Estrogen-induced left ventricular chamber enlargement in ewes

1993 ◽  
Vol 264 (4) ◽  
pp. E490-E496 ◽  
Author(s):  
G. D. Giraud ◽  
M. J. Morton ◽  
L. E. Davis ◽  
M. S. Paul ◽  
K. L. Thornburg
Keyword(s):  
Placebo Group ◽  
Stroke Volume ◽  
Inferior Vena ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Chronic Effect ◽  
Inferior Vena Caval ◽  
Intramuscular Dose ◽  
Left Ventricular Chamber ◽  
Chamber Size

We studied the chronic effect of administration of a single large intramuscular dose of 17 beta-estradiol on left ventricular chamber size and output in the ewe. Fourteen oophorectomized ewes were successfully instrumented and studied, with measurements made of left ventricular, aortic, right and left atrial pressures, left ventricular stroke volume, and left ventricular minor axis dimension. Unanesthetized ewes were studied before and 1, 2, and 3 wk after intramuscular administration of 0.6 mg/kg 17 beta-estradiol (7 ewes) or 1.5 ml sesame oil placebo (7 ewes). Left ventricular end-diastolic pressure-end-diastolic dimension (LVEDP-EDD) and left ventricular end-diastolic pressure-stroke volume (LVEDP-SV) relationships were quantified during graded inferior vena caval occlusion and volume infusion. Left ventricular end-diastolic diameter was larger after estrogen but not after placebo administration. The LVEDP-EDD relationship shifted progressively rightward, indicating left ventricular chamber enlargement in the estrogen group but was unchanged in the placebo group. The plateau limb of the LVEDP-SV relationship in the estrogen group shifted up from a mean stroke volume of 77.1-89.5 ml/beat and did not change in the placebo group. We conclude that administration of a single large intramuscular dose of 17 beta-estradiol resulted in left ventricular chamber enlargement and increased stroke volume in the ewe.

LEFT VENTRICULAR END-DIASTOLIC VOLUME FROM EJECTION FRACTION AND STROKE VOLUME IN PIGS DURING INFERIOR VENA CAVAL OCCLUSION

ASAIO Journal ◽  
2001 ◽  
Vol 47 (2) ◽  
pp. 136
Author(s):  
Cecily J. Gallup ◽  
Santos E. Cabreriza ◽  
Joseph P. Hart ◽  
Rowan F. Walsh ◽  
Henry M. Spotnitz
Keyword(s):  
Ejection Fraction ◽  
Stroke Volume ◽  
Inferior Vena ◽  
Left Ventricular ◽  
Inferior Vena Caval ◽  
End Diastolic Volume

Regional circumferential lengthening patterns in canine left ventricle

1983 ◽  
Vol 245 (5) ◽  
pp. H741-H748 ◽  
Author(s):  
W. Y. Lew ◽  
M. M. LeWinter
Keyword(s):  
Left Ventricle ◽  
Regional Differences ◽  
Inferior Vena ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Elastic Recoil ◽  
Rapid Phase ◽  
Inferior Vena Caval ◽  
Ventricular Filling

We employed sonomicrometers in open-chest dogs to study lengthening of short segments of circumferentially oriented myocardium located at the base, midportion, and apex of the anterior left ventricular free wall. Left ventricular pressure was varied by inferior vena caval occlusion and volume expansion. Diastole was divided into rapid and slow lengthening phases. Rapid lengthening was completed first at the basal site at each of three successive levels of left ventricular diastolic pressure (LVDP). At the base, significant further lengthening occurred during the slow lengthening phase while at the apex virtually all lengthening was completed during the rapid phase. At low LVDPs, peak lengthening rates (dl/dt) were greatest at the apex. As LVDP was increased, regional differences in dl/dt diminished. These results indicate that there is regional variation in the timing of the phases of diastole and in lengthening patterns of the left ventricle. The volume-dependent variation in lengthening rates that we observed is consistent with the concept of regional differences in elastic recoil, which may contribute to active ventricular filling.

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

Left ventricular diastolic function of remodeled myocardium in dogs with pacing-induced heart failure

1998 ◽  
Vol 274 (3) ◽  
pp. H945-H954 ◽  
Author(s):  
Steven B. Solomon ◽  
Srdjan D. Nikolic ◽  
Stanton A. Glantz ◽  
Edward L. Yellin
Keyword(s):  
Heart Failure ◽  
Elastic Properties ◽  
Diastolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Diastolic Filling ◽  
Elastic Recoil ◽  
Systolic Volume ◽  
Left Ventricular Chamber ◽  
Volume Relation

In patients with heart failure, decreased contractility resulting in high end-diastolic pressures and a restrictive pattern of left ventricular filling produces a decrease in early diastolic filling, suggesting a stiff ventricle. This study investigated the elastic properties of the myocardium and left ventricular chamber and the ability of the heart to utilize elastic recoil to facilitate filling during pacing-induced heart failure in the anesthetized dog. Elastic properties of the myocardium were determined by analyzing the myocardial stress-strain relation. Left ventricular chamber properties were determined by analyzing the pressure-volume relation using a logarithmic approach. Elastic recoil was characterized using a computer-controlled mitral valve occluder to prevent transmitral flow during diastole. We conclude that, during heart failure, the high end-diastolic pressures suggestive of a stiff ventricle are due not to stiffer myocardium but to a ventricle whose chamber compliance characteristics are changed due to geometric remodeling of the myocardium. The restrictive filling pattern is a result of the ventricle being forced to operate on the stiff portion of the diastolic pressure-volume relation to maintain cardiac output. Slowed relaxation and decreased contractility result in an inability of the heart to contract to an end-systolic volume below its diastolic equilibrium volume. Thus the left ventricle cannot utilize elastic recoil to facilitate filling during heart failure.

