This study presents an improved method for the measurement of intramyocardial pressure (IMP) using the servo-nulling mechanism. Glass micropipettes (20-24 microns OD) were used as transducers, coated to increase their mechanical resistance to breakage, and placed inside the left ventricular wall with a micropipette holder and manipulator. IMP was measured at the base of the left ventricle in working and nonworking isolated cat hearts that were perfused with Krebs-Henseleit buffer. In working hearts a transmural gradient of systolic IMP oriented from endocardium toward the epicardium was found; the endocardial values for systolic IMP were slightly higher than systolic left ventricular pressure (LVP), by 11-18%. Increases in afterload induced increases in IMP, without changing the systolic IMP-to-LVP ratio. In nonworking hearts with drained left ventricles, the systolic transmural gradient for IMP described for working hearts persisted, but at lower values, and was directly dependent on coronary perfusion pressure. Systolic IMP-to-LVP ratios were always > 1. The diastolic IMP of both working and nonworking hearts exhibited irregular transmural gradients. Our results support the view that generated systolic IMP is largely independent of LVP development.

The maximal negative peak of the first derivative of left ventricular pressure was examined as an index of the end of ventricular ejection by comparing it with the end of aortic flow. Under varying heart rate and afterload situations in anesthetized dogs, a correlation coefficient of 0.982 was obtained with a mean error of less than 0.4 ms. This may be a useful end point for determining systolic time where only ventricular pressure is available.

Chronic hypertension, known to affect the collagen profile of the heart, and exercise result in impaired or improved heart function, respectively. Collagen types I [alpha 1(I)2 and alpha 2(I)] and III [alpha 1(III)3] are the predominant interstitial collagens thought to influence cardiac function, and the ratio of type III to I (collagen III/I) is thought to be a significant factor in the altered relaxation observed in hypertrophy. The present study tested the hypothesis that the myocardial structure and function are different in chronically exercise-trained vs. hypertensive rat hearts. Male rats were either chronically exercised (XTr) or submitted to experimental hypertension by coarctation of the abdominal aorta (Hyp) for 10 wks. Heart rate, blood pressure, and maximal rate of fall of the left ventricular pressure (-dp/dt) were recorded during isoproterenol stimulation. Results showed that both Hyp and XTr had higher heart weight and left ventricular weight-to-body weight ratios (P < 0.05). Mean arterial pressure (MAP) was higher in Hyp and lower in XTr (P < 0.05), whereas (-dP/dt)/MAP was diminished in Hyp but enhanced in XTr. Left ventricular collagen was higher in Hyp than XTr, whereas collagen III/I was reduced in Hyp compared with XTr (P < 0.05). Scanning and transmission electron microscopy also supported an accumulation of left ventricular collagen in Hyp compared with XTr. A negative correlation was observed between collagen III/I and (-dP/dt)/ MAP (r = -0.91; P < 0.05). These results suggest an important relationship between adaptations in left ventricular collagen and the changes in diastolic function observed in both chronic hypertension and exercise cardiac stress.

Myocardial function in sepsis and endotoxin shock is reviewed. Clinical, whole animal, and isolated tissue studies are compared to answer the question whether sepsis and/or endotoxin directly damage the myocardium. Myocardial performance is considered relative to control of preload, afterload, and heart rate. Despite the fact that these vary widely in different studies, there is overwhelming evidence that myocardial performance is depressed in both sepsis and endotoxin shock. The depression is dose related, occurs early after large doses of endotoxin but may follow a hyperdynamic phase in sepsis or after low doses of endotoxin. Endotoxin itself does not appear to be the depressant factor; the final depressant substance(s) is unknown. Calcium transport by the sarcoplasmic reticulum is depressed. This defect is more prominent in the endocardium than in the epicardium. Myocardial adenosinetriphosphatase (ATPase) and norepinephrine stores may be depleted. The septic myocardium has an increased dependence on sympathetic nerve stimulation. There is little evidence that the cause of the myocardial depression is an inadequate coronary blood flow.

Fourier analysis has been applied to simultaneously obtained ventricular pressure, ascending aortic pressure, and aortic flow in the closed-and openchest dog and during infusion with isoproterenol, norepinephrine, and phenylephrine. Partial measurements were also obtained from a sheep and a primate. Impedance moduli and phases were calculated from the ventricular (forcing) and aortic (input) side of the aortic valve and compared. Forcing impedance was similar in form but larger than input impedance, and the phase became positive earlier. Ventricular and aortic powers were calculated and expressed as pressure power, kinetic energy power, and reactive power, along with their harmonic distributions. Mean pressure represented 80 to 91% of total load power but only 20 to 51% of total ventricular power. Calculated efficiency varied from 35% with isoproterenol infusion to 100% with norepinephrine, phenylephrine, and open-chest states. Control efficiency was 78%. The concept of impedance matching was investigated; maximal efficiency occurred with optimal matching. Internal resistance was shown to represent an easily measurable quantity which also partially corresponds to the more complex impedance measurement.KEY WORDS ventricular impedance phenylephrine isoproterenol internal resistance ventricular power norepinephrine ventricular efficiency thoracotomy kinetic energy• Numerous reports have used Fourier series and spectral analysis to describe the complex input impedances of the systemic and pulmonary circuits and the hydraulic power consumed (1-6). The generators providing the inputs into these beds (the right and left ventricles) have largely been ignored in these descriptions, yet their characteristics would appear to be equally important in terms of their ability to match the impedance of the vascular bed supplied for maximum efficiency and power transfer, for purposes of modeling of the cardiovascular system and the design of artificial hearts, and perhaps as another way of describing ventricular performance.Abel (7) and Fronek (8) have previously described an "internal impedance" for the left ventricle using only mean flow and pressure measurements, thereby lumping all the properties that vary with frequency as a "resistance" value. It is feasible, however, to describe the forcing impedance of the ventricle and the hydraulic power produced in the same manner as that used for the input impedances and power consumption of the systemic and pulmonary beds. This report deals with such a concept and with the ability of the pump to match its associated bed in terms of impedance and power transfer at