MRI-determined left ventricular "crescent effect": a consequence of the slight deviation of contents of the pericardial sack from the constant-volume state

During one cardiac cycle, the volume encompassed by the pericardial sack in healthy subjects remains nearly constant, with a transient +/-5% decrease in volume at end systole. This "constant-volume" attribute defines a constraint that the longitudinal versus radial pericardial contour dimension relationship must obey. Using cardiac MRI, we determined the extent to which the constant-volume attribute is valid from four-chamber slices (two-dimensional) compared with three-dimensional volumetric data. We also compared the relative percentage of longitudinal versus radial (short-axis) change in cross-sectional area (dimension) of the pericardial contour, thereby assessing the fate of the +/-5% end-systolic volume decrease. We analyzed images from 10 normal volunteers and 1 subject with congenital absence of the pericardium, obtained using a 1.5-T MR scanner. Short-axis cine loop stacks covering the entire heart were acquired, as were single four-chamber cine loops. In the short-axis and four-chamber slices, relative to midventricular end-diastolic location, end-systolic pericardial (left ventricular epicardial) displacement was observed to be radial and maximized at end systole. Longitudinal (apex to mediastinum) pericardial contour dimension change and pericardial area change on the four-chamber slice were negligible throughout the cardiac cycle. We conclude that the +/-5% end-systolic decrease in the volume encompassed by the pericardial sack is primarily accounted for by a "crescent effect" on short-axis views, manifesting as a nonisotropic radial diminution of the pericardial/epicardial contour of the left ventricle. This systolic drop in cardiac volume occurs primarily at the ventricular level and is made up during the subsequent diastole when blood crosses the pericardium in the pulmonary venous Doppler D wave during early rapid left ventricular filling.     

Impact of pericardial restraint on right atrial mechanics during acute right ventricular pressure load

Optimization of right atrial (RA) mechanics is important for maintaining right ventricular (RV) filling and global cardiac output. However, the impact of pericardial restraint on RA function and the compensatory role of the right atrium to changes in RV afterload remain poorly characterized. In eight open-chest sheep, RA elastance (contractility) and chamber stiffness were measured (RA pressure-volume relations) at baseline and during partial pulmonary artery (PA) occlusion. Data were collected before and after pericardiotomy. With the pericardium intact and partial PA occlusion, RA elastance increased by 28% (P < 0.04), whereas RA stiffness tended to rise (P = 0.08). However, after pericardiotomy, there was a significant fall in both RA elastance (54%, P < 0.04) and stiffness (39%, P < 0.04), and subsequent PA occlusion failed to induce a change in elastance (P > 0.19) or stiffness (P > 0.84). After pericardiotomy, RA elastance and stiffness fell dramatically, and the compensatory response of the right atrium to elevated RV afterload was lost. The ability of the right atrium to respond to changes in RV hemodynamics is highly dependent on pericardial integrity.     

Cardiac function of the leopard shark,Triakis semifasciata

Summary The pressure difference between the cardinal sinus and the pericardium, and the transmural ventricular diastolic pressure at rest and during swimming in the leopard shark, Triakis semifasciata, was measured to characterize the mechanism of cardiac filling in chronically-instrumented fish and to evaluate cardiac responses to swimming. Echo-Doppler and radiographic imaging were also used to fully describe the cardiac cycle. Swimming induces an increase in preload as manifested by a large increment of cardinal sinus pressure (0.26/0.20 [systolic/diastolic] to 0.49/0.32 kPa) which always exceeds pericardial pressure. Increases in both mean ventricular diastolic transmural pressure (0.30–0.77 kPa) and cardinal sinus pressure during swimming suggest increased cardiac filling by vis a tergo as the mechanism for augmenting cardiac output. In contrast to mammals, the fluid-filled pericardial space of elasmobranchs is considerably larger and the pericardium itself does not move in concert with the heart throughout the cardiac cycle. Also, modest increases in heart rate drastically curtail the duration of diastole, which becomes much less than that of systole, a phenomenon not found in mammals. In the absence of tachycardia (<40 bpm), ventricular filling is characterized by a period of early rapid filling, and a late period of filling owing to atrial systole, separated by a period of diastasis. Ventricular filling in elasmobranchs is thus biphasic and is not solely dependent on atrial systole. Atrial diastole is characterized by three filling periods associated with atrial relaxation, ventricular ejection, and sinus venosus contraction. The estimated ventricular ejection fraction of Triakis (80%) exceeds that of the mammalian left ventricle.     

