Left Ventricular Pressure-Volume Relations and Performance as Affected by Sudden Increases in Developed Pressure

Abstract

Left ventricular performance in the isolated dog heart was observed in a preparation in which left ventricular pressure and volume could be monitored continuously while the ventricle contracted isobarically by compressing air into a large chamber. By suddenly reducing the orifice connecting the ventricle to the chamber a constant load was imposed on the ventricle, abruptly forcing it to develop pressure in systole. This pressure increased over the ensuing 3 minutes while both the load and the end-diastolic pressure remained constant, implying that the sudden development of pressure by the ventricle was attended by a positive inotropic effect, otherwise known as homeometric autoregulation. Further studies showed this positive inotropic effect to be a function of the magnitude of the abrupt increase in systolic pressure and the time course of the experiment. /3-adrenergic receptor blockade with propranolol decreased but did not abolish this effect. Infusion of norepinephrine did not enhance it. Increases in ventricular compliance that accompanied loading could not fully account for it. Evidence is presented that this positive inotropic effect may in part be mediated through the release of intrinsic catecholamines when the ventricle is forced to increase its systolic pressure.

The effect of sustained stellate ganglion stimulation on left ventricular contractility in the dog.

“…Kanazawa et al reported that close positive correlation between left ventricular diameter and left ventricular segment length obtained as the same manner exists, and that the end-systolic P-L relationship is thus acceptable for estimating ventricular contractility (Suga and Sagawa 1974; Kanazawa et al 1983;Crozatier et al 1984). Aortic constriction has also been used as an experimental procedure for evaluating left ventricular contractility (Monroe et al 1968;Crozatier et al 1984). In the present study, as shown in Figs.…”

“…However, another report describes a positive relationship between myocardial norepinephrine depletion and defective myocardial contractility ). Actually, the efferent sympathetic nerve is discharged each beat in situ (Felder and Thames 1981), so norepinephrine deple tion seems to disturb the augmentation of contractility by sympathetic nerve excitation (Covell et al 1966;Monroe et al 1968). Thus, it is quite reasonable to assume that cardiac norepinephrine stores would play an important role in maintaining the cardiac contractile state in vivo.…”

The Anrep Effect Reconsidered

“…They, too, dismissed the coronary flow hypothesis of Starling, in view of the findings of Rosenblueth et al (5) and Sarnoff et al (6). As the effect was noted in reserpinized preparations (8,9) they were disinclined to implicate catacholamines in its mechanism. Despite the fact that Sarnoff et al showed an efflux of potassium from the heart after a sudden increase in systolic pressure (10) Blinks and Koch-Weser pointed out differences between the Anrep effect and the Bowditch effect, making it doubtful that similar mechanisms were involved.…”

“…Later, a report from this laboratory showed the effect to be decreased, but not abolished in an isolated heart preparation treated with propranolol (9). Here it was postulated that at least part of the mechanism could be attributed to catacholamines as norepinephrine has been shown to be released by the ventricle in quantities roughly proportional to systolic pressure (12,13).…”

“…Here it was postulated that at least part of the mechanism could be attributed to catacholamines as norepinephrine has been shown to be released by the ventricle in quantities roughly proportional to systolic pressure (12,13). AdThe Journal of Clinical Investigation Volume 51 October 1972mittedly, however, these authors were unable to ascribe a single mechanism to explain completely the "Anrep" effect (9).…”