Simon Rodbard

Blood velocity and endocarditis.

DESPITE the successful use of anitibioties in the treatment of infective endocarditis, the failure of therapy in perhaps onre third of the patients with this condition keeps it in the forefront as a major threat in heart disease.1 2 The increasing incidence of endocarditis following cardiac surgery has also provided an unexpected and disturbing feature of progress in cardiac management.3In addition to the practical problems of management of this disease a number of per plexing clinical and laboratory questions re main. Thus, the argument as to whether the locus of the infection requires previous trauma, inflammation, vascularization,6 or deformity7 remains undecided. The mechanisms in the progression of verrucae and uleerationis, the formationi of thrombi, the validity of spontaneous cures, and the tendency to recurrence, demand re-evaluationi. It is curious that extremnely large quantities of antibiotics are required to halt the growth of inifective agents at the valve, while a thousandth of these concentrations (calculated for extracellular body water) miay destroy the same organisms in other sites in the body or in vitro.Y2 The antibody titers for some of the antigens of the infecting organism mav have little or no inhibitory effect on the mnicrobial growth at the infected valve or artery.3-15There can be little doubt that the circulation is seeded continually by organisms that are swept as emboli from a nidus to all the tissues of the body, with the production of local vascular occlusions; vet these pathogenic showers seldom produce local infections or abscesses. If some of these prob-

The inhibition of coronary atherosclerosis by estrogens in cholesterol-fed chicks.

Chronic administration of estrogens parenterally inhibits coronary atherogenesis in cockerels fed a cholesterol-supplemented diet, although no such prophylactic effect was observed against aorta atherogenesis. This protection of the coronary vessels is associated with depression of the plasma total cholesterol-lipid phosphorus ratio toward normal levels consequent upon estrogen-induced hyperphospholipemia.

Estrogen-Induced Regression of Coronary Atherosclerosis in Cholesterol-Fed Chicks

The present study demonstrates that estrogens reverse previously induced coronary atherosclerosis in cholesterol-fed cockerels, despite the continued presence of the atherogenic stimulus in the diet. Aorta atherogenesis remains unaffected. Hypercholesterolemia is moderately enhanced by estrogen administration; total cholesterol-lipid phosphorus (C/P) ratios are depressed to normal levels, consequent upon estrogen-induced hyperphospholipemia.

Myocardial Tension and Oxygen Uptake

Data obtained in 94 tests in nine anesthetized, thoracotomized dogs were re-examined to determine relationships among oxygen uptake per minute (qO 2), cardiac frequency (F), mean aortic pressure (P), stroke volume (V), and heart weight (G). Statistical analysis supports the concept that during each systole qO2/G is empirically related most closely to the peak mechanical tension (T) developed by a spherical heart, in accord with the relationship qO2/G-b/F = aT, in which a and b are derived constants for each heart. Peak tension is half the product of the mean pressure and the radius (estimated from the stroke volume). Myocardial oxygen uptake is viewed as developing through a mechanical positive feedback mechanism which triggers the shortening of contractile elements. The number of such elements triggered in each beat determines the peak tension, the oxygen requirement of that beat, the resulting energy release, and the work. The oxygen costs of tension increase with the size of the heart since tension must be applied throughout the entire surface of each shell of contractile elements. Mechanical efficiency varies with the square of the stroke radius; it is not directly affected by mean aortic pressure or cardiac frequency. Factors affecting the all-or-none phenomenon, mobilization of tension, myocardial efficiency, the law of the heart, myocardial oxygen uptake, and the coronary flow are discussed in light of these findings.

The spherical dynamics of the heart (myocardial tension, oxygen consumption, coronary blood flow and efficiency).

Abstract Pressure work of the heart has long been known to be more costly in terms of myocardial oxygen consumption and coronary blood flow than an apparently equivalent volume work. This problem was restudied in the dog. Pressure work and volume work were shown to be equivalent when the analysis was carried out from the point of view that the heart behaved like a contracting sphere. Oxygen consumption was then dependent on intramyocardial tension, this being calculated as half the product of the intracardiac radius and pressure. Recalculation of cardiac performance in a number of reports in the literature showed that previously contradictory data could be resolved by this relatively simple relationship. The bases for this type of analysis and a number of physiologic and clinical aspects of cardiac function are discussed.

