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)

We have developed murine models of viral myocarditis induced by encephalomyocarditis (EMC) virus in which severe myocarditis, congestive heart failure and dilated cardiomyopathy occur in high incidence. From these models, we have learned the natural history and pathogenesis and assessed new diagnostic methods and therapeutic and preventive interventions. Mural thrombi in the atria and ventricles, ventricular aneurysms, conduction disturbance and various arrhythmias were seen in these models. Anti-heart antibody were found in sera of mice and myosin isoenzyme were changed during the course of EMC virus myocarditis. Atrial natriuretic polypeptide was markedly increased in the ventricles in these mice. Successive infection with coxsackievirus and EMC virus developed lesions similar to chronic myocarditis. The myocardial uptake of antimyosin antibody was proved to be a useful method of diagnosis of myocarditis. Treatment with the nucleoside analogue, ribavirin and recombinant alpha interferon effectively inhibited myocardial virus replication and reduced myocardial damage. Passive immunization and virus-specific vaccine prevented development of myocarditis. The use of immunosuppressive therapy was associated with greater mortality when administered early in illness and beneficial effects were not seen by later administration. Angiotensin-converting enzyme inhibitor improved myocardial injury and congestive heart failure. A nonselective beta-adrenergic blocker with intrinsic sympathomimetic activity, carteolol, prevented the development of myocardial lesions similar to those in dilated cardiomyopathy after myocarditis in the chronic stage.
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PMID:Lessons from animal experiments in myocarditis. 134 48

Chronic and acute administration of epinephrine or related sympathomimetic agents are typically prescribed for the treatment of clinical disorders such as hypotension, anaphylactic and allergic reactions, and bronchial asthma. In addition to its effects on these infirmaties and on carbohydrate metabolism, epinephrine also exerts a positive inotropic effect on fast-contracting skeletal muscle in a variety of animal species. At present, the precise mechanisms responsible for the inotropic effect are not known. This communication reviews the positive inotropic effects of epinephrine on fast-contracting skeletal muscle and discusses possible mechanisms which might mediate this phenomenon. Epinephrine potentiates muscle twitches via the second messenger, cAMP, secondary to hormone binding to membrane-bound beta-receptors. Cyclic AMP then acts to increase carbohydrate metabolism, alter sodium/potassium exchange, phosphorylate myosin isozymes, and/or alter intracellular calcium exchange. Based on theoretical grounds, the first three mechanisms can be excluded. Therefore, it is tentatively hypothesized that the effect is due to cAMP-enhanced calcium exchange within the muscle fiber and/or to increased influx of extracellular calcium. This notion is consistent with the mechanism of the positive inotropic effects of epinephrine on cardiac tissue. If this hypothesis is correct, it would also suggest a role, at least under some conditions, for extracellular calcium in the process of skeletal muscle excitation-contraction coupling.
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PMID:The positive inotropic effect of epinephrine on skeletal muscle: a brief review. 269 40

The myofibrillar calcium sensitivity of mammalian skeletal muscle and cardiac muscle may be increased by myosin light chain kinase (MLCK)-induced myosin phosphorylation5) 13). Here we report increasing calcium responsiveness of frog skeletal muscle fibres (Tibialis anterior, skinned by freeze drying) by MLCK-induced myosin P-light chain phosphorylation and by the non-glycoside, non-sympathomimetic positive inotropic drug pimobendan. Investigation of myosin light chains by two dimensional gel electrophoresis revealed two phosphorylatable P-light chains (LC-2) having the same isoelectric point (5.3 for the unphosphorylated, 5.1 for the phosphorylated form) but different molecular weights (19 and 18 kD, respectively). This pattern of LC-2 is distinct from mammalian skeletal and cardiac muscle (only one phosphorylatable P-light chain in skeletal, two phosphorylatable P-light chains in cardiac muscle with different isoelectric points, but identical molecular weight). The phosphorylation level was about 0.45 mole phosphate/mole P-light chains and could be increased by 16 +/- 3% by the addition of myosin light chain kinase. This procedure increased the isometric tension at pCa 5.5 by 21 +/- 5% while maximum tension (at pCa 4.3) was not affected by MLCK. The new inotropic drug pimobendan (10(-4) M) increased isometric tension at pCa 6 by 48 +/- 4.5%, but maximal tension was not affected. Another positive inotropic drug, sulmazole, has been shown to potentiate the twitch of intact frog Tibialis anterior muscle23) and to increase force of skinned fibres by 21.7 +/- 3.3% at submaximal activation (pCa 6).
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PMID:Myofibrillar calcium sensitivity modulation: influence of light chain phosphorylation and positive inotropic drugs on skinned frog skeletal muscle. 326 85