Increased oxygen uptake and utilization in the peripheral muscles, rather than cardiac function reserve, may be determinants of increased peak VO2 by cardiac rehabilitation in heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Hasegawa ◽  
T Kono ◽  
K Sakane ◽  
T Matsuoka ◽  
A Soyama ◽  
...  
Keyword(s):  
Heart Failure ◽  
Oxygen Uptake ◽  
Cardiac Function ◽  
Cardiac Rehabilitation ◽  
Systolic Pressure ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Peak Oxygen Consumption ◽  
Volume Index ◽  
Peak Vo2

Abstract Background Peak oxygen consumption (peak VO2) is a major prognostic parameter in heart failure (HF). Previous studies have shown a relationship between peak VO2 and impaired oxygen uptake and utilization in the peripheral muscles. The purpose of this study was to clarify the determinant of increased peak VO2 by cardiac rehabilitation (CR) in patients with HF. Methods We performed echocardiography during upright ramp bicycle cardiopulmonary exercise test in 30 HF patients (61±1 years of age, 80% male) before and 6 months after CR. HR reserve was determined as the change in HR from rest to peak exercise, expressed as a percentage of the predicted maximal HR reserve. Elastance index (EAI) and LV end-systolic elastance index (ELVI) were derived as the ratio of end-systolic pressure to stroke volume index and end-systolic volume index, respectively. End-systolic pressure was estimated from the equation 0.9 × brachial systolic blood pressure. Ventriculo-arterial coupling (VAC) was calculated as the quotient of EAI and ELVI. The ratio of LDEDVI to E/e' mean was used to evaluate LV diastolic compliance. Systemic vascular resistance index was calculated as mean arterial pressure divided by echocardiography calculated cardiac index and multiplied by 80. The arterial venous oxygen content difference (C (A-V) O2 gradient) was calculated by using the Fick equation as: VO2/echocardiography calculated cardiac output. Results Peak VO2 and C (A-V) O2 gradient were increased by CR. However, heart rate reserve, systolic reserve, VAC, diastolic reserve and vasodilation reserve were unchanged by CR (Table 1). Conclusions Increased oxygen uptake and utilization in the peripheral muscles, rather than cardiac function reserve, may be determinants of increased peak VO2 by CR in HF. Table 1 Funding Acknowledgement Type of funding source: None

scholarly journals The effects of malnutrition on cardiac function in African children

2015 ◽  
Vol 101 (2) ◽  
pp. 166-171 ◽  
Author(s):  
Jonathan A Silverman ◽  
Yamikani Chimalizeni ◽  
Stephen E Hawes ◽  
Elizabeth R Wolf ◽  
Maneesh Batra ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Function ◽  
Severe Acute Malnutrition ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Acute Malnutrition ◽  
Volume Index ◽  
Severe Malnutrition ◽  
Systemic Vascular Resistance Index ◽  
Malnourished Children

ObjectiveCardiac dysfunction may contribute to high mortality in severely malnourished children. Our objective was to assess the effect of malnutrition on cardiac function in hospitalised African children.DesignProspective cross-sectional study.SettingPublic referral hospital in Blantyre, Malawi.PatientsWe enrolled 272 stable, hospitalised children ages 6–59 months, with and without WHO-defined severe acute malnutrition.Main outcome measuresCardiac index, heart rate, mean arterial pressure, stroke volume index and systemic vascular resistance index were measured by the ultrasound cardiac output monitor (USCOM, New South Wales, Australia). We used linear regression with generalised estimating equations controlling for age, sex and anaemia.ResultsOur primary outcome, cardiac index, was similar between those with and without severe malnutrition: difference=0.22 L/min/m2 (95% CI −0.08 to 0.51). No difference was found in heart rate or stroke volume index. However, mean arterial pressure and systemic vascular resistance index were lower in children with severe malnutrition: difference=−8.6 mm Hg (95% CI −12.7 to −4.6) and difference=−200 dyne s/cm5/m2 (95% CI −320 to −80), respectively.ConclusionsIn this largest study to date, we found no significant difference in cardiac function between hospitalised children with and without severe acute malnutrition. Further study is needed to determine if cardiac function is diminished in unstable malnourished children.

