Basic determinants of epicardial transudation

1997 ◽  
Vol 273 (3) ◽  
pp. H1408-H1414 ◽  
Author(s):  
R. H. Stewart ◽  
D. A. Rohn ◽  
S. J. Allen ◽  
G. A. Laine
Keyword(s):  
Reflection Coefficient ◽  
Coronary Sinus ◽  
Myocardial Edema ◽  
Hydraulic Conductance ◽  
Linear Increase ◽  
Left Ventricular ◽  
Edema Formation ◽  
Anesthetized Dogs ◽  
The Difference ◽  
Osmotic Reflection Coefficient

Myocardial edema formation, which has been shown to compromise cardiac function, and increased epicardial transudation (pericardial effusion) have been shown to occur after elevation of myocardial venous and lymphatic outflow pressures. The purposes of this study were to estimate the hydraulic conductance and osmotic reflection coefficient for the epicardium and to determine the effect of coronary sinus hypertension and cardiac lymphatic obstruction on epicardial fluid flux (JV,e/Ae). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. JV,e/Ae was determined over 30-min periods for three intracapsular pressures (-5, -15, and -25 mmHg) and two intracapsular solutions exerting colloid osmotic pressures of 7.0 and 2.0 mmHg. Hydraulic conductance was estimated to be 3.7 +/- 0.5 microliters.h-1.cm-2.mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in JV,e/Ae of 16.5 +/- 8.4 microliters.h-1.cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in JV,e/Ae, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.

Unequal right and left ventricular ejection with ectopic beats

1962 ◽  
Vol 203 (6) ◽  
pp. 1141-1144 ◽  
Author(s):  
Jay M. Levy ◽  
Emmanuel Mesel ◽  
Abraham M. Rudolph
Keyword(s):  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Pulmonary Flow ◽  
Anesthetized Dogs ◽  
Ectopic Beats ◽  
The Difference ◽  
The Right ◽  
Ventricular Depolarization

Simultaneous right and left ventricular stroke volumes were measured with electromagnetic flow probes in open-chest, anesthetized dogs. Atrial ectopic beats with normal ventricular depolarization produced differences between right and left ventricular stroke output, although the right and left ventricular pressures were proportionately reduced to an equal extent. This imbalance in volume ejected was a result of the differences in diastolic level, related to peak systolic pressure, in the aorta compared with pulmonary artery. With ventricular ectopic beats, the stimulated ventricle failed to develop the same percentage of control pressure as did the contralateral ventricle. The difference between aortic and pulmonary flow was thus less marked with right ventricular ectopic beats, and exaggerated with left ventricular ectopic beats.

Mechanical cardiopulmonary interdependence

1982 ◽  
Vol 52 (2) ◽  
pp. 333-339 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Chest Wall ◽  
Left Ventricular Pressure ◽  
Pressure Change ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Diastolic Filling ◽  
Elastic Load ◽  
Anesthetized Dogs ◽  
The Difference ◽  
Ventricular Filling

We studied cardiopulmonary interdependence in ten pentobarbital sodium-anesthetized dogs by 1) measuring the increase of left atrial pressure (Pla) required to hold cardiac output (Q) constant on application of a positive end-expiratory pressure (PEEP), 2) determining the reduction of Pla required to mimic the Q fall observed when PEEP was applied while Pla was held constant, and 3) comparing left ventricular pressure-volume curves measured in freshly dead dogs during ventilation with and without PEEP. The atrial pressure changes can be divided into terms for pleural pressure change, lung deformation, and an undefined residual component and can be used to obtain a compliance opposing ventricular filling. Another compliance was derived from the pressure-volume curves. The latter compliance (6.8 ml/cm H2O) significantly exceeded the former (3.9 ml/cm H2O). The difference may have been caused by ventricular interdependence. The respiratory system compliance opposing ventricular filling was approximately one-twentieth of that predicted from lung and chest wall compliances. Deformation of lungs and chest wall appears to be a significant component of the elastic load imposed on ventricular diastolic filling.