scholarly journals Loss of Endogenously Cycling Adult Cardiomyocytes Worsens Myocardial Function

2020 ◽  
Author(s):  
Leigh A Bradley ◽  
Alexander Young ◽  
Hongbin Li ◽  
Helen O Billcheck ◽  
Matthew J Wolf
Keyword(s):  
Myocardial Infarction ◽  
Cell Cycle ◽  
Myocardial Function ◽  
Cultured Cells ◽  
Left Ventricular ◽  
Left Ventricular Chamber ◽  
Adult Cardiomyocytes ◽  
Border Zones ◽  
And Function ◽  
Chamber Size

Rationale: Endogenously cycling adult cardiomyocytes (CMs) increase after myocardial infarction (MI) but remain scare, and are generally thought not to contribute to myocardial function. However, this broadly held assumption has not been tested, mainly because of the lack of transgenic reporters that restrict Cre expression to adult CMs that reenter the cell cycle. Objective: We created and validated a new transgenic mouse, αMHC-MerDreMer-Ki67p-RoxedCre::Rox-Lox-tdTomato-eGFP (denoted αDKRC) that restricts Cre expression to cycling adult CMs and uniquely integrates spatial and temporal adult CM cycling events based on the DNA specificities of orthologous Dre- and Cre recombinases. We then created mice that expressed an inducible Diphtheria toxin (DTA), αDKRC::DTA mice, in adult cycling CMs and examined the effects of ablating these endogenously cycling CMs on myocardial function after Ischemic-Reperfusion (I/R) MI. Methods and Results: A tandem αDKRC transgene was designed, validated in cultured cells, and used to make transgenic mice. The αDKRC transgene integrated between MYH6 and MYH7 and did not disrupt expression of the surrounding genes. Compared to controls, αDKRC::RLTG mice treated with Tamoxifen expressed tdTomato+ in CMs with rare Bromodeoxyuridine (BrdU)+, eGFP+ CMs, consistent with reentry of the cell cycle. We then pre-treated αDKRC::RLTG mice with Tamoxifen to activate the reporter before sham or reperfusion (I/R) myocardial infarction (MI) surgeries. Compared to Sham surgery, the I/R MI group had increased single and paired eGFP+ CMs predominantly in the border zones (5.8 {plus minus} 0.5 vs. 3.3 {plus minus} 0.3 CMs per ten-micron section, N = 8-9 mice per group, n = 16-24 sections per mouse), indicative of cycled CMs. The single to paired eGFP+ CM ratio was ~9 to 1 (5.2 {plus minus} 0.4 single vs. 0.6 {plus minus} 0.2 paired CMs) in the I/R MI group after MI, suggesting that cycling CMs were more likely to undergo polyploidy than replication. The ablation of endogenously cycling adult CMs in αDKRC::DTA mice caused progressive worsening left ventricular chamber size and function after I/R MI, compared to controls. Conclusions: Although scarce, endogenously cycling adult CMs contribute to myocardial function after injury, suggesting that these cells may be physiologically relevant.

scholarly journals Effects of Crystalloid Preloading (20 ml/kg) on Hemodynamics in Relation to Postural Changes in Patients Undergoing Neurosurgical Procedures in Sitting Position

2018 ◽  
Vol 09 (01) ◽  
pp. 080-085
Author(s):  
M. Ranjith ◽  
Prasanna Udupi Bidkar ◽  
K. Narmadalakshmi ◽  
Praveen R. Talawar
Keyword(s):  
Stroke Volume ◽  
Inferior Vena ◽  
Venous Pressure ◽  
Neurosurgical Procedures ◽  
Operating Table ◽  
Sitting Position ◽  
Hemodynamic Parameters ◽  
Inferior Vena Caval ◽  
Postural Changes ◽  
Ringer’S Lactate

ABSTRACT Background: Hemodynamic disturbances are common during positioning the patients from supine to sitting for neurosurgical procedures. The reported incidence of hypotension varies from 5% to 32%. The aim of the study was to study the effect of crystalloid preloading on hemodynamic parameters during positioning the patient from supine to sitting position. Materials and Methods: In this prospective observational trial, 20 patients were enrolled. Two patients had a patent foramen ovale on transesophageal echocardiography and were excluded from the study. All the patients received 20 ml/kg of crystalloid (Ringer's lactate) before initiation of positioning. Physiological hemodynamic parameters such as heart rate, mean arterial pressure, central venous pressure, cardiac output (CO), stroke volume variation (SVV), cardiac index (CI), stroke volume (SV), and maximum and minimum inferior vena caval diameter (IVCD) were recorded after induction, during positioning at 30°, 60° inclination of the operating table and after the final sitting position. Results: Hemodynamic parameters were well maintained during positioning of the patients from supine to sitting position. Crystalloid preloading prevented the hypotension during positioning. There were no significant changes in hemodynamic parameters such as CO, SVR, SVV, CI, and SV. We did not find any correlation with changes in IVCD with changes in CO. Conclusion: A volume of 20 ml/kg of crystalloid preloading before positioning the patient from supine to sitting position maintains the hemodynamic stability and avoids the vasopressor requirement.

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