Celller of l'hy,i"l<>gy a nd l'alh"physi"log y, Uni"....iry "fGiiuingcn, fR G Su mmary During myo.;;trJial ischemia the ph;l~e angle lJl vf the co mple x

In canine hearts the myocardial equilibration processes (temperature, pO2, pCO2, Na+, K+) and the myocardial energy turnover were analyzed at the beginning of a cardioplegically induced cardiac arrest during a coronary perfusion of 10 minutes. The investigated hearts (n = 10) were perfused with the Bretschneider histidine-buffered cardioplegic solution according to the recommendations worked out for clinical use. The results show that during the cardioplegic coronary perfusion of 10 minutes the cooling and temperature equilibration of the myocardium occur considerably faster than the establishment of a new energy steady-state at a very low level. The minimalization of the coronary resistance and of the myocardial O2 consumption are only reached after an extended perfusion period of 7 to 9 minutes. In consequence of the results, the following recommendations can be given for the clinical use of the Bretschneider cardioplegic solution: a) the solution should be used at a temperature of between 5 degrees and 10 degrees C, b) the cardioplegic coronary flow should be between 60 and 80 ml/min . 100 gww, c) the human heart should be perfused for 8 to 10 minutes and, d) the perfusion pressure should be maintained at 40 to 50 mmHg after cardiac arrest has set in. So far the action of equilibration procedures when using the Bretschneider cardioplegic method has not been compared with that of other cardioplegic methods.

No abstract

Cellular and mitochondrial swelling are regarded as typical intra-ischemic alterations ("IIA"), contraction band lesions (CBL), in contrast, as products of post-ischemic reperfusion. The occurrence of both types of structural deterioration was investigated in Purkinje fibres and subendocardial and intramural working myocardium: initially after St. Thomas- or HTK cardioplegia, then during ensuing global ischemia up to the "practical limit of resuscitability", and following post-ischemic reperfusion. Generally, Purkinje fibres are not better preserved than neighbouring working myocardium. Comparing St. Thomas- and HTK cardioplegia, considerable quantitative, but not qualitative differences in the reaction patterns of different cell types or layers arise. Immediately after cardioplegia, CBL are completely lacking in both cell types. During ischemia, CBL occur occasionally in Purkinje fibres and seldom in subendocardial working myocardium, "IIA" predominate. During post-ischemic reperfusion "IIA" tend to reverse in all layers, whereas CBL are found to remain in the subendocardial cell types. In intramural layers, CBL occur only during reperfusion. Thus, we deduce that cardioplegia only modulates the severity of "IIA" and the frequency of CBL, but cannot abolish the particular sensitivity of subendocardial Purkinje fibres to global ischemia. Prerequisites for the development of irreversible CBL are on the one hand ischemic metabolic alterations and corresponding energy deficits, and, on the other hand, a supply of oxygen. The oxygen may be inadequately supplied via diffusion during ischemia or may be subsequently provided by reperfusion.

Clinically applied methods of cardioplegia show very different effects on the rapidity of decay of energy-rich phosphates as well as on kind and progression of ultrastructural alterations of the ischemic myocardium. Comparing the methods of cardioplegia according to Kirklin, St. Thomas's Hospital and Bretschneider (solution HTK) with pure ischemia at 25 degrees C (model A) and Kirklin's or St. Thomas's cardioplegia and subsequent 210 min or HTK cardioplegia and 300 min ischemia at 22 degrees C plus 20 min subsequent reperfusion (model B) leads to the following results: Model A: Compared with pure ischemia cardioplegia according to Kirklin and the St. Thomas's Hospital slows down the decay of the left ventricular ATP-concentration by a mean factor of 3 and the progression of structural alterations of the left ventricular subendocardium by a factor of 2. HTK retards the ATP-decay by a factor of 6, the alterations of ultrastructure by a factor of 6.5. St. Thomas's solution, in contrast to all other methods of cardioplegia, at the onset of ischemia already causes a cellular edema of myocytes; the edema increases during ischemia, and at the ATP-concentration of 4 mumol per gram myocardium is more pronounced than with pure ischemia, Kirklin or HTK. After application of Kirklin's solution, in contrast, a cellular edema of capillary endothelia develops during ischemia, which at 4 mumol ATP is more pronounced than with each of the other methods. Model B: After global ischemia until the ATP-concentration of left ventricular myocardium is 4 mumol/g and a subsequent 20 minutes post-ischemic recovery the ultrastructural alterations in principle resemble those occurring during ischemia (model A).(ABSTRACT TRUNCATED AT 250 WORDS)