Comparative evaluation of pressure and time factors in estimating left ventricular performance

1976 ◽  
Vol 40 (2) ◽  
pp. 196-205 ◽  
Author(s):  
F. L. Abel
Keyword(s):  
Diastolic Pressure ◽  
Time Factors ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Rate Of Change ◽  
Ventricular Performance ◽  
Time To Peak ◽  
Fractional Rate ◽  
Inotropic State ◽  
Developed Pressure

Left ventricular and ascending aortic pressures were measured in open chest mongrel dogs under pentobarbital anesthesia. The data were digitized, averaged, and subgrouped by mean systolic aortic pressures (MSAP), end-diastolic pressure (EDP), and heart rate (HR). Seven raw and 32 derived variable from the pressure, as a function of time, wave forms were analyzed in each subgroup in the control state and following the infusion of catecholamines. A plot of control variability versus sensitivity to norepinephrine indicates that time to peak ventricular pressure (PVP time) is a more sensitive indicator of changes in the inotropic state than such other commonly used variables as max dP/dt, integrated isometric tension, and (max dP/dt)/developed pressure. PVP time also showed less variability with HR, EDP, and MSAP. Regression lines were also fit to the data using a second-order model. This permitted evaluation of experimentally varying either HR, EDP, or MSAP while maintaining the other two constant. PVP time was again one of the better variables in terms of sensitivity to HR, EDP, or MSAP. Vmax, fractional rate of change of power, preejection period, and systolic time were also analyzed and compared with PVP time using averaged data.

Myocardial mechanical alterations during gradual onset long-term hypertension in rats

1981 ◽  
Vol 241 (3) ◽  
pp. H435-H441 ◽  
Author(s):  
J. M. Capasso ◽  
J. E. Strobeck ◽  
E. H. Sonnenblick
Keyword(s):  
Blood Pressure ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Isometric Tension ◽  
Left Renal Artery ◽  
Ventricular Performance ◽  
Time To Peak ◽  
Gradual Onset ◽  
Significant Depression ◽  
Female Wistar Rats

Although a suddenly produced load leads to depressed myocardial contractility, the effects of a slowly induced physiological overload have not been defined. Therefore, a more gradual pressure overload was produced in female Wistar rats by hypertension due to constriction of the left renal artery. Hypertension (systolic blood pressure greater than or equal to 150 mmHg) developed within 3 wk, and blood pressure continued to increase for the next 5 wk. Heart weights in hypertensive animals were elevated by 34% after the onset of hypertension. Isometric and isotonic contractions from left ventricular papillary muscles were recorded at 5, 10, 20, and 30 wk after the onset of hypertension. Total and actively developed isometric tension at all initial muscle lengths were significantly greater in hypertensive animals throughout the 30-wk period. Time to peak tension and time to half relaxation were significantly prolonged. Force-velocity curves demonstrated a significant depression in velocity of shortening at all relative loads in hypertensive muscles that progressed with the duration of hypertension. These studies suggest that myocardial hypertrophy may impart the ability to maintain ventricular performance in terms of force development while speed of shortening decays.

Effect of acute edema on left ventricular function and coronary vascular resistance in the isolated rat heart

1994 ◽  
Vol 267 (3) ◽  
pp. H1054-H1061 ◽  
Author(s):  
A. Rubboli ◽  
P. A. Sobotka ◽  
D. E. Euler
Keyword(s):  
Linear Relationship ◽  
Water Content ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Ventricular Performance ◽  
Developed Pressure ◽  
The Impact

The impact of acute myocardial edema on coronary flow and left ventricular performance was studied in isolated isovolumic rat hearts. After 15 min of aortic perfusion with Krebs-Henseleit buffer, hearts (10/group) were either removed for determination of water content or perfused for another 90 min. Three groups were perfused at a constant pressure of 60, 100, or 140 mmHg, and two groups were perfused at 60 or 140 mmHg with adenosine added. Compared with the 15-min group, there was a significant increase in water content in all groups except the 60-mmHg group (P < 0.005). There was a direct linear relationship between increases in coronary vascular resistance over time and water content (P < 0.0001). A decrease in developed pressure and peak +dP/dt was observed only in those groups that accumulated water. An inverse linear relationship was found between changes in developed pressure and water content (P = 0.0001). Water content had no effect on end-diastolic pressure below 5 ml/g; above 5 ml/g, a direct linear relationship was evident (P = 0.009). The results suggest that myocardial edema increases vascular resistance and decreases systolic performance. End-diastolic pressure is less influenced by edema than either systolic or coronary vascular function.

