Damage of the Heart Muscle Cell 93 



the mechanisms that maintain ionic gradients. Action potentials, 

 although they cannot be generated and propagated, may disappear 

 before the metabolic processes or the contractile proteins are irre- 

 versibly damaged. A decline in ATP has been recorded along with 

 weakened contractile response to electrical stimulation and eventu- 

 ally rigor mortis supervenes in the anoxic heart muscle (Greiner, 

 1952) . After death or in complete anoxia the pH of muscle cells 

 falls with the production of lactic acid according to the glycogen 

 stores available at the time of death. The turnover rate of ATP, 

 too, is affected by change in H ion concentration. The pH depend- 

 ence curve of ATP breakdown is very similar to the myosin-ATPase 

 activity curve and suggests that the two may be related (Bendall, 



1951). 



Ischaemic changes in muscle proteins are, in all probability, 

 similar to those that occur with rigor mortis. Actomyosin not only 

 fails to dissociate and reverse muscle contraction, but abnormal 

 cross linkages form between different filaments (Szent-Gyorgyi 

 1953) . Huxley (1956) , from low angle x-ray studies of muscle in 

 rigor, suggests that the secondary filaments crystallise out per- 

 manently, thus rendering potentially reversible changes in the 

 contractile proteins irreversible. 



RESPONSE OF THE MYOCARDIAL CELL TO ANOXIA AND 



HAEMORRHAGIC SHOCK 



When an organ demands oxygen the need may be met by (1) 

 increasing the blood flow, or (2) increasing the amount of oxygen 

 extracted from the available blood. The heart usually responds by 

 the first method, but there is some evidence, at any rate in the dog's 

 heart, that more oxygen may be extracted under such circumstances 

 (Hackel et al, 1954) , although this is not significant until the in- 

 creased demand becomes extreme. 



As the oxygen supply fails and the muscle cell receives less than 

 is necessary to maintain its normal aerobic metabolism the oxygen 

 tension in the myocardium falls. This shifts the oxidation-reduction 

 system towards a more reduced state. The extent to which in- 

 dividual members of the electron carrier system shift towards the 

 reduced form will be determined by the inherent redox potential 



