Left ventricular functional capacity in the endurance-trained rodent

1990 ◽  
Vol 69 (1) ◽  
pp. 305-312 ◽  
Author(s):  
D. P. Fitzsimons ◽  
P. W. Bodell ◽  
R. E. Herrick ◽  
K. M. Baldwin
Keyword(s):  
Heart Rate ◽  
Systolic Pressure ◽  
Force Production ◽  
Left Ventricular Pressure ◽  
Fold Increase ◽  
Work Load ◽  
Left Ventricular ◽  
Cardiac Myosin ◽  
O2 Uptake ◽  
Training Protocol

Cardiac myosin P-light chain phosphorylation [P-LC(P)] has been proposed to augment myocardial force production. This study was undertaken to examine the potential for cardiac myosin P-LC(P) for both equivalent heart rate and work load in exercising endurance-trained and nontrained rodents. A 10-wk training protocol elicited a significant reduction in submaximal running O2 uptake while enhancing peak O2 uptake (-17 and 10%, respectively, P less than 0.05). Left ventricular functional index during submaximal exercise, obtained with a high-fidelity Millar ultraminiature pressure transducer, indicated that the trained animals were able to maintain peak left ventricular pressure (LVP) in comparison to their sedentary counterparts, even though both heart rate and rate of LVP development were significantly reduced (P less than 0.05). When expressed on the basis of equivalent submaximal heart rate, peak LVP was augmented in the trained animals. Cardiac myosin P-LC(P) was examined under two conditions known to produce disparate responses in trained vs. sedentary animals. For an equivalent work load, we observed parallel increases in P-LC(P) (20%) and systolic pressure (17%) in both groups, even though the trained animals exhibited significantly lower heart rates (P less than 0.05). For an equivalent heart rate, training evoked a significant increase in systolic pressure (26%, P less than 0.05) and caused a slight increase in P-LC(P) relative to the nontrained controls. Cardiac myosin adenosinetriphosphatase was reduced approximately 10% in the trained animals (P less than 0.05), commensurate with a 2.0-fold increase in the V3 (low adenosinetriphosphatase) isomyosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Intraventricular blood pressures in the chicken

1960 ◽  
Vol 198 (1) ◽  
pp. 153-154 ◽  
Author(s):  
H. E. Bredeck
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
The Other ◽  
Blood Pressures ◽  
Left And Right ◽  
The Right ◽  
Made In

Direct heart punctures were made in two groups of unanesthetized chickens to determine the left and right intraventricular blood pressures. One group was composed of nonlaying birds 28–30 weeks old and the other of laying hens 65–67 weeks of age. Heart rates and the respiratory influence on pressure were also measured. Average pressures obtained were 144/0 and 21/ - 1 mm Hg for the left and right ventricle, respectively. Respiratory efforts caused a mean fluctuation in systolic pressure of approximately 8 mm Hg in the left ventricle and 4 mm Hg in the right. With the exception of the right ventricular diastolic blood pressure, there were no significant pressure or pulse rate differences between the two groups. The heart rate and left ventricular pressure were found to be significantly correlated ( P < .01) in both groups of birds.

Left ventricular performance in endotoxin shock in dogs

1982 ◽  
Vol 242 (2) ◽  
pp. H172-H176 ◽  
Author(s):  
W. G. Guntheroth ◽  
J. P. Jacky ◽  
I. Kawabori ◽  
J. G. Stevenson ◽  
A. H. Moreno
Keyword(s):  
Heart Rate ◽  
Average Rate ◽  
Systolic Pressure ◽  
Work Load ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Maximal Velocity ◽  
Ventricular Performance ◽  
Untreated Subject ◽  
Mean Pressure

Endotoxin shock, with maximal velocity of contraction (Vmax) as our index of contractility, showed no myocardial depression in an earlier 4-h study (Guntheroth, Proc. Soc. Exp. Biol. Med. 157: 610--614, 1978). Because of reports of late deterioration, we studied six dogs until spontaneous death (9--18 h). Heart rate nearly doubled and left ventricular filling pressure and aortic mean pressure fell, but Vmax did not change significantly. Because of concern that the marked increase in heart rate may have contributed to an artifactual maintenance of Vmax (due to its frequency dependence, inherent in dp/dt), we studied a final group of five dogs with three additional indicators of contractility. End-systolic pressure-diameter ratio (Emax), ejection fraction (sonar-determined from the minor axis of the left ventricle), and frequency-normalized average rate of generation of power density (FARPD) all fell early and remained low until death. We conclude that myocardial contractility is significantly reduced in endotoxin shock, early and sustained. Its presence is masked somewhat in the untreated subject by the reduced work load, secondary to hypovolemia.