Deleterious effect of ouabain on myocardial function during hypoxia

1989 ◽  
Vol 256 (3) ◽  
pp. H681-H687
Author(s):  
M. J. Cunningham ◽  
C. S. Apstein ◽  
E. O. Weinberg ◽  
B. H. Lorell
Keyword(s):  
Myocardial Function ◽  
Diastolic Pressure ◽  
Lactate Production ◽  
Treated Group ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Fiber Tension ◽  
Coronary Vasodilatation ◽  
Developed Pressure ◽  
Ventricular Distensibility

The effect of cardiac glycosides on myocardial function during hypoxia is controversial. Accordingly, we studied left ventricular performance during hypoxia and reoxygenation in the presence of a mildly inotropic, nontoxic dose of ouabain using isolated, isovolumic, buffer-perfused rabbit hearts. After 15 min of hypoxia, left ventricular developed pressure was less in the ouabain-treated group than in controls (35 +/- 4 vs. 55 +/- 3 mmHg, P less than 0.025). Left ventricular end-diastolic pressure (LVEDP) increased more during hypoxia in the presence of ouabain (9 +/- 1 to 32 +/- 7 with ouabain vs. 9 +/- 1 to 14 +/- 3 mmHg without ouabain, P less than 0.005) despite comparable degrees of coronary vasodilatation and myocardial lactate production in the two groups. When coronary flow was abruptly reduced to zero to eliminate the coronary turgor contribution to diastolic pressure, LVEDP after 15 min of hypoxia in the presence of ouabain was greater than that in control hearts that did not receive ouabain (13 +/- 4 vs. 4 +/- 1 mmHg, P less than 0.05), implicating greater diastolic myocardial fiber tension in the ouabain group during hypoxia. With reoxygenation, recovery of developed pressure was less and end-diastolic pressure remained elevated in the ouabain-treated group when compared with controls. We conclude that a modestly inotropic dose of ouabain exacerbates the decrease in diastolic ventricular distensibility induced by hypoxia, worsens the decline in developed pressure during hypoxia, and impairs recovery during reoxygenation.

Afterload as a primary determinant of ventricular performance

1963 ◽  
Vol 204 (4) ◽  
pp. 604-610 ◽  
Author(s):  
Edmund H. Sonnenblick ◽  
S. Evans Downing
Keyword(s):  
Blood Pressure ◽  
Stroke Volume ◽  
Papillary Muscle ◽  
Work Performance ◽  
Diastolic Pressure ◽  
Muscle Length ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Inotropic State ◽  
Primary Determinant

The importance of aortic blood pressure as a determinant of left ventricular performance was systematically evaluated in the intact cat heart, and compared with the effects of afterloading on work performed by the isotonically contracting isolated cat papillary muscle. In the papillary muscle, at any one muscle length and state of contractility, work was determined by the afterload with which the muscle shortened. In the intact heart, blood pressure (BP) may be considered a gross approximation of the afterload encountered by the contracting ventricle. It was found that at any given initial left ventricular end-diastolic pressure (LVEDP), work performed was a function of the BP. At a constant BP, norepinephrine increased the work performed at any LVEDP by augmenting stroke volume. This work could be further increased by a concomitant increase of BP. Over a broad range, stroke volume was independent of the BP. The state of contractility of the myocardium sets the limits of work; however, work performance remains largely dependent on the BP (afterload). Thus, ventricular performance at a given constant inotropic state is the product of two largely independent variables, the preload (establishing initial muscle length) and the afterload.

Right ventricular performance during ischemia: an anatomic and hemodynamic analysis

1977 ◽  
Vol 233 (4) ◽  
pp. H505-H513 ◽  
Author(s):  
H. Brooks ◽  
R. Holland ◽  
J. Al-Sadir
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Time To Peak ◽  
Contractile Parameters ◽  
Significant Depression ◽  
Right Ventricular Performance ◽  
The Right

This study in the pig was designed to characterize right ventricular (RV) contractile responses during infarction involving three areas of the heart--anteroseptal, anterolateral, and inferoseptal. Porcine coronary architecture was studied from multicolor vinyl casts. Distribution of blood supply to ventricular myocardium and papillary muscles was defined by intra-arterial dye injection. High-fidelity pressure and flow data were measured simultaneously in both ventricles following ligation of approximately equal lengths of the anterior descending, left circumflex, or posterior descending arteries. In the three groups, weight of myocardium involved by the occluded artery was comparable and there was significant depression of left ventricular performance, more pronounced in the two anterior infarcts. However, in anterolateral infarction, despite the obligatory drop in RV flow, there was no significant alteration in RV end-diastolic pressure (EDP), peak rate of rise of RV pressure (dP/dt), or time-to-peak developed dP/dt. In contrast, with both anteroseptal and inferoseptal infarctions there were significant alterations in all RV contractile parameters, at increased levels of RVEDP, signifying a primary depression in RV contractile state. With inferoseptal infarction, further occlusion of the right coronary near its origin produced a more exaggerated and selective RV contractile abnormality and, in half of the animals, varying degrees of acute tricuspid insufficiency.

