SUMMARY The mechanical properties of the normal left ventricular wall during diastole were studied in 15 chronically instrumented, conscious dogs. Left ventricular minor and major axis diameters and equatorial wall thickness were measured with implanted pulse-transit ultrasonic dimension transducers. Left ventricular and pleural pressures were measured with high fidelity micromanometers. Circumferential mural stress was calculated by using an ellipsoidal shell theory; circumferential strain was calculated by using a natural strain definition. The static elastic properties of the myocardium were estimated by fitting the stress-strain values at the points of diastasis during a vena caval occlusion to an exponential function. A modified creep test was used to evaluate the series viscous properties of the myocardium. Acute increases in systolic and diastolic loading were produced by inflating implanted aortic occluders for 15 minutes in five dogs. In these dogs, the static stress-strain curves were not altered significantly after this period of pressure loading, indicating tbat short-term series viscous properties are negligible. Parallel viscous properties were evaluated in 10 dogs by means of the variable rate stretch test of dynamic diastolic filling. A viscoelastic model incorporating a parallel viscous element fit the dynamic stress-strain data better and predicted the static elastic properties more accurately than a simple exponential model. Thus, the mechanical characteristics of the diastolic left ventricle can be represented most precisely by a viscoelastic model that includes a parallel viscous element.AN EXPONENTIAL relationship between ventricular pressure and volume during diastole was first demonstrated by Frank.1 Influenced by Blix, 2 Frank concluded that this observation represented a fundamental relationship between diastolic force and length within the ventricular wall. During the past two decades there has been a renewed interest in describing the mechanical properties of diastolic myocardium, and numerous investigators have confirmed Frank's observations in a variety of experimental preparations. "5 On the basis of these studies it generally has been accepted that, in both the isolated and the intact heart, an exponential relationship exists between left ventricular pressure and volume during diastole. 6 However, several authors recently have suggested that fitting pressure-volume or pressure-dimension data from a single diastolic filling period with a simple exponential function may be an oversimplification. "12 Indeed, previous experiments that demonstrated exponential pressure-dimension curves in the intact heart utilized static measurements during induced volume changes.13 So far as we are aware, there are no directly measured data in the literature which indicate that ventricular pressure and di- Received July 9,1976; accepted for publication December 10,1976. mensions are exponentially related during the dynamic filling of a single diastole. The diastolic mechanical properties of isolate...
A B S T R A C T In order to evaluate the effects of atrial contraction on left ventricular function, the pressure gradient technique was used to measure instantaneous aortic blood flow and pressure in nine patients, six having complete heart block and three having normal sinus rhythm. From these data both left ventricular stroke volume and stroke work were calculated. Ventricular rate was controlled by transvenous right ventricular pacing over a range of 50-158 beats/min. At each heart rate, beats which were not preceded by a P wave served as controls. The other beats were divided into six groups according to the duration of the preceding PR interval. The results indicated that stroke volume and stroke work were always affected similarly. In one patient the presence of a P wave did not alter the subsequent stroke volume significantly. In the other patients, beats preceded by P waves had stroke volumes greater than the controls. In general, there was no difference in stroke volume for beats preceded by a P wave having a PR interval within the range of 0.05-0.20 sec. As the PR interval lengthened beyond 0.20 sec stroke volume tended to decrease, especially at more rapid heart rates. The absolute increase in stroke volume after a beat preceded by a P wave (PR interval 0.05-0.20 sec) was quite variable among the patients. For a given patient the absolute increase in stroke volume was essentially independent of heart rate. The percentage change in stroke volume, however, was always greater as the heart rate increased.
Phasic left ventricular wall force and wall thickness were monitored with appropriate transducers to provide a direct measurement of circumferential wall stress in open-chest dogs. Left ventricular pressure and measurements of chamber geometry were used to estimate the wall stress using several geometric models. During the initial control period, peak and end-ejection measured wall stresses were 207 ± 19 and 104 ± 13 g/cm 2 , respectively. The best estimates of these values were 198 ± 18 and 117 ± 11 g/cm 2 obtained from a modified thin-wall ellipse formula in which the midwall rather than the endocardial radius was used. Wide variations in hemodynamic conditions were produced with intravenous infusions of nitroglycerin, phenylephrine, and isoproterenol. Comparison of directly measured and estimated values during all control periods and during the response to these interventions showed that both the modified thin-wall ellipse and a thick-wall ellipse were generally accurate predictors of the measured wall stress. All other models tended to underestimate measured stress. The sensitivity of the estimated wall stress computed by the models to geometric measurement errors was also evaluated. A thick-wall sphere was the most sensitive to both circumferential length and wall thickness measurement errors, and a thick-wall ellipse was the least sensitive. All models examined were relatively insensitive to base-to-apex length measurement errors.
This study was undertaken to determine whether coronary blood flow can be regulated in response to coronary arterial occlusions briefer than a single diastole. The possible involvement of metabolic vs. myogenic mechanisms in such regulation was investigated. Eleven conscious dogs with experimentally produced complete heart block, chronically implanted electromagnetic flow probes, and pneumatic occluders on the left circumflex coronary artery were studied. Diastolic coronary occlusions lasting 100 to 400 msec were performed at paced heart rates of 40, 60, and 120 beats/min. At a heart rate of 60 beats/min, a 200-msec occlusion was sufficiently long to produce a significant reactive hyperemic response; 400-mec occlusions resulted in larger responses, while 100-msec occlusions did not generate a discernible response. The onset of reactive hyperemia was delayed from the end of the occlusion until the first post-occlusion systole. The length of this delay could be altered by changing the heart rate or occlusion duration, but no significant response was detected before the first post-occlusion systole. This characteristic of the data is more consistent with a metabolic than with a myogenic mechanism. If the response is metabolic, the data demonstrate that autoregulation of coronary flow by such a mechanism is very rapid, occurring during the first systole in which a flow deficit is detected by the myocardium.
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