High-energy phosphates and function in isolated, working rabbit hearts

1987 ◽  
Vol 253 (5) ◽  
pp. H1215-H1223 ◽  
Author(s):  
E. D. Lewandowski ◽  
Sr. Devous MD ◽  
R. L. Nunnally
Keyword(s):  
Heart Rate ◽  
Nuclear Magnetic Resonance ◽  
Cardiac Output ◽  
Left Ventricular Pressure ◽  
Work Load ◽  
Rabbit Heart ◽  
High Energy ◽  
Left Ventricular ◽  
High Energy Phosphates ◽  
And Function

An isolated, working, rabbit heart has been developed for use with nuclear magnetic resonance (NMR) spectroscopy. This model is functionally stable over a 4-h period and displays classic hemodynamic responses to work-load changes. Control 31P spectra of this preparation (n = 5) were obtained with simultaneous recordings of left ventricular pressure (LVP), LVP differentiated with respect to time (dP/dt), heart rate (HR), and cardiac output (CO). ATP, phosphocreatine (PCr), and hemodynamics remained stable over a 90-min perfusion. Hearts were also subjected to 13.5 min of global ischemia (IS) at 37 degrees C followed by 60 min of reperfusion (RE, n = 7) or 45 min of chronic IS (n = 6). Contraction ceased within 60 s of IS. PCr loss was rapid, reaching undetectable limits by 11 min. ATP loss was gradual and bore no relationship to functional loss. ATP fell to 60 +/- 4% (means +/- SE) of pre-IS levels after 13.5 min of IS. With RE, PCr returned to control levels, whereas ATP values remained depressed for the entire 60 min. Functional activity resumed with RE, but dP/dt did not rise above 85 +/- 7% of preischemic values. No correlation between residual ATP at the end of IS and functional recovery during RE was evident.

Left ventricular function during chronic endotoxemia in swine

1988 ◽  
Vol 254 (2) ◽  
pp. H324-H330 ◽  
Author(s):  
K. Lee ◽  
H. van der Zee ◽  
S. W. Dziuban ◽  
K. Luhmann ◽  
R. D. Goldfarb
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Salmonella Enteritidis ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Inotropic State ◽  
Pressure Development ◽  
Hyperdynamic Sepsis

Cardiac performance was studied in 15 chronically instrumented awake pigs during chronic endotoxemia (CET) induced by intravenous infusion of low doses of endotoxin. We sought to test the hypothesis that left ventricular inotropic state was depressed during the stage of chronic endotoxemia when cardiac output, heart rate, and left ventricular systolic pressures are elevated, termed "hyperdynamic sepsis". Left ventricular pressure, internal short axis diameter (SAX), pulmonary artery blood flow, and electrocardiogram were recorded. After initial surgical preparation, each pig was observed for 7-10 days to measure representative basal values. Each pig was then reoperated on day 10 to implant an endotoxin-loaded osmotic pump whose output, infused Salmonella enteritidis endotoxin at a rate calculated to be 10 micrograms.kg-1.h-1 for up to 7 days. Cardiac performance was monitored by measuring dP/dt, heart rate, stroke volume, end-diastolic diameter, percent change in diameter, and the slope of the end-systolic pressure diameter relationship (ESPDR). Data from the basal days were pooled and compared with the data obtained each day of CET by two-way analysis of variance. Ten of 15 pigs survived more than 2 days of CET; 5 died before the morning of the second CET day. The surviving pigs demonstrated elevated systolic pressures, left ventricular maximum rate of pressure development (+dP/dtmax and -dP/dtmax), heart rates, and cardiac output. However, both ESPDR and percent SAX shortening were significantly depressed during both CET days. We conclude that cardiac inotropic state is depressed during hyperdynamic sepsis as indicated by the load-independent parameter ESPDR and confirmed by depressed percent SAX shortening.