Right atrial pressure as measure of ventricular constraint in newborn lambs

Although the lungs and pericardium constrain the heart and limit cardiac output, no method exists to assess this constraint in sick newborns. We hypothesize that a useful estimate of ventricular constraint may be obtained by measuring right atrial pressure (P(RA)) in the newborn. To test this hypothesis, we measured P(RA), thoracic inferior vena caval pressure (P(IVC); saline-filled catheters), and ventricular constraint (pericardial pressure, P(PER); liquid-containing balloon) in 4-wk-old (neonatal, n = 12) and 3-day-old (newborn, n = 6) anesthetized lambs. The measurements were made while LV filling pressure was altered (0-20 mmHg) and while positive end-expiratory pressure (PEEP) was maintained at 2.5 or 15 cmH2O. In all of the lambs, a strong linear relationship (r) existed between P(RA) and P(PER) (P(RA) = 1.19 P(PER) + 0.0, r = 0.99) and between P(IVC) and P(PER) (P(IVC) = 1.24 P(PER) + 0.1, r = 0.99; PEEP of 2.5 cmH2O). Similar relationships were also observed with increased PEEP (P(RA) = 1.29 P(PER)-1.2, r = 0.98 and P(IVC) = 1.32 P(PER)-1.2, r = 0.97). Because P(RA) provides an accurate measure of ventricular constraint in the normal lamb, it may be a useful measure of ventricular constraint in the sick newborn.     

Opening the pericardium during pulmonary artery constriction improves cardiac function.

During acute pulmonary hypertension, both the pericardium and the right ventricle (RV) constrain left ventricular (LV) filling; therefore, pericardiotomy should improve LV function. LV, RV, and pericardial pressures and RV and LV dimensions and LV stroke volume (SV) were measured in six anesthetized dogs. The pericardium was closed, the chest was left open, and the lungs were held away from the heart. Data were collected at baseline, during pulmonary artery constriction (PAC), and after pericardiotomy with PAC maintained. PAC decreased SV by one-half. RV diameter increased, and septum-to-LV free wall diameter and LV area (our index of LV end-diastolic volume) decreased. Compared with during PAC, pericardiotomy increased LV area and SV increased 35%. LV and RV compliance (pressure-dimension relations) and LV contractility (stroke work-LV area relations) were unchanged. Although series interaction accounts for much of the decreased cardiac output during acute pulmonary hypertension, pericardial constraint and leftward septal shift are also important. Pericardiotomy can improve LV function in the absence of other sources of external constraint to LV filling.     

Relationship between right ventricular wave speed and elastance in dogs

Wave speed (c) must be known to separate forward- and backward-going waves during wave-intensity analysis, which measures the energy transported by the waves in the circulation. c is related to elastance; the present study was performed to measure right ventricular (RV) c during the cardiac cycle and to compare c with RV elastance. In 7 dogs, we measured right atrial, pulmonary arterial, pericardial and 2 RV pressures, and pulmonary arterial flow. A pulse generator was connected to the RV apex, and c was measured by determining the transit time between the 2 high-fidelity RV pressure transducers; the distance was measured roentgenographically. Eight sonomicrometry crystals were implanted in the RV endocardium to calculate RV volume and, thereby, elastance. RV c ranged from approximately 1 m/s during diastole to approximately 4 m/s during systole. Log-log plots of c vs. elastance were linear. These slopes represent the power relationships between c and elastance and ranged from 0.30 to 0.56; for the combined data, it was 0.31. Given knowledge of c, forward- and backward-going waves can be identified and their energy quantitated. In the canine RV, c is approximately proportional to 1/3 the power of elastance: log c = 0.31.log E - 2.05.     

