Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Drug use among athletes has become a recognised problem in sports. Athletes may use drugs for therapeutic indications, for recreational or social reasons, as ergogenic aids or to mask the presence of other drugs during drug testing. Stimulants were some of the first drugs used and studied as ergogenic aids. Amphetamines may increase time to exhaustion by masking the physiological response to fatigue. Caffeine may improve utilisation of fatty acids as a fuel source thereby sparing muscle glycogen. Cocaine and other sympathomimetic drugs have little or no effect on athletic performance. Anabolic steroids appear to have the potential to increase lean muscle mass and strength under certain conditions. Human growth hormone may also be used for an anabolic effect, but data on this effect are lacking. Erythropoietin may represent a pharmacological alternative to blood doping by increasing red blood cell mass. The use of narcotic analgesics is not necessarily ergogenic but can be harmful if used to allow participation of an athlete with a severe injury. According to the American College of Sports Medicine alcohol does not possess an ergogenic effect. However, it may be used to reduce anxiety or tremor prior to competition. Marijuana does not increase strength. Tobacco products may produce psychomotor effects or control appetite which may be beneficial to some athletes. Other drugs used by athletes include beta-blocking agents, diuretics, and a variety of nutritional supplements. In addition, diuretics and probenecid may be taken to mask drug contents in the urine. Whether the ergogenic effects are real or perceived, the potential for adverse effects exists for all of these drugs. Potential health complications represent a serious risk to an otherwise healthy population. Further research on the long term health risks in athletes taking ergogenic drugs is needed.
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PMID:Enhancement of athletic performance with drugs. An overview. 168 20

Adult male rats were maintained on a nutritionally adequate liquid diet, or laboratory chow and water (controls), for 7 days. They were then anaesthetized and parotid flow was recorded after isoprenaline or pilocarpine stimulation, each collected over two, timed sampling periods--an initial 5 min and a subsequent 15 min. The isoprenaline-induced flow rates in liquid diet rats were reduced to 45 and 30% of those in control rats for the first and subsequent samples respectively (p less than 0.02). After pilocarpine stimulation there were no significant differences in the first samples, but in the subsequent samples the flow rate in liquid diet rats was reduced to 54% of that in controls (p less than 0.001). The parotid gland weights were reduced by 35% in liquid diet rats compared to controls (p less than 0.05). On computerized planimetric analysis, parotids (from rats that had not been given secretagogues) had significantly smaller mean acinar areas, mean acinar profile perimeters and mean acinar transection diameters after liquid feeding (p less than 0.001). The findings support the notion that there is a functional reserve capacity available in atrophied glands to support the relatively fast flow that occurs on initial stimulation but which becomes exhausted during sustained stimulation. This exhaustion occurs more severely and more rapidly in the low-volume, protein-rich saliva elicited by sympathomimetic stimulation than in the high-volume, low-protein saliva formed in response to parasympathomimetic stimulation.
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PMID:The effects of a liquid diet on initial and sustained, stimulated parotid salivary secretion and on parotid structure in the rat. 222 54

For the treatment of severe attacks of asthma, too, inhalable beta 2-sympathomimetic agents form the basis of drug therapy. It is, further, necessary to apply these agents systemically together with theophylline, the best approach to pre-status and status asthmaticus being continuous i.v. application following a bolus administration (dose of beta 2-sympathomimetic 0.04 mg/kg x min, for theophylline 10-15 micrograms/kg x min). Furthermore, 50-200 mg prednisolone equivalent are administered i.v. Secretolysis and increased expectoration are ensured by a copious supply of liquids, inhalation of saline mists, administration of acetyl cysteine or ambroxol, together with physical-therapeutic measures. Also important is the administration of oxygen and the calming of the anxious, agitated patient by adopting a relaxed, calm approach and devoting the patient sufficient attention. The uncritical use of sedatives (cave: depressive effect on respiration) is to be rejected. If, despite increasing the dose of the beta 2-sympathomimetic agent (approx. 0.06 micrograms/kg x min), no improvement is seen after 1-2 hours, or if global respiratory failure develops or exhaustion of the respiratory musculature is threatening, intensive monitoring and care should be initiated. If necessary, the patient is intubated and ventilated; in therapy-refractory situations, bronchoalveolar lavage should be employed as an adjunctive measure.
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PMID:[Treatment of the severe asthma attack and status asthmaticus]. 268 29