Differences in distensibility between the anterior and posterior walls of the left ventricle in dogs

1991 ◽  
Vol 69 (3) ◽  
pp. 334-340
Author(s):  
Zhao-Nian Zhou ◽  
Sheng-Jing Dong ◽  
Eldon R. Smith ◽  
John V. Tyberg
Keyword(s):  
Left Ventricle ◽  
Length Change ◽  
Posterior Wall ◽  
Anterior Wall ◽  
Left Ventricular ◽  
Transmural Pressure ◽  
Segment Length ◽  
Anesthetized Dogs ◽  
Pericardial Pressure ◽  
The Difference

Nonuniformity of myocardial systolic and diastolic performance in the normal left ventricle has been recognized by a number of investigators. Lack of homogeneity in diastolic properties might be caused by or related to differences in the distensibility of different regions of the left ventricular (LV) wall. Thus, we compared the end-diastolic transmural pressure–strain relations in both the anterior and posterior LV walls in seven anesthetized dogs during two interventions (pulmonary artery constriction and aortic constriction). Transmural pressure was defined as the difference between LV intracavitary pressure and local pericardial pressure. LV pressure was measured using a micromanometer; pericardial pressures over the LV anterior and posterior wails were measured with balloon transducers. Circumferentially oriented pairs of sonomicrometer crystals were implanted in the midwall of the anterior and posterior walls of the LV to measure segment lengths. Strains were calculated as (L – L0)/L0, where L was the instantaneous segment length and L0 was the segment length when transmural pressure was zero. The pattern of end-diastolic transmural pressure–strain relations was similar in ail dogs. The change in strain in the posterior wall was always greater than that in the anterior wall. Opening the pericardium did not affect the difference in distensibility of the anterior and posterior walls. The results suggest that the posterior wall is more compliant than the anterior wall (that is, for a given difference in transmural pressure, the local segment length change of the posterior wall was greater). This seems consistent with other observations, which suggest that the posterior wall might make a greater contribution to diastolic filling.Key words: regional ventricular function, diastolic suction, elastic properties.

Measurement of myocardial PCO2 with a microelectrode: its relation to coronary sinus PCO2

1979 ◽  
Vol 236 (1) ◽  
pp. H29-H34
Author(s):  
R. B. Case ◽  
A. Felix ◽  
M. Wachter
Keyword(s):  
Coronary Sinus ◽  
Coronary Flow ◽  
Coronary Occlusion ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Co2 Efflux ◽  
Arterial Pco2 ◽  
Pco2 Electrode ◽  
The Difference

A micro-PCO2 electrode, with dimensions of 1 x 10 mm, and a 63% response time of 14 s was inserted into the left ventricular myocardium of the pentobarbital-anesthetized dog. Continuous recordings were made of myocardial PCO2 (PmCO2), arterial PCO2 (PaCO2), and coronary sinus PCO2 (CSPCO2) during variation of respiratory rate. PmCO2 and CSPCO2 were compared at varying coronary flow. PmCO2 was similar to and closely followed changes in CSPCO2. The difference between PmCO2 and CSPCO2 was -0.52 +/- 3.63 (SD) mmHg, and PmCO2 exceeded PaCO2 by 20.69 +/- 5.12 mmHg. After coronary occlusion, PmCO2, rose promptly, but CSPCO2 was only slightly elevated until the occlusion was released, when a CO2 efflux into the coronary sinus occurred. It is concluded that the electrode measures extracellular PCO2 and that extracellular and myocardial PCO2 are essentially equal. PmCO2 rises rapidly following coronary occlusion.

Early changes in protein synthesis in epicardial coronary artery of pressure-overloaded heart

1996 ◽  
Vol 270 (2) ◽  
pp. H685-H691 ◽  
Author(s):  
M. Gerova ◽  
O. Pechanova ◽  
V. Stoev ◽  
M. Kittova ◽  
I. Bernatova ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Coronary Artery ◽  
Left Ventricular ◽  
Leucine Incorporation ◽  
Experimental Conditions ◽  
Coronary Wall ◽  
Anesthetized Dogs ◽  
The Difference ◽  
Ventricle Volume ◽  
Right Ventricle Volume

In anesthetized dogs, a 4-h, approximately 30% increase in blood pressure induced by constriction of the abdominal aorta brought about an increase in the total RNA content in the left anterior descending coronary artery (LADCA) and the left ventricular (LV) myocardium (9.05 +/- 1.72 and 11.06 +/- 4.68%, respectively) but not in the left circumflex coronary artery (LCCA). Under the same experimental conditions, [14C]leucine incorporation increased in LADCA and LV myocardium (45.34 +/- 13.54 and 58.07 +/- 11.91%, respectively), but not in LCCA. The data indicate an early shift in protein synthesis in LADCA and simultaneously in the myocardium during a short-term pressor event. The difference in the shift of protein synthesis in the two main branches of the left coronary artery was related to the quantitatively different deformation of the LADCA and LCCA due to different deformation of the underlying myocardium and/or of the annulus fibrosus atrioventricularis during changes in the left or right ventricle volume [M. Gerova, E. Barta, M. Stolarik, and J. Gero, Am. J. Physiol. 262 (Heart Circ. Physiol. 31): H1049-H1053, 1992]. The results support the hypothesis that the deformation and/or rate of deformation of cells in the coronary wall may trigger an increase in protein synthesis. Changes in protein synthesis in the myocardium and LADCA were found to be reversible 2 h after releasing the aortic constriction.