scholarly journals Addition of a β1-Blocker to Milrinone Treatment Improves Cardiac Function in Patients with Acute Heart Failure and Rapid Atrial Fibrillation

Cardiology ◽  
2019 ◽  
Vol 142 (4) ◽  
pp. 195-202
Author(s):  
Shigeki Kobayashi ◽  
Takeki Myoren ◽  
Toshiro Kajii ◽  
Michiaki Kohno ◽  
Takuma Nanno ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
New York ◽  
Cardiac Function ◽  
Acute Decompensated Heart Failure ◽  
Stroke Volume Index ◽  
Heart Association ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Volume Index

Background: Tachycardia worsens cardiac performance in acute decompensated heart failure (ADHF). We investigated whether heart rate (HR) optimization by landiolol, an ultra-short-acting β1-selective blocker, in combination with milrinone improved cardiac function in patients with ADHF and rapid atrial fibrillation (AF). Methods and Results: We enrolled9 ADHF patients (New York Heart Association classification IV; HR, 138 ± 18 bpm; left ventricular [LV] ejection fraction, 28 ± 8%; cardiac index [CI], 2.1 ± 0.3 L/min–1/m–2; pulmonary capillary wedge pressure [PCWP], 24 ± 3 mm Hg), whose HRs could not be reduced using standard treatments, including diuretics, vasodilators, and milrinone. Landiolol (1.5–6.0 µg/kg–1/min–1, intravenous) was added to milrinone treatment to study its effect on hemodynamics. The addition of landiolol (1.5 µg/kg–1/min–1) significantly reduced HR by 11% without changing systolic blood pressure (BP) and resulted in a significant decrease in PCWP and a significant increase in stroke volume index (SVI), suggesting that HR reduction restores incomplete LV relaxation. Administration of more than 3.0 µg/kg–1/min–1 of landiolol decreased BP, CI, and SVI. Conclusion: The addition of landiolol at doses of <3.0 µg/kg/min to milrinone improved cardiac function in decompensated chronic heart failure with rapid atrial fibrillation by selectively reducing HR.

scholarly journals Loss of Estrogen Receptor Alpha (ERα) Exacerbates Experimental Pulmonary Arterial Hypertension (PAH)

2018 ◽  
Vol 2 (1) ◽  
Author(s):  
Annie Gensel ◽  
Andrea Frump ◽  
Tim Lahm
Keyword(s):  
Pulmonary Artery ◽  
Severe Disease ◽  
Systolic Pressure ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Volume Index ◽  
Protective Effects ◽  
Artery Remodeling ◽  
Cardiopulmonary System ◽  
Pulmonary Artery Remodeling

Background and Hypothesis: PAH is a sexually dimorphic cardiopulmonary disease characterized by excessive vasoconstriction and pulmonary artery remodeling, leading to right ventricular (RV) failure and death. While women are more likely to develop PAH, they exhibit more favorable hemodynamics and increased survival compared to men. These improved outcomes in women with PAH have been linked to protective effects of the sex steroid 17ß-estradiol (E2). While E2’s receptor ERα is protective in the systemic vasculature, its function in the cardiopulmonary system has not been explored. We hypothesized that loss of ERα exacerbates PAH. Experimental Design: Studies were performed in male and female wild type (WT) or ERα loss-of-function mutant (ERαmut) rats with monocrotaline (MCT)-induced PAH as well as disease-free controls. We quantified hemodynamics (RV catheterization), RV structure and function (echocardiography) and pulmonary artery remodeling (Verhoff-van Giesson staining). Lung tissues were analyzed for expression of pulmonary vascular homeostatic regulators BMPR2 and apelin and pro-survival regulator ERK (Western blot). P<0.05 (ANOVA) was considered significant. Results: ERαmut rats did not differ hemodynamically from WT controls. However, after MCT administration, ERαmut rats exhibited more severe disease than WT MCT rats (demonstrated by increased RV hypertrophy, RV systolic pressure, total pulmonary resistance index, as well as decreased cardiac index and stroke volume index (p<0.05). Interestingly, female ERαmut MCT rats exhibited more severe disease than their male counterparts. Apelin expression decreased in ERαmut MCT lungs compared to WT and ERαmut controls (p<0.05). Furthermore, female WT MCT lungs exhibited preserved apelin expression compared to male WT MCT (p<0.05). BMPR2 expression in ERαmut MCT lungs decreased compared to WT and ERαmut controls, as well as WT MCT (p<0.05). Conclusion: Loss of ERα aggravates MCT-PAH, indicating that ERα exerts protective effects in the cardiopulmonary system. Harnessing ERα signaling may represent a novel treatment strategy for women and men with PAH.