Oxygen delivery and myocardial function in rabbit hearts perfused with cell-free hemoglobin

1992 ◽  
Vol 72 (2) ◽  
pp. 476-483 ◽  
Author(s):  
V. W. MacDonald ◽  
R. M. Winslow
Keyword(s):  
Oxygen Uptake ◽  
Myocardial Function ◽  
Oxygen Affinity ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Free Hemoglobin ◽  
Langendorff Preparation ◽  
Oxygen Gradients ◽  
Developed Pressure ◽  
Krebs Henseleit Buffer

Isolated rabbit hearts were perfused with Krebs-Henseleit buffer that contained 1.5 g/dl hemoglobin Ao [HbAo; PO2 at which half-saturation of hemoglobin occurs = 12 Torr], human hemoglobin cross-linked between alpha-chains with bis(3,5-dibromosalicyl)fumarate (alpha alpha-Hb; PO2 at which half-saturation of hemoglobin occurs = 30 Torr), or fatty acid-free bovine serum albumin (BSA). Myocardial performance and oxygen uptake were determined at different aortic PO2's [arterial PO2 (PaO2)] by use of an isovolumic Langendorff preparation. Function and oxygen uptake were comparable among the three different groups of hearts at an average mean PaO2 of 557 Torr. As PaO2 decreased, myocardial function was preserved better in hearts perfused with hemoglobin than in hearts perfused with Krebs-Henseleit buffer alone or with BSA. Hearts perfused with either HbAo or alpha alpha-Hb exhibited similar 10% decreases in left ventricular developed pressure and rate of change in left ventricular developed pressure at PaO2 of 141 Torr compared with a 58% decrease with BSA. However, corresponding venous PO2's were lower with HbAo (20 Torr) than with alpha alpha-Hb (35 Torr), and oxygen uptake decreased by 36% with HbAo but remained constant with alpha alpha-Hb. These data suggest that although myocardial function can be sustained over a fairly broad range of hemoglobin oxygen affinities, tissue oxygen gradients and myocardial oxygen uptake are maintained better by cell-free hemoglobin with an oxygen affinity in the normal physiological range.

Abstract 4370: Intramyocardial Administration of Erythropoietin Promotes Cell Proliferation, Induces Early Angiogenesis and Attenuates Cardiac Remodeling

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ralf Gäbel ◽  
Christian Klopsch ◽  
Dario Furlani ◽  
Wenzhong Li ◽  
Can Yerebakan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Peripheral Blood ◽  
Diastolic Pressure ◽  
Troponin T ◽  
Interstitial Fibrosis ◽  
Capillary Density ◽  
Left Ventricular ◽  
Border Zone ◽  
Ki 67 ◽  
Ventricular Performance

Erythropoietin (EPO) protects the ischemic myocardium from heart failure development after myocardial infarction (MI). However, little is known about its intracardiac cell proliferation and early angiogenesis. We hypothesize that EPO may contribute to cell proliferation, angiogenesis and eventually induce a beneficial remodeling process. Following permanent LAD ligation in rats, EPO (3000 U/kg; n=99) or saline (n=95) was delivered along the infarction border. In control animals without MI (n=55) saline was injected intramyocardially. After 6 weeks follow-up, left ventricle was catheterized and analyzed for cardiac performance. The level of eNOS mRNA was dramatically increased 9.3 fold in non-infarcted area of EPO treated rats at 24 h detected by real time PCR and confirmed by immunohistology. We found a 45 % enhancement in Ki-67+ cell numbers near the infarction at 48 h after EPO treatment (n=6, P<0.001). Hematopoietic cell lineages including c-Kit+ and CD34+ cells were augmented in the peripheral blood after 48h. Capillary density was enhanced by 17% as early as 1 week (n=6, P<0.001). Myocyte apoptosis was reduced by 41% and 37% at border zone after 1 and 6 weeks (n=6, P<0.05). Cardiac troponin T level, a highly sensitive and specific indicator of myocardial cell death, was significantly reduced in peripheral blood 2 weeks after EPO injection (n=5, P<0.05). Cardiomyocyte size and interstitial fibrosis at 6 weeks were decrease by 13% and 23% (n=6, P=0.015, P<0.001). Intramyocardial EPO delivery enhanced left ventricular performance at baseline and Dobutamine stress conditions compared with MI rats (cardiac output: 65% and 71% increase at baseline and stress; end-diastolic pressure: 51% and 53% reduction respectively, n=11–14, P<0.05). To conclude, intramyocardial EPO delivery induces early cell poliferation, angiogenesis and attenuates post MI remodeling.