Heat loss from the heart in dogs

1962 ◽  
Vol 202 (1) ◽  
pp. 41-44 ◽  
Author(s):  
Robert J. Adolph ◽  
Gianni Pinardi ◽  
Robert F. Rushmer
Keyword(s):  
Temperature Gradient ◽  
Heat Loss ◽  
Temperature Difference ◽  
Coronary Sinus ◽  
Left Ventricular ◽  
Average Temperature ◽  
Coronary Sinus Flow ◽  
Physical Measurements ◽  
Anesthetized Dogs ◽  
Sinus Flow

Thermistors were inserted into the coronary sinus and the root of the aorta in anesthetized dogs to record the temperature difference between the left ventricular coronary inflow and outflow. Coronary sinus flow was directly measured with an indwelling cannula. Heat loss from the coronary vasculature was then calculated as the product of the temperature gradient and the coronary sinus flow. The average temperature difference during control periods was about .5 C (range, .24–.88 C). Isoproterenol, l-epinephrine, and acetylstrophanthidin all increased the temperature gradient, the coronary sinus flow, and, therefore, the myocardial heat loss. A small but significant amount of heat was lost from the epicardial surface of the left ventricle to the lungs in the closed-chest dog. Direct physical measurements of heat loss avoid many of the uncertainties inherent in estimates of wasted energy based on the energy equivalent of myocardial oxygen consumption.

Myocardial tissue pressure and blood flow during coronary sinus pressure modulation in anesthetized dogs

1992 ◽  
Vol 73 (5) ◽  
pp. 2184-2191 ◽  
Author(s):  
B. Cantin ◽  
J. R. Rouleau
Keyword(s):  
Arterial Pressure ◽  
Coronary Sinus ◽  
Left Ventricular ◽  
Myocardial Tissue ◽  
Tissue Pressure ◽  
Pressure Transducers ◽  
Coronary Pressure ◽  
Anesthetized Dogs ◽  
Pressure Modulation ◽  
Sinus Pressure

To determine whether coronary sinus outflow pressure (Pcs) or intramyocardial tissue pressure (IMP) is the effective back pressure in the different layers of the left ventricular (LV) myocardium, we increased Pcs in 14 open-chest dogs under maximal coronary artery vasodilation. Circumflex arterial (flowmeter), LV total, and subendocardial and subepicardial (15-microns radioactive spheres) pressure-flow relationships (PFR) and IMP (needle-tip pressure transducers) were recorded during graded constriction of the artery at two diastolic Pcs levels (7 +/- 3 vs. 23 +/- 4 mmHg). At high Pcs, LV, aortic and diastolic circumflex arterial pressure, heart rate, myocardial oxygen consumption, and lactate extraction were unchanged; IMP in the subendocardium did not change (130/19 mmHg), whereas IMP in the subepicardium increased by 17 mmHg during systole and 10 mmHg during diastole (P < or = 0.001), independently of circumflex arterial pressure. Increasing Pcs did not change the slope of the PFR; however, coronary pressure at zero flow increased in the subepicardium (P < or = 0.008), whereas in the subendocardium it remained unchanged at 24 +/- 3 mmHg. Thus Pcs can regulate IMP independently of circumflex arterial pressure and consequently influence myocardial perfusion, especially in the subepicardial tissue layer of the LV.

Restraining effect of intact pericardium during acute volume loading

1992 ◽  
Vol 262 (6) ◽  
pp. H1725-H1733 ◽  
Author(s):  
R. J. Applegate ◽  
W. E. Johnston ◽  
J. Vinten-Johansen ◽  
H. S. Klopfenstein ◽  
W. C. Little
Keyword(s):  
Left Ventricular ◽  
Transmural Pressure ◽  
Equilibrium Analysis ◽  
Volume Loading ◽  
Fluid Infusion ◽  
Anesthetized Dogs ◽  
Similar Range ◽  
Cardiac Volumes ◽  
The Difference ◽  
Lv Volume

