Gerard A. Kaiser

Electroaugmentation of Ventricular Performance and Oxygen Consumption by Repetitive Application of Paired Electrical Stimuli

When a depolarizing stimulus is delivered to the ventricle immediately following the refractory period, little extrasystolic contraction occurs and repetitive paired stimulation then results in a marked and sustained improvement of ventricular performance which has been termed electroaugmentation. The present study characterizes this augmentation and its effects on myocardial oxygen consumption (MVO2). In 45 experiments on 14 dogs in which mean aortic pressure and stroke volume were held constant by right heart bypass, a change from single to paired stimulation at identical contraction rates markedly increased the performance of the left ventricle as evidenced by shortening of ejection time increase in left ventricular dp/dt, stroke power, and peak ejection rate, and sometimes a fall in end diastolic pressure. Similar resul were obtained after administration of resepine or nethalide. In 15 experiments on 11 dogs the stroke volume of the left ventricle was varied during single and paired stimulation. Improvement in left ventricular performance during paired stimulation was always evidenced by increased speed of contractic and an upward displacement of the curvesrelating end diastolic pressure to stroke powe mean and peak ejection rates, and some times by an upward displacement of the curves relating end diastolic pressure to stroke volume and stroke work. In eight experiments MV˙O2 was determined during single and paired stimulation, stroke volume, mean aortic pressure, and contraction rate being held constant. Paired stimulation always increased MV˙O2 the average increase being 35%. Despite the rise in MV˙O2, a reduction in the tension-time index always occurred. These studies indicate that repetitive paired stimulation exerts a powerful and sustained positive inotropic in fluence on the mammalian ventricle and that at a relatively constant level of external world the increased velocity of ventricular contraction which accompanies this effect results in an increase in MV˙O2.

The Architecture of the Heart in Systole and Diastole Technique Of Rapid Fixation And Analysis Of Left Ventricular Geometry

Techniques for rapid fixation of the canine left ventricle in systole or diastole that have permitted analysis of ventricular geometry under known hemodynamic conditions are described. Six ventricles were arrested at and diastole, 7 at end ejection, and 7 in diastole following acute ventricular overdistension. The architecture of the ventricles was analyzed from measurements of the fixed ventricles and silicone-rubber casts of the ventricular cavities. In ventricles of matched weights, the average reduction, from end diastole to end ejection, of the apex to mitral valve distance was 4.6%, while that from apex to aortic valve was less than 1%. The minor internal equator was reduced by 26%, the midwall radius by 16%, and the outer radius by 8.5%. The ratio of the average end-diastolic volume minus end-systolic volume to the end-diastolic volume (analogous to stroke volume/end-diastolic volume) averaged 59%. The average wall thickness was 28% greater in systolic than in diastolic ventricles. The papillary muscle volume averaged 5.0%e of ventricular volume at end diastole and 14.7% at end systole. The area of the mitral valve orifice averaged 28% less at end systole than at end diastole; this area was 39% more in the hearts subjected to over-transfusion than in those with normal filling pressures. These data provide a framework for construction of a geometric model suitable for use in analyses of the mechanics of left ventricular contraction. Moreover, the methods described offer the possibility of correlating ventricular geometry and ultrastructure with cardiac function in normal and in abnormal hearts.

An Intrinsic Adrenergic Vasodilator Mechanism in the Coronary Vascular Bed of the Dog

The question of whether the coronary blood vessels contain an intrinsic adrenergic mechanism for vasodilatation has been examined by studying the response of the coronary vessels of the dog to isoproterenol. Initially, coronary blood flow, coronary sinus PO2, mean arterial pressure, and heart rate were measured continuously in anesthetized, open-chest animals. When isoproterenol, 0.1 to 0.3 μg/kg/min, was given intravenously, coronary flow and coronary sinus PO2 always increased in spite of tachycardia and a reduced or unchanged arterial pressure. Although this response suggested a primary vasodilating effect of isoproterenol, a vasodilatation consequent to increased myocardial activity or an extracardiac factor could not be eliminated. Accordingly, additional studies were performed in an isolated heart arrested with potassium and perfused with whole blood at constant rates of flow. Isoproterenol was given by single injections and constant infusions and always produced a decrease of perfusion pressure. These decreases could be blocked by nethalide and, as indicated by measurements of myocardial oxygen uptake and coronary venous PO2, did not depend upon increased myocardial metabolism or decreased myocardial oxygenation. With injections of 0.01, 0.1, 1.0, and 10.0 μg of isoproterenol, the decreases averaged respectively 3, 8, 14, and 26% of the control pressures. It is concluded that the coronary vessels of the dog do contain an intrinsic adrenergic mechanism for vasodilatation.

Observations on the Role of Diminished Oxygen Tension in the Functional Hyperemia of Skeletal Muscle

The hypothesis that lowered tissue oxygen tension acting on vascular smooth muscle can explain functional hyperemia in skeletal muscle was examined in ten dogs. A comparison was made between the blood flow increment that accompanied rapid, rhythmic contraction of a gastrocnemius muscle and the flow change that occurred in the same muscle at rest during its perfusion with venous blood obtained from the resting or contracting gastrocnemius muscle of the opposite leg. Blood PO2, pH, and PCO2 were measured in samples of venous blood from the muscle. There was no evidence that the perfusion circuit traumatized the perfused blood. During functional hyperemia, the increases in blood flow averaged 173%, and the average venous PO2, was 25 mm Hg. During venous perfusion, the maximum increases in blood flow averaged 56%, and the average venous PO2, was 23 mm Hg. When the muscle was stimulated to contract during its perfusion with venous blood, increases in blood flow occurred which averaged 143%, despite additional falls in venous blood PO2 that averaged only 3 mm Hg. These studies suggest that the effect of lowered PO2 on vascular smooth muscle does not produce sufficient vasodilatation to explain functional hyperemia in skeletal muscle.