Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3614_Библиотеки_им_академика_М_И_Перельмана

Hibernation immediately attracted the attention of basic scientists and several experimental models and studies were quickly under­taken. us, Ross and Heusch described hibernating myocardium as the result of a proportionate reduction in blood supply and con­tractile function, the so called perfusion– contraction matching. is idea gained immediate consensus, both in the acute experimental models and in some clinical settings (i.e. short- term hibernation), while a chronic perfusion– contraction matching (i.e. chronic hi­bernation) resulted in a long- lasting and, to some extent, semantic controversy:reduced versus preserved baseline ow in hibernating myocardium.–  How could hibernation, which is an expression of ischaemia, exist in the presence of normal ow? Of course all de­pends on the denition of ischaemia and, amazingly, as late as 1994 there was no clear accepted denition of ischaemia. e majority of studies reported reduced resting ow in the hibernating segments, but others found no reduction. As a result, the idea that hiberna­tion is consequent to repetitive episodes of post- ischaemic stunning developed. Even this hypothesis seems unrealistic, as stunning and hibernation are distinct entities with respect to their origin and nat­ural history. Stunning occurs on reperfusion, hibernation needs re­perfusion to be established! Another mystery relates to the intrinsic cause and consequences of the downregulation of contractility of hibernating myocardium, which has been considered either ‘smart’ or ‘selsh’. ‘Smart’ because it is capable of adapting to unfavourable circumstances by appropriately downregulating its biochemical and physiological activity as an act of self- preservation. By contrast, for