Creatine phosphokinase heart

Takahashi, R. Ushikubo, S. Oimomi, M. and Shinki, T. Creatine phosphokinase isoenzymes of human heart muscle and skeletal muscle. Clin. Chim. Acta (1972),... 

Five repeated exposures of 200 ppm for 12.5 min every 4 d resulted in increased cardiac-specific creatine phosphokinase activity in the blood (pooled data measured at 2 h after the first, third, and fifth exposures) and ectopic heart beats during the first 2 min after injection of norepinephrine (after the fifth exposure) but failed to induce cardiac lesions (histopathologic examinations at 14 d postexposure) (O Flaherty and Thomas 1982). The rats were restrained and anesthetized. 

Saks, V.A. Chernousova, C.B. Cukovsky, D.E. Smirnov, V.N. Chazov, E.L Studies of energy transport in heart cells. Mitochondrial isoenzyme of creatine phosphokinase kinetic properties and regulatory action of Mg " ions. Eur. J. Biochem., 57, 273-290 (1975)... 

Enzymes, which are normally produced in cells, are released into the blood when cells are injured. For example, after a heart attack, there is an increase in blood levels of creatine phosphokinase (CPK) and other enzymes such as lactate dehydrogenase (LDH). The extent of damage and the rate of recovery can be estimated by periodically measuring the levels of these enzymes. Measurement of the MB isozyme of CPK is also used as an aid in diagnosis. 

Myocardial infarction occurs when the blood supply to the heart muscle is blocked for an extended time. If this lack of blood supply, called ischemia, is prolonged, the myocardium suffers irreversible cell damage and muscle death, or infarction. When this happens, the concentration of cardiac enzymes in the blood rises dramatically as the dead cells release their contents into the bloodstream. Although many enzymes are liberated, three are of prime importance. These three enzymes, creatine phosphokinase (CPK), lactate dehydrogenase (LDH), and aspartate aminotransferase/serum glutamate-oxaloacetate transaminase (AST/SGOT), show a characteristic sequential rise in blood serum level following myocardial infarction and then return to normal. This enzyme profile, shown in the ac-... 

These data give the clinician an accurate picture of the nature of the diseased tissue. For a heart attack victim, only creatine phosphokinase isoenzyme 2 (CPK II, the predominant heart isoenzyme) will be elevated in the three days following the heart attack. CPK I (brain) and CPK III (skeletal muscle) levels will remain unchanged. Similarly, only LDH 1, the lactate dehydrogenase isoenzyme made in heart muscle, will be elevated. The levels of LDH 2-5 will remain within normal values. 

This syndrome is a combination of symptomatic effects produced by antipsychotic drug therapy. Symptoms and signs include hyperpyrexia, muscle rigidity, altered mental status (e.g., catatonia) and cardiovascular instability (e.g., unstable heart rate and blood pressure). Acute renal failure may ultimately occur. Diagnostic signs include elevated creatine phosphokinase (CPK) and myoglobinuria. 

Creatine phosphokinase (CK), one of the proteins measured to follow Ann Jeina s myocardial infarction (see Chapter 6) is present in cells as dimers (two subunits). The dimers may be homodimers (two identical subunits of either the M [muscle] isozyme or the B [brain] isozyme), or heterodimers (MB) The MB isozyme is produced only by the heart and readily released from injured cardiomyocytes into the blood (see Chapter 6). 

The creatine formed is released from the liver and travels throngh the bloodstream to other tissues, particularly skeletal muscle, heart, and brain, where it reacts with ATP to form the high-energy compound creatine phosphate (see Fig. 47.6). This reaction, catalyzed by creatine phosphokinase (CK, also abbreviated as CPK), is reversible. Therefore, cells can use creatine phosphate to regenerate ATP. 

HOE-642, a selective sodium-hydrogen exchange subtype 1 inhibitor (Scholz et al. 1995), when given at 1 iM together with tetrodotoxin (44 jiM) protected isolated rat hearts from ischaemic/reper-fusion injury and lowered creatine phosphokinase activity in the coronary effluent in comparison to that observed in the non-treated hearts (Eng et al. 1998). 

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