Damage of the Heart Muscle Cell 91 



sarcomere, and they then interdigitate (Huxley, 1956) . In the re- 

 laxed state filaments slide easily along each other. During contrac- 

 tion this sliding is brought about by internal forces, probably by 

 obliquely orientated cross linkages between actin and myosin fila- 

 ments. There is no actual shortening of myosin filaments until they 

 are crowded together by extreme shortening of the sarcomeres. 

 Szent-Gyorgyi describes a "plasticizing" effect of ATP. After a 

 change in muscle length has occurred, either by stretching or short- 

 ening, the plasticizing quality allows the muscle to regain a tension 

 about equal to that originally held. Without this effect a muscle be- 

 comes rigid and responds to slow stretch with an increase in tension, 

 finally tearing if the stretch goes too far. 



K ions are involved in some way, we have seen, in the work of 

 the cardiac muscle. They are necessary for optimal work and main- 

 tenance of the stability of isolated heart muscle mitochondria. 

 Muscle poor in K ions fatigues easily and develops less tension. 

 During contraction K+ leaves the muscle cell and Na+ enters 

 through the semi-permeable cell membrane (Hodgkin, 1951) . At 

 the end of this phase Na+ is extruded actively and K ions than 

 diffuse in, driven against the concentration gradient by the poten- 

 tial gradient, to re-establish an equilibrium with a relatively high 

 concentration of K+ and low concentration of Na+ in the cell. 



From these considerations it follows that myocardial metabolism 

 can be upset through (1) disturbances in energy production, and 

 (2) disturbances in energy utilisation. Instances of (1) are met 

 with in the ischaemia of coronary occlusion, haemorrhagic shock 

 and ventricular fibrillation. A special instance is heart failure as- 

 sociated with Beri Beri. Under group (2) comes cardiac failure. 



Energy production can fail at any level of the catalysed pro- 

 cesses concerned in its machinery. Since these are closely interre- 

 lated it is not surprising that one perverted phase of metabolism 

 may lead to changes in other metabolic pathways, as in the case of 

 diabetes mellitus. On the other hand, as with cardiac ischaemia, the 

 disturbance may remain more localised. Interference with the co- 

 carboxylase mechanism, as in haemorrhagic shock and coro- 

 nary occlusion, blocks the incorporation of carbohydrate catabolism 

 into the Krebs cycle. It further interrupts fatty-acid catabolism 