Quantification of left and right ventricular kinetic energy using four-dimensional intracardiac magnetic resonance imaging flow measurements

We aimed to quantify kinetic energy (KE) during the entire cardiac cycle of the left ventricle (LV) and right ventricle (RV) using four-dimensional phase-contrast magnetic resonance imaging (MRI). KE was quantified in healthy volunteers (n = 9) using an in-house developed software. Mean KE through the cardiac cycle of the LV and the RV were highly correlated (r(2) = 0.96). Mean KE was related to end-diastolic volume (r(2) = 0.66 for LV and r(2) = 0.74 for RV), end-systolic volume (r(2) = 0.59 and 0.68), and stroke volume (r(2) = 0.55 and 0.60), but not to ejection fraction (r(2) < 0.01, P = not significant for both). Three KE peaks were found in both ventricles, in systole, early diastole, and late diastole. In systole, peak KE in the LV was lower (4.9 ± 0.4 mJ, P = 0.004) compared with the RV (7.5 ± 0.8 mJ). In contrast, KE during early diastole was higher in the LV (6.0 ± 0.6 mJ, P = 0.004) compared with the RV (3.6 ± 0.4 mJ). The late diastolic peaks were smaller than the systolic and early diastolic peaks (1.3 ± 0.2 and 1.2 ± 0.2 mJ). Modeling estimated the proportion of KE to total external work, which comprised ～0.3% of LV external work and 3% of RV energy at rest and 3 vs. 24% during peak exercise. The higher early diastolic KE in the LV indicates that LV filling is more dependent on ventricular suction compared with the RV. RV early diastolic filling, on the other hand, may be caused to a higher degree of the return of the atrioventricular plane toward the base of the heart. The difference in ventricular geometry with a longer outflow tract in the RV compared with the LV explains the higher systolic KE in the RV.     

Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis

Pressure waves are thought to travel from the left atrium (LA) to the pulmonary artery (PA) only retrogradely, via the vasculature. In seven anesthetized open-chest dogs, a balloon was placed in the LA, which was rapidly inflated and deflated during diastole, early systole, and late systole. High-fidelity pressures were measured within and around the heart. Measurements were made at low volume [LoV; left ventricular end-diastolic pressure (LVEDP) = 5-9 mmHg], high volume (HiV; LVEDP = 16-19 mmHg), and HiV with the pericardium removed. Wave-intensity analysis demonstrated that, except during late systole, balloon inflation created forward-going PA compression waves that were transmitted directly through the heart without measurable delay; backward PA compression waves were transmitted in-series through the pulmonary vasculature and arrived after delays of 90 +/- 3 ms (HiV) and 103 +/- 5 ms (LoV; P < 0.05). Direct transmission was greater during diastole, and both direct and series transmission increased with volume loading. Pressure waves from the LA arrive in the PA by two distinct routes: rapidly and directly through the heart and delayed and in-series through the pulmonary vasculature.     

A novel technique for measurement of pericardial pressure

To determine whether pericardial liquid pressure accurately measures pericardial constraint, we developed a technique in which a catheter was positioned perpendicular to the epicardial surface. This device, which occupies little or no pericardial space, couples the thin film of liquid to a transducer. In six open-chest dogs, we also measured left ventricular (LV) end-diastolic pressure (LVEDP) and anteroposterior and septum-to-free wall diameters. LVEDP was raised incrementally to approximately 25 mmHg by saline infusion. With the use of the product of the two diameters as an index of area (A(LV)), LVEDP-A(LV) relationships were obtained with the pericardium closed and again after the pericardium had been widely opened to obtain the isovolumic difference in LVEDP (DeltaLVEDP). In all dogs, the technique yielded values of pericardial pressure equal to DeltaLVEDP as well as equal to that measured using a previously placed balloon transducer in the same location and at the same A(LV). We conclude that, when the pressure of the pericardial liquid is appropriately measured, it (in addition to the balloon-measured contact stress) defines the diastolic constraining effect of the pericardium. Furthermore, we suggest that earlier measurements of pericardial "liquid pressure" were low, due to an artifact of measurement.     