To determine the effect of the intact pericardium on ventricular end-diastolic pressures (EDP) during acute volume loading, we measured left ventricular (LV) and right ventricular (RV) micromanometer pressure and LV volume using a conductance catheter in eight open-chest, anesthetized dogs. A range of LV pressure and volume was obtained by intravascular volume expansion with the pericardium intact and then over a similar range after removal of the pericardium. Pericardial pressure (Pper) was calculated using static equilibrium analysis as the difference between LVEDP with the pericardium present and absent at a constant LV volume. At the beginning of the fluid infusion (LVEDP 7.3 +/- 1.7 mmHg and RVEDP 4.4 +/- 2.6 mmHg, mean +/- SD), Pper was not different from zero (-1.0 +/- 2.3 mmHg, P not significant). The onset of pericardial restraint (Pper greater than or equal to 0 mmHg) occurred when LVEDP was 9.1 +/- 2.9 mmHg and RVEDP was 4.1 +/- 2.9 mmHg. At low cardiac volumes before fluid infusion, RV transmural pressure was positive and significantly greater than the near zero Pper. After the onset of pericardial restraint, however, RVEDP and Pper increased similarly and were related according to Pper = 1.1 (+/- 0.34) RVEDP - 4.2 (+/- 2.6) mmHg, standard deviation 0.6 +/- 0.8 mmHg, r = 0.98 +/- 0.10. These data indicate that the intact pericardium behaves in two functionally distinct ways. At low cardiac volumes, Pper is zero and the pericardium does not affect LV filling. RV transmural pressure is positive and greater than Pper.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanical workload-myocardial water content relationship in isolated rat hearts

1997 ◽  
Vol 273 (1) ◽  
pp. H271-H278
Author(s):  
E. R. Schertel ◽  
R. M. Daye ◽  
D. E. McClure ◽  
T. Lai ◽  
M. Miyamoto ◽  
...  
Keyword(s):  
Water Content ◽  
Isolated Heart ◽  
Left Ventricular Pressure ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Edema Formation ◽  
Perfused Rat Heart ◽  
Rat Hearts ◽  
Heart Preparation ◽  
Isolated Rat

We tested the hypothesis that the mechanical workload of the heart inversely determines the rate of myocardial edema formation in an isolated, perfused rat heart preparation. Heart rate (HR) was varied in three groups by pacing at 125 (HR125), 250 (HR250), or 350 beats/min (HR350). Left ventricular pressure (LVP) was varied in two additional groups by pacing at 250 beats/min and with the addition of either epinephrine (Epi) or propranolol (Pro) to the perfusate. In five otherwise identical groups, variation of coronary vascular resistance was minimized by adenosine. Myocardial water content (MWC) varied significantly and inversely with HR in the HR125, HR250, and HR350 groups. MWC of the HR250 group was significantly less than that of the Pro group but did not differ from the Epi group. However, when adenosine was used, MWC had significant inverse relationships with HR and LVP. We concluded that the mechanical workload of the heart inversely determines the rate and degree of myocardial edema formation in this isolated heart preparation, and both HR and LVP are determinants of this relationship.

Intramyocardial distribution of blood flow in hemorrhagic shock in anesthetized dogs

1976 ◽  
Vol 230 (1) ◽  
pp. 41-49 ◽  
Author(s):  
EL Carlson ◽  
SL Selinger ◽  
J Utley ◽  
JI Hoffman
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Coronary Resistance ◽  
Anesthetized Dogs ◽  
Diastolic Coronary Flow

In 34 anesthetized, open-chest dogs aortic blood pressure was kept at 35-40 mmHg for 3 h to determine if maldistribution of coronary blood flow (CBF) could contribute to the irreversibility of hemorrhagic shock. Six dogs were pretreated with phenoxybenzamine (PBZ) and 11 dogs (3 with PBZ) received hypertonic mannitol infusions in late hemorrhage. Changes of heart rate, cardiac output, and peripheral resistance were similar to those described by others. In untreated dogs total and left ventricular CBF fell, as did coronary vascular resistance. However, minimal coronary resistance after transient ischemia rose progressively and the ratio of subendocardial:subepicardial flow fell, as did the percentage of diastolic coronary flow. Mannitol infusion returned CBF and steady-state and minimal postischemic coronary resistance to control values and also returned to normal the increased myocardial water content found in late hemorrhage. Phenoxybenzamine delayed but did not prevent the rise of coronary vascular resistance or decreased subendocardial flow. These studies suggest that there may be subendocardial ischemia, possibly due to myocardial edema, in hemorrhagic shock.

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