scholarly journals The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jingtao Na ◽  
Haifeng Jin ◽  
Xin Wang ◽  
Kan Huang ◽  
Shuang Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Expression Patterns ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Luciferase Reporter ◽  
Left Ventricular Ejection ◽  
Tunel Staining ◽  
Ventricular Ejection Fraction

Abstract Background Heart failure (HF) is a clinical syndrome characterized by left ventricular dysfunction or elevated intracardiac pressures. Research supports that microRNAs (miRs) participate in HF by regulating  targeted genes. Hence, the current study set out to study the role of HDAC3-medaited miR-18a in HF by targeting ADRB3. Methods Firstly, HF mouse models were established by ligation of the left coronary artery at the lower edge of the left atrial appendage, and HF cell models were generated in the cardiomyocytes, followed by ectopic expression and silencing experiments. Numerous parameters including left ventricular posterior wall dimension (LVPWD), interventricular septal dimension (IVSD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LEVDP), heart rate (HR), left ventricular pressure rise rate (+ dp/dt) and left ventricular pressure drop rate (-dp/dt) were measured in the mice. In addition, apoptosis in the mice was detected by means of TUNEL staining, while RT-qPCR and Western blot analysis were performed to detect miR-18a, HDAC3, ADRB3, cMyb, MMP-9, Collagen 1 and TGF-β1 expression patterns. Dual luciferase reporter assay validated the targeting relationship between ADRB3 and miR-18a. Cardiomyocyte apoptosis was determined by means of flow cytometry. Results HDAC3 and ADRB3 were up-regulated and miR-18a was down-regulated in HF mice and cardiomyocytes. In addition, HDAC3 could reduce the miR-18a expression, and ADRB3 was negatively-targeted by miR-18a. After down-regulation of HDAC3 or ADRB3 or over-expression of miR-18a, IVSD, LVEDD, LVESD and LEVDP were found to be decreased but LVPWD, LVEF, LVFS, LVSP, + dp/dt, and −dp/dt were all increased in the HF mice, whereas fibrosis, hypertrophy and apoptosis of HF cardiomyocytes were declined. Conclusion Collectively, our findings indicate that HDAC3 silencing confers protection against HF by inhibiting miR-18a-targeted ADRB3.

scholarly journals Electrophysiological effects of right and left vagal nerve stimulation on the ventricular myocardium

2014 ◽  
Vol 307 (5) ◽  
pp. H722-H731 ◽  
Author(s):  
Kentaro Yamakawa ◽  
Eileen L. So ◽  
Pradeep S. Rajendran ◽  
Jonathan D. Hoang ◽  
Nupur Makkar ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nerve Stimulation ◽  
Regional Differences ◽  
Left Ventricular Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Ventricular Pressure ◽  
Electrophysiological Effects

Vagal nerve stimulation (VNS) has been proposed as a cardioprotective intervention. However, regional ventricular electrophysiological effects of VNS are not well characterized. The purpose of this study was to evaluate effects of right and left VNS on electrophysiological properties of the ventricles and hemodynamic parameters. In Yorkshire pigs, a 56-electrode sock was used for epicardial ( n = 12) activation recovery interval (ARI) recordings and a 64-electrode catheter for endocardial ( n = 9) ARI recordings at baseline and during VNS. Hemodynamic recordings were obtained using a conductance catheter. Right and left VNS decreased heart rate (84 ± 5 to 71 ± 5 beats/min and 84 ± 4 to 73 ± 5 beats/min), left ventricular pressure (89 ± 9 to 77 ± 9 mmHg and 91 ± 9 to 83 ± 9 mmHg), and dP/d tmax (1,660 ± 154 to 1,490 ± 160 mmHg/s and 1,595 ± 155 to 1,416 ± 134 mmHg/s) and prolonged ARI (327 ± 18 to 350 ± 23 ms and 327 ± 16 to 347 ± 21 ms, P < 0.05 vs. baseline for all parameters and P = not significant for right VNS vs. left VNS). No anterior-posterior-lateral regional differences in the prolongation of ARI during right or left VNS were found. However, endocardial ARI prolonged more than epicardial ARI, and apical ARI prolonged more than basal ARI during both right and left VNS. Changes in dP/d tmax showed the strongest correlation with ventricular ARI effects ( R2 = 0.81, P < 0.0001) than either heart rate ( R2 = 0.58, P < 0.01) or left ventricular pressure ( R2 = 0.52, P < 0.05). Therefore, right and left VNS have similar effects on ventricular ARI, in contrast to sympathetic stimulation, which shows regional differences. The decrease in inotropy correlates best with ventricular electrophysiological effects.

