Abstract
In myocardial perfusion, blood acts not only as a source of oxygenation and nutrients and a pathway for removal of metabolites, but also as a coolant and a heat sink. At increasing heart rate the pumping efficiency decreases and the heat generation increases. Increased temperature leads to increase of aggregation of red cells and to apparent increase in the rigidity of red cells. It is also known that clotting of blood becomes more rapid at increased temperatures. Thus, even a marginal increase of temperature at any specific site of the myocardium might form a vicious circle affecting heart nourishment and heart performance. In his studies of cancer, von Ardenne showed localized tissue necrosis at 41°C, while Rigby and Dintenfass considered ‘melting’ of molecular collagen as a factor in the elastic properties and function of myocardium (which might have an example in rheumatic heart disease). Phase transition of collagen depends on its chemical composition which might differ in different parts of the heart. There is also little information permitting definite statement on existence of hot spots in the heart as duration of heat generation required would be of 300 sec duration while current evidence suggests 60 sec duration under experimental conditions. Nevertheless, the total evidence of thermal changes in the blood rheology and in the rheology of myocardium suggests that thermal mechanisms could be of importance in heart pathology.
Keywords
Get full access to this article
View all access options for this article.
