By using excised postmortem hearts obtained from 15 mongrel dogs with the pericardium intact, we investigated mechanical interactions between the four heart chambers from the standpoint of ventricular pressure-volume relationships. The interactions investigated were those between (1) the atrium and the ventricle, (2) the right ventricle and left ventricles, (3) the atrium and one ventricle vs. the other ventricle, and finally (4) the left and right atrium and the right ventricle vs. the left ventricle. For these purposes, we inserted compliant balloons into the four heart chambers without injuring the pericardium, i.e., we incised the base of the atria which was not covered with the pericardium. We obtained the right and/or left ventricular pressure-volume relationships under a constant pressure in three other heart chambers by changing the height of the reservoir connected to each balloon. As a result, both ventricular pressure-volume relationships were hardly affected by an increase in the atrial pressure ranging from 5 to 30 cm H2O with the pericardium removed, although the ventricle became less compliant due to an increase of the same magnitude of the opposite ventricular pressure. On the other hand, the effect of an increase in atrial pressure was distinct with the pericardium intact. Also, all mechanical interactions were enhanced dramatically with the intact pericardium. Thus, the pericardium plays an important role in these mechanical interactions, especially when the filling pressures of all heart chambers increase simultaneously. Clinically, these findings may be important to understanding ventricular functions as related to various heart disease-especially acute heart failure.

We examined the effects of aortic input impedance alteration on left ventricular pressure, aortic flow and ejected volume (integral value of aortic flow), in an isolated blood perfused ejecting canine heart, with special reference to end-systolic values. A hydraulic model which stimulates an aortic input impedance was attached to the aortic root of an excised heart. Left ventricular end-diastolic pressure was kept constant by electrical pacing. Three coronary arteries were perfused with arterial blood from support dogs. When the peripheral resistance in the hydraulic model was changed, there were inverse linear relationships between stroke volume and mean left ventricular systolic pressure and between ejected volume and pressure at end-systole. Time interval from the onset of contraction to end-systole did not change. Thus the relation between stroke volume and mean left ventricular pressure obtained by changes in peripheral resistance is governed by a source resistance, which can be considered as the contractile state of the ventricle. When the capacitance (arterial compliance) was changed, there was no inverse linear relation between stroke volume and mean systolic pressure. In many cases, there was an inverse linear relationship between ejected volume and pressure at end-systole. However, an increase in capacitance prolonged the time interval from the onset of contraction to end-systole. We conclude that the end-systolic pressure-ejected volume relationship in the ejecting heart is governed not only by contractility but also by arterial capacitance.

SUMMARY We examined the effects of graded reduction of afterload on the global left ventricular and regional myocardial functions as well as coronary hemodynamics in hearts with regional ischemia. We used isolated, paced canine hearts that were loaded with a hydraulic system that simulated the aortic input impedance of the dog's arterial tree. The loading conditions could be quantitatively and sequentially changed by the reduction of the systemic vascular resistance of the hydraulic system, while the preload was kept constant using a variable-height reservoir connected to the left atrium. The heart was perfused with arterial blood from a support dog. Mean coronary perfusion pressure was maintained equal to mean aortic pressure (AoP) by a servo-controlled pump. Then, the left circumflex branch was constricted to an approximate 50% flow reduction of the preischemic control condition. The myocardial lengths at ischemic and nonischemic regions were measured with two pairs of ultrasonic crystals.In the hearts without ischemia, cardiac output continued to increase, from 535 14 to 1181 74 ml/min (p < 0.01), as mean AoP decreased from 111 4 to 52 + 3 mm Hg (p < 0.01), although mean coronary blood flow decreased by approximately 50 %. During regional ischemia, at control pressures, performance of the ischemic region diminished from 0.94 + 0.15 to 0.77 + 0.15 mm (p < 0.05). With a small decrease in afterload, from 98 ± 6 to 86 ± 3 mm Hg, performance improved slightly as in the normal region. With a larger reduction in afterload, from 86 ± 3 to 55 ± 6 mm Hg, performance of the ischemic region decreased from 0.77 ± 0.15 to 0.61 ± 0.15 mm (p < 0.05) while cardiac output increased. Thus, there appears to be a bimodal change in performance: a baseline performance, perfusion pressure-mediated decrease and a second, afterload-modulated change.THE REDUCTION of aortic blood pressure (AoP) in the heart with myocardial ischemia lowers left ventricular tension and myocardial metabolic requirements, and decreases coronary blood flow at the same time. Thus, the reduction of AoP has both favorable and unfavorable myocardial effects. Therefore, whether or not the AoP should be decreased is important for the treatment of patients with coronary arterial stenosis.Many investigators'-' have reported the relationship between regional coronary blood flow and the mechanical function in an experimental model in which the afterload pressure was not controlled. Additionally, the effect of the alteration in AoP on ischemic myocardial function has been reported in the heart with an occlusion of a coronary arterial branch. 82 However, there have been only a few reports concerning the relationship between afterload pressure and ischemic myocardial function in a heart with an incomplete coronary stenosis rather than a complete occlusion.Sasayama et al."3 reported that the reduction of AoP aggravated the ischemic myocardial function and its elevation improved it in a heart with a stenosis of the coronary arterial branch. However, Wyatt et al. 14 prove ...