Flow Through Collapsible Tubes: Augmented Flow Produced by Resistance at the Outlet

The physical laws describing the character of flow through blood vessels may depart radically from those which have been developed by engineers and physicists for uniform flow through rigid tubes of uniform diameter. These deviations are marked in the case of flow through collapsible tubes, such as blood vessels and valves. At critically high velocities, the flow pattern may be transformed from a quiet, uniform smooth-flowing stream to an interrupted series of jets with the production of audible sound and with marked energy losses. The present study deals primarily with the paradoxically increased flow which may take place through collapsible tubes when a resistance is added to the outlet from the system. This marked deviation from the laws for rigid tubes is attributed to the vessel-distending effects of the added resistance, and to the inhibition of the phenomenon of recurrent collapsibility. The present in vitro experiments are used to attempt to explain certain paradoxical findings in flow through the collapsible tube systems of the body.

Arrival time and calibrated contour of the pulse wave, determined indirectly from recordings of arterial compression sounds☆☆☆★★★

Abstract A new, safe, indirect method for obtaining a calibrated ascending limb of the arterial pulse wave and its arrival time at the site of measurement is described. The time from onset of the Q wave of the electrocardiogram until the registration of the arterial compression sound of Korotkoff (Q-K time) is shown to be related to the arrival time of the pulse wave at the artery under the cuff. A plot of the Q-K time against the pressure in the sphygmomanometer cuff permits the construction of a calibrated contour of the pulse wave. This relationship was confirmed by intra-arterial puncture techniques. The Q-K time is unaffected by changes in the blood flow through the extremity compressed by the cuff. The Q-K time is shortened and the slope of the upstroke is made more steep by generalized exertion, epinephrine, and norepinephrine. Analysis suggests that the shortening and the change in slope may be manifestations of an increase in pulse-wave velocity.

Physical Factors in the Progression of Stenotic Vascular Lesions

An explanation of the progression of stenotic lesions was sought in animal experiments. After surgical decrease of the lumen of arteries, progressive ingrowth of fibrous connective tissue led to the development of stenosis with changes in the artery that resembled those of coarctation. These changes are explained by the action of local blood pressures. Phenomena such as progressive stenosis, valvulogenesis, patterns of lipid infiltration, medial hypertrophy, thinning, and cystic change are discussed in terms of the concepts derived from these studies.

Direct measurement of bronchial arterial flow.

A method is described for the measurement of the collateral pulmonary blood flow in the thoracotomized dog by utilization of a flow-meter which measures flow into an aortic sac from which the bronchial arteries arise. This preparation maintains the normal perfusing pressures and diminishes phase changes in the arterial pulse waves. The bronchial vascular resistance is increased by an increase in the insufflation air pressure, by bilateral vagotomy, or by the administration of l-epinephrine into the bronchial arterial circulation. The bronchial vascular resistance was decreased after a transitory interruption of the bronchial arterial blood flow (reactive hyperemia). After administration of serotonin in the bronchial artery, a transient increase in resistance was followed by a marked decrease. Intrapulmonary vascular injections produced only a decrease in resistance. The present data demonstrate the sensitivity of the preparation described.

Pressor Mechanisms Induced by Intracranial Compression

A sudden rise in intracranial pressure initiates a three-fold cardiovascular response in the dog. Within one second after the onset of compression, the blood pressure rises sharply, presumably as a result of a direct neurogenic stimulus to the arterioles; the pressure then levels off in a few seconds. A second pressor effect is apparently due to the secretion into the blood stream of graded amounts of nor-epinephrine-like materials at the onset of compression; this rise is delayed about 12 seconds, a period perhaps associated with its circulation to the arterioles. In some experiments, a heart rate increase occurs at this time. It is shown by a special technique that the circulating blood volume increases about 10 per cent during this period. With the offset of compression all these effects disappear in the same order. The potential role of these mechanisms in the blood pressure regulating complex is discussed.