scholarly journals A proof of principle study of atomoxetine for the prevention of vasovagal syncope: the Prevention of Syncope Trial VI

EP Europace ◽  
2019 ◽  
Vol 21 (11) ◽  
pp. 1733-1741 ◽  
Author(s):  
Robert S Sheldon ◽  
Lucy Lei ◽  
Juan C Guzman ◽  
Teresa Kus ◽  
Felix A Ayala-Paredes ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Stroke Volume ◽  
Vasovagal Syncope ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Study Drug ◽  
Norepinephrine Transporter ◽  
Volume Index ◽  
Head Up Tilt ◽  
Invasive Techniques

Abstract Aims There are few effective therapies for vasovagal syncope (VVS). Pharmacological norepinephrine transporter (NET) inhibition increases sympathetic tone and decreases tilt-induced syncope in healthy subjects. Atomoxetine is a potent and highly selective NET inhibitor. We tested the hypothesis that atomoxetine prevents tilt-induced syncope. Methods and results Vasovagal syncope patients were given two doses of study drug [randomized to atomoxetine 40 mg (n = 27) or matched placebo (n = 29)] 12 h apart, followed by a 60-min drug-free head-up tilt table test. Beat-to-beat heart rate (HR), blood pressure (BP), and cardiac haemodynamics were recorded using non-invasive techniques and stroke volume modelling. Patients were 35 ± 14 years (73% female) with medians of 12 lifetime and 3 prior year faints. Fewer subjects fainted with atomoxetine than with placebo [10/29 vs. 19/27; P = 0.003; risk ratio 0.49 (confidence interval 0.28–0.86)], but equal numbers of patients developed presyncope or syncope (23/29 vs. 21/27). Of patients who developed only presyncope, 87% (13/15) had received atomoxetine. Patients with syncope had lower nadir mean arterial pressure than subjects with only presyncope (39 ± 18 vs. 69 ± 18 mmHg, P < 0.0001), and this was due to lower trough HRs in subjects with syncope (67 ± 30 vs. 103 ± 32 b.p.m., P = 0.006) and insignificantly lower cardiac index (2.20 ± 1.36 vs. 2.84 ± 1.05 L/min/m2, P = 0.075). There were no significant differences in stroke volume index (32 ± 6 vs. 35 ± 5 mL/m2, P = 0.29) or systemic vascular resistance index (2156 ± 602 vs. 1790 ± 793 dynes*s/cm5*m2, P = 0.72). Conclusion Norepinephrine transporter inhibition significantly decreased the risk of tilt-induced syncope in VVS subjects, mainly by blunting reflex bradycardia, thereby preventing final falls in cardiac index and BP.

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function. Methods In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results Baseline characteristics were not different in the empagliflozin (n = 22) and placebo (n = 20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 h; day 1: 48.4 ± 34.7 g/24 h; p < 0.001) as well as urinary volume (1740 ± 601 mL/24 h to 2112 ± 837 mL/24 h; p = 0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/eʹ) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p = 0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/s; day 1: 0.73 ± 0.2 m/sec; p = 0.003). Conclusions Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function. Trial registration EudraCT Number: 2016-000172-19; date of registration: 2017-02-20 (clinicaltrialregister.eu)

Resistance exercise enhances oxygen uptake without worsening cardiac function in patients with systolic heart failure: a systematic review and meta-analysis