Abstract 16574: Heart Failure Biomarkers (NT-proBNP, Gal-3, sST2) Correlate With Right Ventricular Systolic Pressure and Provide Insight to Poor CRT Response: A BIOCRT Substudy

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Roderick C Deaño ◽  
Jackie Szymonifka ◽  
Qing Zhou ◽  
Jigar H Contractor ◽  
Zachary Lavender ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Fold Increase ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Cardiac Transplant ◽  
Right Ventricular Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Crt Response

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.

Cardiovascular response to cycle exercise during and after pregnancy

1989 ◽  
Vol 66 (1) ◽  
pp. 336-341 ◽  
Author(s):  
S. P. Sady ◽  
M. W. Carpenter ◽  
P. D. Thompson ◽  
M. A. Sady ◽  
B. Haydon ◽  
...  
Keyword(s):  
Heart Rate ◽  
Maximal Exercise ◽  
Cardiovascular Response ◽  
Work Load ◽  
Cycle Ergometry ◽  
Maximal Heart Rate ◽  
O2 Uptake ◽  
Cycle Exercise ◽  
Vascular Beds ◽  
Response To Exercise

Our purpose was to determine if pregnancy alters the cardiovascular response to exercise. Thirty-nine women [29 +/- 4 (SD) yr], performed submaximal and maximal exercise cycle ergometry during pregnancy (antepartum, AP, 26 +/- 3 wk of gestation) and postpartum (PP, 8 +/- 2 wk). Neither maximal O2 uptake (VO2max) nor maximal heart rate (HR) was different AP and PP (VO2 = 1.91 +/- 0.32 and 1.83 +/- 0.31 l/min; HR = 182 +/- 8 and 184 +/- 7 beats/min, P greater than 0.05 for both). Cardiac output (Q, acetylene rebreathing technique) averaged 2.2 to 2.8 l/min higher AP (P less than 0.01) at rest and at each exercise work load. Increases in both HR and stroke volume (SV) contributed to the elevated Q at the lower exercise work loads, whereas an increased SV was primarily responsible for the higher Q at higher levels. The slope of the Q vs. VO2 relationship was not different AP and PP (6.15 +/- 1.32 and 6.18 +/- 1.34 l/min Q/l/min VO2, P greater than 0.05). In contrast, the arteriovenous O2 difference (a-vO2 difference) was lower at each exercise work load AP, suggesting that the higher Q AP was distributed to nonexercising vascular beds. We conclude that Q is greater and a-vO2 difference is less at all levels of exercise in pregnant subjects than in the same women postpartum but that the coupling of the increase in Q to the increase in systemic O2 demand (VO2) is not different.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Stress Echocardiography in Hyperthyroidism

1999 ◽  
Vol 84 (7) ◽  
pp. 2308-2313 ◽  
Author(s):  
George J. Kahaly ◽  
Stephan Wagner ◽  
Jana Nieswandt ◽  
Susanne Mohr-Kahaly ◽  
Thomas J. Ryan
Keyword(s):  
Heart Rate ◽  
Ejection Fraction ◽  
Stroke Volume ◽  
Stress Echocardiography ◽  
Maximal Exercise ◽  
Stroke Volume Index ◽  
Work Load ◽  
Left Ventricular ◽  
Volume Index ◽  
Systolic Volume

