Muscle enzymes, release

Myocardial infarction (Ml), also known as coronary thrombosis, is one of the commonest causes of mortality and morbidity in adults. Ml is usually diagnosed by a history of cnishing chest pain, characteristic ECG changes and cardiac muscle enzyme release. 

During severe liver damage, an ei zyme (Ei of practice problem 12) is release into the bloodstream. After severe exercis a muscle enzyme, Es, that catalyzes the sacr... 

The second messenger linking activation of surfece receptors by spasmogens in smooth muscle to release of intracellular Ca " has been identified as IP3. IP3 is formed by activated receptor stimulation of a cell membrane enzyme, PLC, which hydrolyses a lipid constituent of the cell membrane, phosphatidylinositol bisphosphate (PIP2 Fig. 9.4). 

Skeletal muscles also contribute enzymes to blood. Again, the cause may be poor perfusion, hypotliermia, or direct trauma to the muscles (crush injuries). Infection, inflammation (polymyositis), degenerative changes (dystrophies), drugs, and alcohol (alcoholic myopathy) wid cause enzyme leakage from myocytes. Enzyme release from muscles and other tissues also occurs as a result of anesthesia. 

Determination of LDH Lactate dehydrogenase (LDH) catalyzes the equilibrium reaction of pyruvate to lactate. The activity of serum LDH is due to the presence of the enzyme released from damaged organs and tissues such as liver, heart, skeletal muscle, erythrocytes, etc. because LDH is located in the cytoplasm of the cells. Therefore, the activity of LDH is useful for screening for the existence of cell injuries, estimation of damaged tissues, and evaluation of treatment of diseases. LDH has five isoenzymes, and their patterns are of diagnostic importance. 

The proteins are broken down in a discrete fashion that remains unknown, but certainly does not involve lysosomal enzyme release or even lysosome formation in the muscle. The amino acids are freed, most are reutilized for protein synthesis, but alanine which constitutes only 5% of the muscle amino acid component and to a smaller extent glutamine are transported from muscle to liver where the amino acids are used in the process of gluconeogenesis. 

Contraction of muscle follows an increase of Ca " in the muscle cell as a result of nerve stimulation. This initiates processes which cause the proteins myosin and actin to be drawn together making the cell shorter and thicker. The return of the Ca " to its storage site, the sarcoplasmic reticulum, by an active pump mechanism allows the contracted muscle to relax (27). Calcium ion, also a factor in the release of acetylcholine on stimulation of nerve cells, influences the permeabiUty of cell membranes activates enzymes, such as adenosine triphosphatase (ATPase), Hpase, and some proteolytic enzymes and facihtates intestinal absorption of vitamin B 2 [68-19-9] (28). 

Figure 4. The citrate cycle. There is complete oxidation of one molecule of acetyl-CoA for each turn of the cycle CH3COSC0A + 2O2 - 2CO2 + H2O + CoASH. The rate of the citrate cycle is determined by many factors including the ADP/ATP ratio, NAD7NADH ratio, and substrate concentrations. During muscle contraction, Ca is released from cellular stores (mainly the sarcoplasmic reticulum) and then taken up in part by the mitochondria (see Table 2). Ca " activates 2-oxoglutarate and isocitrate dehydrogenases (Brown, 1992). Succinate dehydrogenase may be effectively irreversible. Enzymes ...

Following massive crush injury, myoglobin released from damaged muscle fibers colors the urine dark red. Myoglobin can be detected in plasma following a myocardial infarction, but assay of serum enzymes (see Chapter 7) provides a more sensitive index of myocardial injury. 

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