Effects of changes in left ventricular loading and pleural pressure on mitral flow

The cause of the fall in left ventricular (LV) stroke volume (SV) during a fall in pleural pressure (Pp1) has been in dispute for over a century. We have defined the changes in the temporal relationship between LV inflow (Qm) and outflow (Qa) in a canine preparation to test the mutually exclusive hypotheses that the fall in LVSV is caused only by changes during diastole (e.g., ventricular interdependence) or only by changes during systole (e.g., afterload). The ability of the experimental preparation to measure the results of acute changes in right heart volume or output and acute changes in LV afterload was validated in open-chest studies with and without pericardial constraint. In closed-chest studies, with a fall in Pp1 during a Mueller maneuver Qm reached both its inspiratory minimum and expiratory maximum before Qa in 80% of the Mueller maneuvers, invalidating both hypotheses, which each required that one flow lead the other in 100% of the Mueller maneuvers. Review of individual records suggested that if the rapid changes in Pp1 occurred during systole, Qa could vary in a manner independent of the preceding Qm. These studies suggest that both diastolic and systolic events may contribute to the fall in SV, while causing opposite changes in LV volumes.     

Increased right ventricular output and central pulmonary reservoir function support rise in pulmonary blood flow during adenosine infusion in the ovine fetus

Although adenosine markedly increases fetal pulmonary blood flow, the specific changes in pulmonary trunk (PT), ductus arteriosus (DA), and conduit pulmonary artery (PA) flow interactions that support this increased flow are unknown. To address this issue, seven anesthetized late-gestation fetal sheep were instrumented with PT, DA, and left PA micromanometer catheters and transit-time flow probes. Blood flow profile and wave intensity analyses were performed at baseline and after adenosine infusion to increase PA flow approximately fivefold. With adenosine infusion, DA mean and phasic flows were unchanged, but increases in mean PT (500 ± 256 ml/min, P = 0.002) and the combined left and right PA flow (479 ± 181 ml/min, P < 0.001) were similar (P > 0.7) and related to a larger flow-increasing forward-running compression wave arising from right ventricular (RV) impulsive contraction. Moreover, while the increased PT flow was confined to systole, the rise in PA flow spanned systole (316 ml/min) and diastole (163 ml/min). This elevated PA diastolic flow was accompanied by a 170% greater discharge from a PT and main PA reservoir filled in systole (P < 0.001), but loss of retrograde blood discharge from a conduit PA reservoir that was evident at baseline. These data suggest that 1) an increase in fetal pulmonary blood flow produced by adenosine infusion is primarily supported by a higher PT blood flow (i.e., RV output); 2) about two-thirds of this increased RV output passes into the pulmonary circulation during systole; and 3) the remainder is transiently stored in a central PT and main PA systolic reservoir, from where it discharges into the lungs in diastole.     

