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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 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”.