The Pathophysiology of Myocardial Perfusion [antikvár]

About This BookThis book developed from a futile attempt to update my 1971 monograph on coronary collaterals [1]. I had the impression that knowledge about the collateral circulation of the heart had so rapidly progressed that a revision of the earlier text was necessary. Especially clinical cardiologists had become interested in the topic and the presence or absence of collaterals began to influence the decision whether or not to bypass a coronary obstruction by surgery.Studies in experimental animals had advanced to a point where hemodynamic and morphologic investigation did not necessarily lead to a further advancement of knowledge.The remaining and most important unsolved problem was: "what makes collateral grow?" Is it a metabolite of anaerobic metabolism?, a tissue hormone?, a vascular growth factor similar to nerve growth factor?These questions stirred our interest to study myocardial ischemia more closely in the hope to find the magic chemical that expands physiologic autoregulation to a point where ischemic heart muscle makes vessels grow which prevent death.We had no clue (and we continue to live with our ignorance) as to the possible nature of this probably biochemical transmitter. All we know is that ischemia is the most potent known influence which stimulates growth of collaterals. It was therefore quite natural that we became interested in myocardial ischemia which we studied with the instrument available to us, the electron microscope. These electron-microscopic studies were carried out in human biopsy material obtained during open heart surgery after elective cardiac arrest followed by periods of ischemia. This is essentially a "no-flow" state which was compared to the "low-flow" state of regional myocardial ischemia studied in experimental animals after acute occlusion of a coronary artery. The difference between these states is, as will be pointed out in the respective chapters, the existence of leucotactic mediators which appear very early in regional "low-flow" ischemia but not in global "no-flow" ischemia. Since the development of collaterals is also accompanied by inflammatory reactions involving polymorphonuclear leucocytes and monocytes it was reasonable to assume that collateral growth is stimulated by a transmitter associated with leuco taxis. Since the concentration of these compounds in tissue may reach values of 10"' molar we calculated that about 20 kg of infarcted dog myocardium are needed for an attempt to isolate, purify and test these mediators. This would require about 100 kg of heart muscle or about 500