A 2D FE model of the heart demonstrates the role of the pericardium in ventricular deformation

During pulmonary artery constriction (PAC), an experimental model of acute right ventricular (RV) pressure overload, the interventricular septum flattens and inverts. Finite element (FE) analysis has shown that the septum is subject to axial compression and bending when so deformed. This study examines the effects of acute PAC on the left ventricular (LV) free wall and the role the pericardium may play in these effects. In eight open-chest anesthetized dogs, LV, RV, aortic, and pericardial pressures were recorded under control conditions and with PAC. Model dimensions were derived from two-dimensional echocardiography minor-axis images of the heart. At control (pericardium closed), FE analysis showed that the septum was concave to the LV; stresses in the LV, RV, and septum were low; and the pericardium was subject to circumferential tension. With PAC, RV end-diastolic pressure exceeded LV pressure and the septum inverted. Compressive stresses developed circumferentially in the septum out to the RV insertion points, forming an arch-like pattern. Sharp bending occurred near the insertion points, accompanied by flattening of the LV free wall. With the pericardium open, the deformations and stresses were different. The RV became much larger, especially with PAC. With PAC, the arch-like circumferential stresses still developed in the septum, but their magnitudes were reduced, compared with the pericardium-closed case. There was no free wall inversion and flattening was less. From these FE results, the pericardium has a significant influence on the structural behavior of the septum and the LV and RV free walls. Furthermore, the deformation of the heart is dependent on whether the pericardium is open or closed.     

Differential modulation of right ventricular strain and right atrial mechanics in mild vs. severe pressure overload

Increased right atrial (RA) and ventricular (RV) chamber volumes are a late maladaptive response to chronic pulmonary hypertension. The purpose of the current investigation was to characterize the early compensatory changes that occur in the right heart during chronic RV pressure overload before the development of chamber dilation. Magnetic resonance imaging with radiofrequency tissue tagging was performed on dogs at baseline and after 10 wk of pulmonary artery banding to yield either mild RV pressure overload (36% rise in RV pressure; n = 5) or severe overload (250% rise in RV pressure; n = 4). The RV free wall was divided into three segments within a midventricular plane, and circumferential myocardial strain was calculated for each segment, the septum, and the left ventricle. Chamber volumes were calculated from stacked MRI images, and RA mechanics were characterized by calculating the RA reservoir, conduit, and pump contribution to RV filling. With mild RV overload, there were no changes in RV strain or RA function. With severe RV overload, RV circumferential strain diminished by 62% anterior (P = 0.04), 42% inferior (P = 0.03), and 50% in the septum (P = 0.02), with no change in the left ventricle (P = 0.12). RV filling became more dependent on RA conduit function, which increased from 30 ± 9 to 43 ± 13% (P = 0.01), than on RA reservoir function, which decreased from 47 ± 6 to 33 ± 4% (P = 0.04), with no change in RA pump function (P = 0.94). RA and RV volumes and RV ejection fraction were unchanged from baseline during either mild (P > 0.10) or severe RV pressure overload (P > 0.53). In response to severe RV pressure overload, RV myocardial strain is segmentally diminished and RV filling becomes more dependent on RA conduit rather than reservoir function. These compensatory mechanisms of the right heart occur early in chronic RV pressure overload before chamber dilation develops.     

Assessment and consequences of the constant-volume attribute of the four-chambered heart

The constant-volume hypothesis regarding the four-chambered heart states that total pericardial volume remains invariant throughout the cardiac cycle. Previous canine studies have indicated that the pericardial volume remains constant within 5%; however, this hypothesis has not been validated in humans using state-of-the-art technology. The constant-volume hypothesis has several predictable functional consequences, including a relationship between atrial ejection fraction and chamber equilibrium volumes. Using cardiac magnetic resonance (MR) imaging (MRI), we measured the extent to which the constant-volume attribute of the heart is valid, and we tested the accuracy of the predicted relationship between atrial ejection fraction and chamber equilibrium volumes. Eleven normal volunteers and one volunteer with congenital absence of the pericardium were imaged using a 1.5-T MR scanner. A short-axis cine-loop stack covering the entire heart was acquired. The cardiac cycle was divided into 20 intervals. For each slice and interval, pericardial volumes were measured. The slices were stacked and summed, and total pericardial volume as a function of time was determined for each subject. In the normal subjects, chamber volumes at ventricular end diastole, end systole, and diastasis were measured. Pericardial volume remained invariant within 5 +/- 1% in normal subjects; maximum variation occurred near end systole. In the subject with congenital absence of the pericardium, total heart volume, defined by the epicardial surface, varied by 12%. The predictions of the relationship between atrial ejection fraction and chamber equilibrium volumes were well fit by MRI data. In normal subjects, the four-chambered heart is a constant-volume pump within 5 +/- 1%, and constant-volume-based modeling accurately predicts previously unreported physiological relationships.     

Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole: model-based prediction with in vivo validation

Previous studies in healthy humans have established that the (approximately 850 ml) volume enclosed by the pericardial sac is nearly constant over the cardiac cycle, exhibiting a transient approximately 5% decrease (approximately 40 ml) from end diastole to end systole. This volume decrease manifests as a "crescent" at the ventricular free wall level when short-axis MRI images of the epicardial surface acquired at end systole and end diastole are superimposed. On the basis of the (near) constant-volume property of the four-chambered heart, the volume decrease ("crescent effect") must be restored during subsequent early diastolic filling via the left atrial conduit volume. Therefore, volume conservation-based modeling predicts that pulmonary venous (PV) Doppler D-wave volume must be causally related to the radial displacement of the epicardium (Delta) (i.e., magnitude of "crescent effect" in the radial direction). We measured Delta from M-mode echocardiographic images and measured D-wave velocity-time integral (VTI) from Doppler PV flow of the right superior PV in 11 subjects with catheterization-determined normal physiology. In accordance with model prediction, high correlation was observed between Delta and D-wave VTI (r=0.86) and early D-wave VTI measured to peak D-wave velocity (r=0.84). Furthermore, selected subjects with various pathological conditions had values of Delta that differed significantly. These observations demonstrate the volume conservation-based causal relationship between radial pericardial displacement of the left ventricle and the PV D-wave-generated filling volume in healthy subjects as well as the potential role of the M-mode echo-derived radial epicardial displacement index Delta as a regional (radial) parameter of diastolic function.     

Experimental cardiac tamponade: correlation of pressure, flow velocity, and echocardiographic changes

Seven episodes of experimental cardiac tamponade were induced in five anesthetized closed-chest dogs. Simultaneous pericardial and intracavitary pressures were synchronized with superior vena caval and transvalvular pulsed-Doppler flow tracings. The earliest indication of tamponade was the development of a negative transmural right atrial pressure that occurred during early ventricular diastole and was associated with echocardiographic evidence of right atrial collapse. This was also associated with reversal of diastolic flow in the superior vena cava and with diminished early diastolic flow velocity across the tricuspid as well as the mitral valve. During more advanced cardiac tamponade, the transmural right atrial pressure became negative during both early and late ventricular diastole as well as during isovolumic ventricular systole. This was associated with a disappearance of early diastolic ventricular filling and right ventricular diastolic collapse as observed on two-dimensional echocardiography. In hypotensive cardiac tamponade (cardiac output diminished by 70%), the decreased transmural right atrial pressure that developed during ventricular systole was accompanied by diminished antegrade flow in the superior vena cava. In advanced and hypotensive tamponade, ventricular filling occurred mainly during atrial contraction.     

Influence of the pericardium on right and left ventricular filling in the dog

We compared the influence of the pericardium on left and right ventricular (LV, RV) filling by measuring LV and RV pressures and segment lengths (SL, LV free wall, and RV inflow and outflow tracts) in six open-chest, pentobarbital sodium-anesthetized dogs before and after pericardiectomy. End-diastolic pressure (EDP) was varied by partial caval occlusion and dextran infusion. At each site the ln EDP-SL relation was fitted by linear regression and characterized by its slope and 1-Torr EDP intercept. The slope and 1-Torr intercept of the LV ln EDP-SL relation changed variably after pericardiectomy, but in each dog a change occurred that shifted this relation downward. In contrast, the RV inflow tract slope invariably decreased significantly after pericardiectomy, whereas its intercept was unchanged in all but one dog. The RV outflow tract results were similar to the inflow tract but less consistent. By the use of the raw EDP-SL data points, we calculated that the absolute contribution of the pericardium to EDP (i.e., the effective pericardial surface pressure) was similar at the three sites. However, as EDP values increased the proportional contribution of the pericardium to right ventricular end-diastolic pressure (RVEDP) increased, whereas that to left ventricular end-diastolic pressure (LVEDP) remained relatively constant. As a result, at the higher EDP values tested, the pericardium was responsible for a larger proportion of RVEDP than LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)     