Abstract P109: Alteration in Intracellular Calcium During Cardiac Arrest

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Satoshi Takeda ◽  
Hiroshi Yoshida ◽  
Takeki Ogawa
Keyword(s):  
Cardiac Arrest ◽  
Intracellular Calcium ◽  
Cell Injury ◽  
Diastolic Pressure ◽  
Pulseless Electrical Activity ◽  
Left Ventricular Pressure ◽  
Cardiac Metabolism ◽  
Left Ventricular ◽  
Free Calcium ◽  
Developed Pressure

AIM: A cytosolic free calcium is an important regulator of cardiac metabolism and contractility, and an increased [Ca2+]i has been implicated in irreversible cell injury and contractile dysfunction. We investigated intracellular calcium ([Ca2+]i) dynamics during cardiac arrest, especially in pulseless electrical activity (PEA) and asystole. METHODS: Rat hearts (n=18) were perfused with a Langendorff system and loaded with Fura-2/AM, as a [Ca2+]i marker, and BCECF/AM, as a pHi marker. Surface fluorescence of the heart was recorded with an intracellular ion analyzer. A latex balloon was inserted into the left ventricle to monitor left ventricular pressure. Sustained normo-thermic cardiac arrest was induced for 20 min by clamping the aortic cannula. RESULTS: After clamping (cardiac arrest), the left ventricular developed pressure decreased significantly, from 84.3±11 mmHg to 3.88±0.7 mmHg (p<0.01) at 2min. The rhythm was PEA in all cases in this period, followed by asystole. The amplitude of the [Ca2+]i transient (0.30±0.03) was maintained at 2 min, but further significant increases were observed in both systolic (1.14±0.04, p<0.01) and diastolic levels of [Ca2+]i (0.84±0.04, p<0.05), when compared with pre-arrest levels. The [Ca2+]i transient disappeared 4.7±0.6 min. The diastolic [Ca2+]i increased gradually after 5 min to 20 min. This diastolic [Ca2+]i increase was parallel with the increase in left ventricular end diastolic pressure (indicated ischemic contracture). The pHi increased (to 7.6±1.0) immediately after clamping. Thereafter pHi decreased rapidly and remained steady (at pH 6.6±0.6). CONCLUSIONS: The change in the [Ca2+]i-pressure relationship rather than change in the amplitude of the [Ca2+]i transient was the main contributor in the early cardiac arrest phase. The diastolic [Ca2+]i increase might induce irreversible cell injury in the late cardiac arrest phase.

Ventricular function in the newborn lamb

1965 ◽  
Vol 208 (5) ◽  
pp. 931-937 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Ventricular Function ◽  
Diastolic Pressure ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Ventricular Mechanics ◽  
Inotropic State ◽  
Ejection Rate ◽  
Norepinephrine Infusion

The present study was initiated with the objective of evaluating in the newborn those aspects of ventricular mechanics which form the basis of the Frank-Starling relation, and which permit a determination of changes in the inotropic state of the heart. Left ventricular function was studied in lambs, 12 hr to 5 days old, utilizing a preparation designed to permit control and measurement of systemic arterial pressure (AP), cardiac output, heart rate (HR), and temperature. Continuous measurements of arterial Po2 and pH were made. These data permitted the construction of ventricular function curves relating stroke volume, mean ejection rate, and stroke work and power to left ventricular end-diastolic pressure, at constant AP and HR. In all preparations the Frank-Starling relation was found to be operative. Norepinephrine infusion, 1–2 µg/kg per min, resulted in a substantial increment of both force and speed parameters, thereby demonstrating the ability of the newborn heart to alter its inotropic state. Severe metabolic acidosis did not inhibit the response of the myocardium to norepinephrine.

Ventricular performance and myocardial water content during hemodilution in dogs

1978 ◽  
Vol 235 (6) ◽  
pp. H767-H775 ◽  
Author(s):  
G. A. Geffin ◽  
M. A. Vasu ◽  
D. D. O'Keefe ◽  
D. G. Pennington ◽  
A. J. Erdmann ◽  
...  
Keyword(s):  
Water Content ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Stroke Work ◽  
Ventricular Performance ◽  
End Diastolic Volume ◽  
Lv Mass ◽  
Right Heart Bypass ◽  
Water Gain

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.

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