2017 ◽  
Vol 23 (1) ◽  
pp. 73-89 ◽  
Author(s):  
Francisco V. Santos ◽  
Gaspar R. Chiappa ◽  
Sergio Henrique Rodolpho Ramalho ◽  
Alexandra Correa Gervazoni Balbuena de Lima ◽  
Fausto Stauffer Junqueira de Souza ◽  
...  
Keyword(s):  
Heart Failure ◽  
Systematic Review ◽  
Oxygen Uptake ◽  
Cardiac Function ◽  
Resistance Exercise ◽  
Meta Analysis ◽  
Systolic Heart Failure

scholarly journals Empagliflozin does not change cardiac index nor systemic vascular resistance but rapidly improves left ventricular filling pressure in patients with type 2 diabetes: a randomized controlled study 

2020 ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  
Keyword(s):  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Hemodynamic Parameters ◽  
Mitral Inflow ◽  
Ventricular Filling Pressure

Abstract Background: In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function.Methods: In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results: Baseline characteristics were not different in the empagliflozin (n=22) and placebo (n=20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 hrs; day 1: 48.4 ± 34.7 g/24 hrs; p<0.001) as well as urinary volume (1740 ± 601 mL/24 hrs to 2112 ± 837 mL/24 hrs; p=0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/e’) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p=0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/sec; day 1: 0.73 ± 0.2 m/sec; p=0.003). Conclusions: Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function.

scholarly journals Effects of Normoxia, Hyperoxia, and Mild Hypoxia on Macro-Hemodynamics and the Skeletal Muscle Microcirculation in Anesthetised Rats

2021 ◽  
Vol 8 ◽  
Author(s):  
Elisa Damiani ◽  
Erika Casarotta ◽  
Fiorenza Orlando ◽  
Andrea Carsetti ◽  
Claudia Scorcella ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Negative Impact ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Microvascular Density ◽  
Vessel Density ◽  
Volume Index ◽  
Flow Index ◽  
Flow Quality ◽  
Mild Hypoxia

Objectives: Excessive oxygen (O2) administration may have a negative impact on tissue perfusion by inducing vasoconstriction and oxidative stress. We aimed to evaluate the effects of different inhaled oxygen fractions (FiO2) on macro-hemodynamics and microvascular perfusion in a rat model.Methods: Isoflurane-anesthetised spontaneously breathing male Wistar rats were equipped with arterial (carotid artery) and venous (jugular vein) catheters and tracheotomy, and randomized into three groups: normoxia (FiO2 21%, n = 6), hyperoxia (FiO2 100%, n = 6) and mild hypoxia (FiO2 15%, n = 6). Euvolemia was maintained by infusing Lactate Ringer solution at 10 ml/kg/h. At hourly intervals for 4 h we collected measurements of: mean arterial pressure (MAP); stroke volume index (SVI), heart rate (HR), respiratory rate (by means of echocardiography); arterial and venous blood gases; microvascular density, and flow quality (by means of sidestream dark field videomicroscopy on the hindlimb skeletal muscle).Results: MAP and systemic vascular resistance index increased with hyperoxia and decreased with mild hypoxia (p &lt; 0.001 in both cases, two-way analysis of variance). Hyperoxia induced a reduction in SVI, while this was increased in mild hypoxia (p = 0.002). The HR increased under hyperoxia (p &lt; 0.05 vs. normoxia at 3 h). Cardiax index, as well as systemic O2 delivery, did not significantly vary in the three groups (p = 0.546 and p = 0.691, respectively). At 4 h, microvascular vessel surface (i.e., the percentage of tissue surface occupied by vessels) decreased by 29 ± 4% in the hyperoxia group and increased by 19 ± 7 % in mild hypoxia group (p &lt; 0.001). Total vessel density and perfused vessel density showed similar tendencies (p = 0.003 and p = 0.005, respectively). Parameters of flow quality (microvascular flow index, percentage of perfused vessels, and flow heterogeneity index) remained stable and similar in the three groups.Conclusions: Hyperoxia induces vasoconstriction and reduction in skeletal muscle microvascular density, while mild hypoxia has an opposite effect.