In 15 healthy, not specifically trained volunteers (age: 26.6 +/- 2.7 years) single equipotent doses of a selective beta 1-blocker with intrinsic sympathomimetic activity (ISA) (200 mg Epanolol-Visacor; V) and of a selective beta 1-blocker without ISA (100 mg Metoprolol; M) were compared with placebo (P) with respect to their influence upon physical performance capacity and metabolism in a random, double blind, cross-over experimental setting. The subjects underwent three step by step incremental treadmill tests and three treadmill endurance tests until volitional exhaustion. Maximum running speed and maximum oxygen uptake were used as measures of maximum performance capacity. Running speed and oxygen uptake related to individual anaerobic threshold, and running time and running distance in the endurance tests were used as measures of endurance capacity. Both maximum and endurance performances were reduced significantly by beta-blockade. No relevant differences were discerned between V and M. The uniform reduction in exercise heart rate with both beta-blockers demonstrated the application of equipotent doses. At rest, heart rate was significantly higher under V than under M. Carbohydrate metabolism was unaffected, both beta-blockers showing equal inhibition of lipolysis during exercise. We conclude that intrinsic sympathomimetic activity has no influence upon physical performance and metabolism during selective beta 1-blockade.
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PMID:Effects on physical performance of intrinsic sympathomimetic activity (ISA) during selective beta 1-blockade. 288 3

Possession of beta-1-selectivity and intrinsic sympathomimetic activity (ISA) by beta-adrenergic blocking drugs have been found to modify the effects of these drugs on heart rate, blood pressure and pulmonary airway resistance both at rest and during exercise. In a randomised, double-blind, cross-over, placebo-controlled trial, 21 healthy male volunteers took placebo, propranolol (non-selective with no ISA), metoprolol (beta-1-selective with no ISA) and pindolol (non-selective with ISA) on separate occasions prior to an exercise test using the same protocol each time. Heart rate, blood pressure and peak respiratory flow rate (PEFR) were measured before exercise and at exhaustion. No significant differences in percentage increase in heart rate after exercise were detected between placebo and all the three beta-blockers. All three drugs were associated with significantly lower percentage increases in systolic blood pressure with exercise compared to placebo; with metoprolol and propranolol causing lower increases than pindolol. The index of myocardial oxygen consumption, MVO2, was highest with pindolol. PEFR was reduced most by propranolol. Possession of beta-1-selectivity and ISA by beta-blocking drugs modifies their effects on cardio-respiratory responses to exercise amongst indigenous Kenyans.
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PMID:Influence of beta-blockade with beta-1-selectivity or intrinsic sympathomimetic activity on some cardiorespiratory responses to exercise. 790 31

We investigated myocardial interstitial norepinephrine kinetics in both the ischemic and nonischemic regions during reperfusion after 40 min of coronary occlusion in anesthetized cats. By use of a cardiac dialysis technique, dialysate norepinephrine contents from both regions were monitored as an index of myocardial interstitial norepinephrine levels. For vehicle perfusate (n = 8), the accumulated dialysate norepinephrine level in the postischemic region decreased from 3,010 +/- 923 pg/ml at 30-40 min of occlusion to 957 +/- 178 pg/ml at 0-10 min of reperfusion and returned to near control level at 30-40 min of reperfusion. After 40 min of reperfusion, there were no significant differences in tyramine (100 micrograms/ml, norepinephrine-releasing sympathomimetic amine)-induced norepinephrine release between both regions. For perfusate containing 100 microM desipramine (neural uptake inhibitor, n = 6), at 0-10 min of reperfusion, the dialysate norepinephrine in the postischemic region did not significantly decrease. The dialysate norepinephrine then returned to near preocclusion level at 30-40 min of reperfusion. These data suggest that reperfusion rapidly returns accumulated myocardial norepinephrine to the preischemic level and neuronal norepinephrine uptake greatly contributes to this return in the early phase of reperfusion. Forty minutes of coronary occlusion cause neither norepinephrine exhaustion nor irreversible impairment of norepinephrine uptake function in nerve terminals.
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PMID:Regional myocardial interstitial norepinephrine kinetics during coronary occlusion and reperfusion. 876 58