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In experiments on anaesthetized dogs the arterial blood pressure and the left ventricular pressure were enhanced by intraarterial blood transfusion. The circumflex branch of the left coronary artery was perfused by constant blood pressure at 65, 100 or 200 mm Hg. After elimination of the sinus node the heart rate was kept constant at 150 beats per minute by electrical stimulation of the right auricle. The metabolically regulated component of coronary resistance of the circumflex branch was kept constant by a maximal pharmacological dilatation. On this condition the coronary blood flow decreases with increasing left intraventricular systolic pressure. The coronary resistance increases. The increasing coronary resistance with increasing intraventricular blood pressure is caused by an enhancement of the extravascular component because the perfusion pressure and hematocrit were constant, and the coronary vessel maximal dilated. The rise of coronary resistance with increasing intraventricular blood pressure depends on the height of perfusion pressure. Low perfusion pressure is combined with a marked increase, while the increase is small in the experiments with high perfusion pressure. The pathophysiological significance of the results has been discussed.

In Experimenten an narkotisierten Hunden wurde durch intracoronare Isoproterenolinfusionen die maximale Druckanstiegsgeschwindigkeit im linken Ventrikel (dp/dt max) vergrosert. Dabei wurde nach Ausschaltung des Sinusknotens die Herzfrequenz durch elektrische Reizung des rechten Herzohres konstant gehalten. Die intravasale (metabolisch regulierte) Komponente des Einfluswiderstandes wurde durch eine maximale pharmakologische Dilatation konstant gehalten. Die extravasale Komponente des Einfluswiderstandes steigt mit zunehmendemdp/dt max an, und zwar wahrend der Systole. Der diastolische Einfluswiderstand bleibt konstant. Da gleichzeitig die Diastole auf Kosten der Systole langer wird, ist der Widerstandsanstieg wahrend des ganzen Herzcyclus relativ gering.

Bei elektrischer Reizung des Herzens (rechtes Herzohr) nach Ausschaltung des Sinusknotens finden sich in dem untersuchten Frequenzbereich von 60–220 Schlagen in der Minute normale Systolen- und Diastolenzeiten. Wird durch eine maximale pharmakologische Coronardilatation die intravasale Komponente des Coronarwiderstandes konstant gehalten, so last sich mit steigender Frequenz in allen Experimenten eine Zunahme der extravasalen Komponente des Coronarwiderstandes nachweisen. Diese Zunahme wird durch die relative Zunahme der Systolenzeit auf Kosten der Diastolenzeit hervorgerufen. Die Zunahme der extravasalen Komponente der Coronarwiderstandes ist relativ gering, weil eine Abnahme des systolischen Einstromwiderstandes die Wirkung der Systolenverlangerung vermindert. Die extravasale Komponente des diastolischen Einstromwiderstandes ist frequenzunabhangig.

In Experimenten an narkotisierten Hunden wurde durch i.v. Injektionen eines Barbiturates bei gleichzeitigen Bluttransfusionen, die den arteriellen Blutdruck konstant hielten, der enddiastolische Druck im linken Ventrikel erhoht. Die Herzen wurden nach Ausschalten des Sinusknotens uber das rechte Herzohr elektrisch mit 150 Impulsen in der Minute stimuliert. Die metabolische Komponente des Einfluswiderstandes wurde durch eine pharmakologische, maximale Dilatation der Coronargefase konstant gehalten. Die Coronardurchblutung bei maximaler pharmakologischer Dilatation sinkt mit steigendem end-diastolischen Druck ab. Die extravasale Komponente des Einfluswiderstandes steigt mit zunehmendem enddiastolischen Druck wahrend der Systole, der Diastole und des Gesamtcyclus an. Die Systolendauer nimmt mit steigendem enddiastolischen Druck zu.

The effects of coronary dilatators were studied in isolated, isovolumetrically beating guinea pig hearts at different Ca++-concentrations of the perfusion fluid. In all experiments hypoxic dilatation of the vessels was absent because the coronary venous partial pressure of oxygen was higher than 50 mm Hg. The coronary dilatation caused by six of the investigated substances—Nifedipine, Prenylamin, Verapamil, Lidoflazin, Dipyridamol and Hexobendin—could be suppressed by increasing of the Ca++-concentration of the perfusion fluid. Therefore the mechanism of action on the smooth muscles of the coronary vessels has to be explained by a calcium antagonistic effect of these substances. The contractility of the myocardium is influenced in different ways. Nifedipine, Verapamil and Prenylamin show negative inotropic effects, which are also compensated by increasing the Ca++-concentration. In contrast Hexobendin, Lidoflazin and Dipyridamol show no negative or even a small positive inotropic effect. The effects of nitroglycerine and carbochromen are not affected by changes of the extracellular Ca++-concentration.