The effects of daily activity and autonomic nerve tone on the fluctuation of ambulatory blood pressure were studied in hypertensive patients. The autonomic nerve tone was measured by frequency domain analysis of the RR interval. Physical activity was evaluated by a walk count, converted to a walk rate (WR), recorded using a digital Holter ECG fitted with an accelerometer, with simultaneous monitoring of blood pressure (Bp). Average values of the WR, H and L/H components were calculated for the 15 min. period just prior to Bp monitoring. The relationship between the average WR, H and L/H values and the Bp was determined by a linear regression analysis. Hypertension was classified into three types, autonomic nerve dominant (AN), exercise dominant (EX), and irregular (IR), based on a high correlation coefficient between Bp and either H or L/H (AN type), between Bp and WR (EX type), or no significant correlation between Bp and any of the parameters (IR type). Of the thirty hypertensive patients studied 11 were classified as AN, 12 as EX, and 7 as IR. Patients of the EX type had significantly lower Bp than patients in the other two classes. Furthermore, all of the IR type patients showed non-dipper type hypertension, suggesting that the Bp regulation mechanisms were impaired. The results suggest the significance of simultaneous monitoring of physical activity and autonomic nerve function at the time of Bp monitoring.

SUMMARY The relationship between cardiac output (CO) and peripheral resistance (Rp) was examined under the following conditions for coronary perfusion: constant coronary flow perfusion; perfusion with a pressure equal to mean aortic pressure (AoP perfusion); and perfusion with a pressure equal to the mean AoP -30 mm Hg (AoP -30 mm Hg perfusion). We also examined the coronary pressure-flow relationship. For these studies, we used paced, isolated, ejecting canine hearts, which were loaded by a hydraulic system that simulated the input impedance of a dog's systemic arterial tree.The CO in the constant coronary flow perfusion continued to increase with the reduction of Rp. The CO in the AoP perfusion became maximal at a slightly subphysiologic Rp, or at an average mean AoP of 65 mm Hg. This mean AoP was closely associated with the lower limit of the autoregulation of coronary blood flow. In the AoP -30 mm Hg perfusion, the mean AoP at which CO became maximal was 72 mm Hg and the corresponding coronary perfusion pressure appeared to be lower than the lower limit of the perfusion pressure range for coronary flow autoregulation. The Rp value at that point was slightly higher than the physiologic range.We conclude that when coronary perfusion pressure changes with mean AoP, and when left ventricular enddiastolic pressure is fixed, there is a clear optimal Rp at which CO becomes maximal, and this optimal Rp is higher if coronary perfusion pressure is biased from mean AoP to a significant degree.BENEFICIAL EFFECTS have been reported in afterload-reducing therapy for the treatment of congestive heart failure. They are achieved from alterations in ventricular systolic loading and ventricular filling pressure through the use of peripheral vasodilator drugs.'17 Reduced systemic vascular resistance (SVR) improves left ventricular systolic loading, and it can both raise the cardiac output (CO) and lower the myocardial oxygen needs in severe congestive heart failure due to ischemic or nonischemic heart disease. '-7 However, afterload-reducing therapy may not always be beneficial, especially when the aortic pressure (AoP) is reduced to the extent of causing a deficit of coronary flow relative to the metabolic need.It is possible to produce beneficial hemodynamic effects with little or no change in mean arterial pressure (MAP). MAP is related to CO and SVR by the formula MAP = CO X SVR (assuming right atrial pressure is negligible). Thus, if the percent increase in CO produced by afterload-reducing therapy is of the same magnitude as the decrease in the SVR, there may be little or no change in MAP. Chatterjee et al.8 observed unloading of the ventricle in terms of the reduction of SVR without a decrease in MAP. Therefore, it is important to examine how the reduction of SVR alters AoP and CO and to determine the minimal safe level of AoP for coronary circulation. The purpose of this study was to determine experimentally how far SVR or AoP can be reduced so as to achieve maximal CO without coronary ischemia. We also examined the ...