Muscle mimics

T1, as the thallous ion (Tl+), has been used for imaging heart function under stress and rest conditions since about 1975. The thallous ion distributes in viable heart muscle as a potassium ion mimic, through the Na+-K+ ATPase pump. Clinical images with 201T1 show the infarcted regions of the heart as cold spots or without radioactivity. 2 T1 decays by electron capture with a... 

The clinical picture in male children can closely resemble Duchenne-type muscular dystrophy in adults, it mimics limb-girdle dystrophy or polymyositis. The early and severe involvement of respiratory muscles in most patients with AMD is a distinctive clinical clue. Respiratory failure and pulmonary infection are the most common causes of death. 

Antibodies against the muscle-specific receptor kinase mimic myasthenia gravis 724... 

Figure 13.22 The decrease in phosphocreatine concentration in the muscle during stimulation. Electrical stimulation of muscle in the laboratory is used to mimic sprinting activity in the muscle. Data from Hultman Sjoholm (1983). The units for the concentration of phosphocreatine are pmole per gram dry weight of muscle taken by biopsy. Note apparent differences in concentration when data are presented as wet or dry weight.

Electrical stimulation of muscle to mimic sprinting (Eigure 13.22). 

The anxiolytic properties of 5-HT3 receptor antagonists have been demonstrated in several animal models of anxiety. In these models, the 5-HT3 antagonists mimic the anxiolytic effects of the benzodiazepines but differ from the latter in their lack of sedative, muscle relaxant and anticonvulsant action. These compounds appear to be extremely potent... 

Salbutamol is a selective bet02-agonist and therefore mimics the sympathetic system resulting in tachycardia and fine tremor. Salbutamol causes potassium loss leading to the development of muscle cramps. It also leads to headache. Constipation is not a side-effect of salbutamol but is commonly associated with the use of antimuscarinics. 

By using drugs that mimic or block the actions of chemical transmitters, we can selectively modify many autonomic functions. These functions involve a variety of effector tissues, including cardiac muscle, smooth muscle, vascular endothelium, exocrine glands, and presynaptic nerve terminals. Autonomic drugs are useful in many clinical conditions. However, a very large number of drugs used for other purposes have unwanted effects on autonomic function. 

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