In 9 dogs the heart rate was kept constant by electrical stimulation of the right auricle after elimination of the sinus node. Hypercapnia was induced by increasing inspiratory carbonic acid concentration at constant oxygen concentration. The mean arterial carbonic acid partial pressure increased from 40.5 to 70.5 mm Hg. The mean pH decreased from 7.30–7.14. Under these conditions the coronary flow did not change. Systolic and diastolic aortic pressure, left ventricular pressure, and the maximal rate of pressure rise in the left ventricle remained unchanged. Alterations of coronary blood flow caused by increased carbonic acid concentrations as described by other authors can be explained by a change of hemodynamic conditions.

The idiopathic periostal hyperostosis with dysproteinemia shows typical symptoms: acute onset with high fever and severe pain in the forearms and the praetibial area, periostal reaction along the ulnae and tibiae accompanied by hypalbuminemia and alpha2-globulin increase. The clinical entity has yet been described in only 2 cases. Our own case illustrates the longterm follow-up. The differential diagnosis especially of Caffey-Syndrom is discussed.

Heart rate (calculated beat to beat) and excursions of the thoracic wall were registered continuously during exchange transfusions in the newborn period (N equals 29). Short time changes of heart rate ranging from 5 to 10 (N equals 11) and from 11 to 25 beats per minute (N equals 11) were usually present before exchange transfusion. In two cases "silent" (i.e. short time changes of heart rate lower than 5 bpm) heart rate pattern was registered before and in another two cases appeared during the exchange transfusions. This pattern is of prognostic value, 3 of these 4 children showed severe complications during the therapeutic procedure. Of particular interest is, that the "silent" pattern could be detected before other clinical signs of shock appeared. Monitoring heart frequency (beat to beat) therefore gives the possibility to start the therapy of complications early.

Der Stromungswiderstand in den Koronargefasen last sich in zwei Komponenten einteilen, einmal in eine extravasale Komponente und zum anderen in eine intravasale Komponente. Die intravasale Komponente wird im wesentlichen durch den Tonus der Widerstandsgefase, d. h. der Arteriolen bestimmt und wird durch den Herzstoffwechsel reguliert. Ein gesundes Koronarsystem kann mit Hilfe dieser Komponente den Stromungswiderstand und damit die Durchblutung um den Faktor 4 bis 5 verandern.

In unseren fruheren Untersuchungen an isolierten Herzen konnte gezeigt werden, das das Epontol eine konzentrationsabhangige, coronarerweiternde Wirkung hat (Dudziak et al. 1970). Der Coronardurchflus ubertraf den fur einen bestimmten Sauerstoffverbrauch zu erwartenden Wert, so das von einer den nutritiven Bedarf ubersteigenden Luxusdurchblutung gesprochen werden konnte.

The influence of increasing perfusion pressure in the coronary arteries on cardiac contractility and oxygen consumption was studied in isovolumetrically working, empty beating, and potassium arrested guinea-pig hearts. Raising the coronary perfusion pressure from 60 to 80 cm H2O increased left ventricular peak systolic pressure by 19.4±2.8%, coronary flow by 47.7±8.0% and oxygen consumption by 32.7±6.2% (N=17). At a constant perfusion pressure hypoxia increased the coronary flow by 111.8±16.4% (N=19), but did not alter the contractility of the heart or its oxygen consumption. Increasing pressure without changing flow, raised pressure in the left ventricle by 26.5±4.8% and myocardial oxygen consumption by 20.3±3.4% (N=14). The end-diastolic pressure and the heart rate remained unchanged in all experiments. From these findings it may be concluded that the pressure in the coronary vessels — independent of the flow rate — exercises a positive inotropic effect, thereby increasing metabolism. This can be explained by increased fibre tension, caused by an extension of the coronary vessels, the so-called “garden-hose-effect”.