Abstract 15016: Peak Oxygen Consumption Achieved at the End of Cardiac Rehabilitation Predicts Survival in Patients With Coronary Heart Disease

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Salvatore Carbone ◽  
Youngdeok Kim ◽  
Sergey Kachur ◽  
Alban De Schutter ◽  
Hayley E Billingsley ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Oxygen Consumption ◽  
Heart Disease ◽  
Cardiac Rehabilitation ◽  
Peak Oxygen Consumption ◽  
Mortality Data ◽  
Term Survival ◽  
Long Term Survival ◽  
Peak Vo2

Introduction: Several patients with coronary heart disease (CHD) present reduced survival despite completing cardiac rehabilitation (CR), suggesting that the level of cardiorespiratory fitness (CRF) achieved might remain suboptimal. The purposes of this study were: 1) to examine the independent association of peak oxygen consumption (VO 2 ), a measure of CRF, at post-CR with long-term survival; and 2) to establish an optimal cut-off for peak VO 2 at post-CR that best predicts mortality risk. Methods: 853 patients with CHD (mean age of 64±10 years old) who were referred to CR between January 1, 2000, and June 30, 2013, at Ochsner Medical Center were analyzed for this study. We measured pre- and post-CR peak VO 2 . Mortality data were collected using National Death Index. Cox proportional hazard regression model was used to examine the risk of all-cause mortality associated with peak VO 2 at post-CR, independent of peak VO 2 at pre-CR and related changes during CR. Contal and O’Quigley’s method were used to determine the optimal cut-off for peak VO 2 at post-CR based on a split-sample approach. Results: Mean peak VO 2 at post-CR was 21.01±6.25 mL/kg/min (75% and 51% predicted peak VO2 using Wasserman and FRIEND Registry equations, respectively). During a mean follow-up of 6.55 years, 106 subjects (12.4%) died. Peak VO 2 at post-CR independently predicted mortality (Hazard Ratio: 0.82 [0.77-0.87], p<0.001). We identified peak VO 2 of ≥17.6 kg/mL/min as optimal cut-off best predicting survival ( Figure 1, Panel A ) and the %predicted peak VO2 at post-CR ≥62.1% using Wasserman ( Figure 1, Panel B ) and ≥41.4% using FRIEND Registry ( Figure 1, Panel C ) as the alternative optimal cut-offs. Conclusions: In patients with CHD undergoing CR, post-CR peak VO 2 independently predicts long-term survival. These results suggest that patients with CHD presenting a peak VO 2 lower than the cut-off identified herein may benefit from additional sessions of CR or higher intensity exercise training.

Hemodynamic and metabolic effects of exercise in Crotalaria-induced pulmonary hypertension in rats

1984 ◽  
Vol 57 (6) ◽  
pp. 1829-1833 ◽  
Author(s):  
L. J. McNabb ◽  
K. M. Baldwin
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Vascular Resistance ◽  
Resistance Index ◽  
Stroke Volume Index ◽  
Exercise Duration ◽  
Left Ventricular ◽  
Metabolic Effects ◽  
Volume Index ◽  
Work Index

The hemodynamic and metabolic effects of exercise were measured in Crotalaria-induced pulmonary hypertension in rats. The Crotalaria group had increased preexercise heart rate, mean pulmonary arterial pressure (PAP), arteriovenous O2 content difference, right ventricular work index (RVWI), and total pulmonary vascular resistance index (TPVRI) and decreased mean systemic blood pressure (BP), arterial O2 content (CaO2), venous O2 content (CvO2), cardiac index (CI), stroke volume index (SVI), and left ventricular work index (LVWI). The Crotalaria group during exercise had increased PAP, RVWI, TPVRI, and total systemic vascular resistance index and decreased BP, O2 consumption, CaO2, CvO2, CI, SVI, LVWI, O2 pulse index, and exercise duration. It is hypothesized that abnormal right ventricular function was a primary factor in the reduced exercise tolerance of the Crotalaria group.

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