered into recent controlled trials of ventricular (85% of patients) or supraventricular arrhythmias (15%). Most patients were middle-aged male Caucasians with significant heart disease. The most serious adverse event was proarrhythmia, occurring in 56 patients (4.3%). Of these, 27 had hemodynamic compromise due to malignant ventricular arrhythmias. Most had a history of sustained ventricular tachycardia, myocardial infarction, congestive heart failure (CHF) or cardiomyopathy, or a combination of these. The other 29 had nonsevere events; 38% continued taking sotalol. Proarrhythmia was manifested by torsades de pointes in 24 of the 56 patients. No universal causal relation was found with commonly associated factors such as bradycardia, hypokalemia and long QT interval. The mean QT and QTc at baseline within 1 week of a severe proarrhythmic event were greater than those of patients not having proarrhythmia. Nineteen patients (1%) discontinued therapy with sotalol because of drug-related CHF. Predisposing conditions included low initial baseline ejection fraction, history of CHF, cardiomyopathy or cardiomegaly, or both, male gender and age greater than 65 years. Heart failure usually occurred within 7 to 30 days of initiating therapy. The most common reason for premature discontinuation of the drug in patients treated for sustained ventricular tachycardia was ineffectiveness (39%), whereas adverse effects were the most common reasons among patients treated for complex ventricular ectopy (21%). Dyspnea and bradycardia were the most common cardiovascular effects, and fatigue, dizziness and asthenia the most common noncardiac, adverse effects. Although frequently reported, these adverse effects resulted in discontinuation of only 1 to 4% of the patients at risk.(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1990 Jan 02
PMID:Clinical safety profile of sotalol in patients with arrhythmias. 240 37

Sotalol is a unique beta-adrenergic blocking agent with additional actions characteristic of Vaughn-Williams class III antiarrhythmic agents in experimental models. To test the efficacy of sotalol to suppress ventricular arrhythmias, a 6 week parallel, placebo-controlled out-patient study of two doses (320 and 640 mg/day, in two divided doses) was performed in four hospitals in 56 patients with chronic premature ventricular complexes at a frequency of 30/h or more (mean +/- SE, 528 +/- 60/h) on 48 hour ambulatory electrocardiographic recording. During a placebo week, no change occurred in arrhythmia frequency (532 +/- 76/h). Subsequent sotalol therapy significantly reduced median arrhythmia frequency in patients receiving both low (n = 19) and high (n = 18) doses compared with that in patients receiving placebo (by 77 and 83%, respectively, versus 6%; p less than 0.001). Twenty-two (59%) of 37 sotalol-treated patients, 11 in each group, reached the prospectively defined criterion of efficacy (greater than or equal to 75% arrhythmia reduction) versus 2 (11%) of 19 placebo control patients (p less than 0.001). Sotalol reduced the median frequency of couplets by 94% (p less than 0.0001) and that of runs by 89% (p less than 0.0007). The electrocardiographic effects of sotalol included reductions in heart rate (by 17 to 27%) and increases in the QTc (by 6 to 9%) and PR (by 6%) intervals. Ejection fraction was unchanged. The most common adverse side effect was fatigue, but drug discontinuation was required in only three patients taking 640 mg/day. No proarrhythmic events or biochemical abnormalities were observed. In summary, sotalol displays significant antiarrhythmic activity of moderately high degree with good tolerance in doses of both 320 and 640 mg/day. Its antiarrhythmic actions are distinguished from those reported for other beta-blockers by its effects on the QTc interval and its moderately high degree of antiarrhythmic activity.
J Am Coll Cardiol 1986 Oct
PMID:Multicenter trial of sotalol for suppression of frequent, complex ventricular arrhythmias: a double-blind, randomized, placebo-controlled evaluation of two doses. 242 52


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