Exertion symptoms occur frequently in subjects with hyperthyroidism. Using stress echocardiography, exercise capacity and global left ventricular function can be assessed noninvasively. To evaluate stress-induced changes in cardiovascular function, 42 patients with untreated thyrotoxicosis were examined using exercise echocardiography. Studies were performed during hyperthyroidism, after treatment with propranolol, and after restoration of euthyroidism. Twenty- two healthy subjects served as controls. Ergometry was performed with patients in a semisupine position using a continuous ramp protocol starting at 20 watts/min. In contrast to control and euthyroidism, the change in end-systolic volume index from rest to maximal exercise was lower in hyperthyroidism. At rest, the stroke volume index, ejection fraction, and cardiac index were significantly increased in hyperthyroidism, but exhibited a blunted response to exercise, which normalized after restoration of euthyroidism. Propranolol treatment also led to a significant increase of delta (Δ) stroke volume index. Maximal work load and Δ heart rate were markedly lower in hyper- vs. euthyroidism. Compared to the control value, systemic vascular resistance was lowered by 36% in hyperthyroidism at rest, but no further decline was noted at maximal exercise. The Δ stroke volume index, Δ ejection fraction, Δ heart rate, and maximal work load were significantly reduced in severe hyperthyroidism. Negative correlations between free T3 and diastolic blood pressure, maximal work load, Δ heart rate, and Δ ejection fraction were noted. Thus, in hyperthyroidism, stress echocardiography revealed impaired chronotropic, contractile, and vasodilatatory cardiovascular reserves, which were reversible when euthyroidism was restored.

Abstract 13421: Ventricular and Arterial Elastance During Isometric Handgrip Exercise and Post-exercise Circulatory Arrest in Heart Failure With and Without Preserved Ejection Fraction

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Naoki Fujimoto ◽  
Keishi Moriwaki ◽  
Issei Kameda ◽  
Masaki Ishiyama ◽  
Taku Omori ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Circulatory Arrest ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Isometric Handgrip ◽  
Arterial Elastance ◽  
Post Exercise

Introduction: Isometric handgrip (IHG) training at 30% maximal voluntary contraction (MVC) lowers blood pressure in hypertensive patients. Impacts of IHG exercise and post-exercise circulatory arrest (PECA), which isolates metaboreflex control, have been unclear in heart failure (HF). Purpose: To investigate the impacts of IHG exercise and PECA on ventricular-arterial stiffness and left ventricular (LV) relaxation in HF with preserved (HFpEF) and reduced ejection fraction (HFrEF). Methods: We invasively obtained LV pressure-volume (PV) loops in 20 patients (10 HFpEF, 10 HFrEF) using conductance catheter with microtip-manometer during 3 minutes of IHG at 30%MVC and 3 minutes of PECA. Hemodynamics and LV-arterial function including LV end-systolic elastance (Ees) by the single-beat method, effective arterial elastance (Ea), and time constant of LV relaxation (Tau) were evaluated every minute. Results: At rest, HFpEF had higher LV end-systolic pressure (ESP) and lower heart rate than HFrEF with similar LV end-diastolic pressure (EDP). The coupling ratio (Ees/Ea) was greater in HFpEF than HFrEF (1.0±0.3 vs. 0.6±0.3, p<0.01). IHG for 3minutes similarly increased heart rate in HFpEF (by 10±8 bpm) and HFrEF (by 14±6 bpm). IHG also increased end-diastolic and LVESP (134±21 vs. 158±30 mmHg and 113±25 vs. 139±25 mmHg) in both groups (groupхtime effect p≥0.25). In HFpEF, Ees, Ea and Ees/Ea (1.0±0.3 vs. 1.1±0.4) were unaffected during IHG. In HFrEF, IHG induced variable increases in Ea. LV end-systolic volume and the ESPV volume-axis intercept were larger, and Ees at IHG 3 rd min was greater (1.30±0.7 vs. 3.1±2.1 mmHg/ml, p<0.01) than baseline, resulting in unchanged Ees/Ea at IHG 3 rd min (0.6±0.3 vs. 0.8±0.4, p≥0.37). Tau was prolonged only in HFrEF during IHG and was returned to the baseline value during PECA. During the first 2 minutes of PECA, LVESP was lower than that at IHG 3 rd min only in HFpEF, suggesting less metaboreflex control of blood pressure in HFpEF during IHG. Conclusions: IHG exercise at 30%MVC induced modest increases in LV end-systolic and end-diastolic pressures in HFpEF and HFrEF. Although the prolongation of LV relaxation was observed only in HFrEF, the ventricular and arterial coupling was maintained throughout the IHG exercise in both groups.

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