The pericardium and cardiac transmural filling pressure in the fetal sheep

Fetal pericardial physiology may be important for understanding normal and abnormal circulatory states. Right atrial, pericardial, thoracic, and amniotic fluid pressures were measured simultaneously in chronically-instrumented, near-term fetal sheep. Fourteen experiments were performed in 8 fetuses 4-21 days after surgery. The pressure gradient from the right atrium to the amniotic fluid and its components (transatrial, transpericardial and transthoracic pressures) were measured during control and with rapid infusion and withdrawal of blood. Under control conditions, right atrial minus amniotic pressure was 3.2 +/- 1.8 (SD) torr, right atrial minus pericardial pressure 2.5 +/- 1.7, pericardial minus thoracic pressure 0.6 +/- 0.7, and thoracic minus amniotic pressure 0.1 +/- 1.4. At right atrial pressures above control, pericardial minus thoracic pressure rose linearly with right atrial minus thoracic pressure. The average regression coefficient was 0.50 with an intercept of -1.5 torr. Administration of dextran-saline solution (121% of estimated blood volume) over 2-4 hs in 10 experiments did not reduce the pericardial minus thoracic to right atrial minus thoracic pressure relationship. Fluid added to the pericardium of three lambs progressively shifted the pericardial minus thoracic to right atrial minus thoracic pressure relationship up and to the left. The pericardial minus thoracic to right atrial minus thoracic pressure relationship was unaffected by fetal growth. Thus, the fetal pericardium affects cardiac filling pressures. The affect of the pericardium is increased markedly by pericardial liquid but is unchanged during growth.     

Coronary circulatory pressure gradients

The pressure gradients of the canine coronary circulation were measured in 37 dogs during control and following eight interventions: left stellate ganglion or left vagosympathetic trunk stimulation, as well as isoproterenol, acetylcholine, noradrenaline, adenosine, phenylephrine, or adrenaline infusions. During control, pressure gradients in the epicardial coronary arteries (measured from the aorta to coronary artery branch) were 15.2 +/- 1 mmHg (1 mmHg (1 mmHg = 133.32 Pa) during systole and 10.6 +/- 1.5 mmHg during diastole. Adrenaline increased this systolic gradient, while acetylcholine and phenylephrine decreased it. In contrast, the pressure gradients in the small coronary arteries (from the branch of an epicardial artery to the pressure in an obstructed coronary artery) were 56 +/- 1.3 mmHg during systole and 63.7 +/- 1.3 mmHg during diastole. These gradients were increased by phenylephrine during both systole and diastole, noradrenaline and adrenaline during diastole and decreased by isoproterenol (systolic), left vagosympathetic trunk stimulation (diastolic), acetylcholine (systolic and diastolic), and adenosine (diastolic). The microcirculation and small vein gradients during control were 16.4 +/- 1.2 mmHg during systole and 8.5 +/- 0.8 mmHg during diastole. Decreases in this gradient were produced by isoproterenol, acetylcholine, and adenosine during systole and adenosine during diastole. These observations are consistent with the concept that the coronary circulation has considerable regulatory capacity in all of its component parts. Specifically, epicardial arteries appear to function as both conduits and as resistance vessels, small arteries as major resistance vessels, and the microcirculation and small veins as both capacitors and resistors.