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.

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 Right ventricle to pulmonary artery coupling in patients undergoing transcatheter aortic valve implantation

Heart ◽  
2018 ◽  
Vol 105 (2) ◽  
pp. 117-121 ◽  
Author(s):  
Ibrahim Sultan ◽  
Arturo Cardounel ◽  
Islam Abdelkarim ◽  
Arman Kilic ◽  
Andrew D Althouse ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Stroke Volume Index ◽  
Left Ventricular ◽  
Volume Index ◽  
Left Ventricular Ejection ◽  
Ventricular Ejection Fraction ◽  
Transcatheter Aortic Valve ◽  
All Cause Mortality

ObjectivesTo evaluate the prognostic value of the ratio between tricuspid annular plane systolic excursion (TAPSE)-pulmonary artery systolic pressure (PASP) as a determinant of right ventricular to pulmonary artery (RV-PA) coupling in patients undergoing transcatheter aortic valve replacement (TAVI).BackgroundRV function and pulmonary hypertension (PH) are both prognostically important in patients receiving TAVI. RV-PA coupling has been shown to be prognostic important in patients with heart failure but not previously evaluated in TAVI patients.MethodsConsecutive patients with severe aortic stenosis who received TAVI from July 2011 through January 2016 and with comprehensive baseline echocardiogram were included. All individual echocardiographic images and Doppler data were independently reviewed and blinded to the clinical information and outcomes. Cox models quantified the effect of TAPSE/PASP quartiles on subsequent all-cause mortality while adjusting for confounders.ResultsA total of 457 patients were included with mean age of 82.8±7.2 years, left ventricular ejection fraction (LVEF) 54%±13%, PASP 44±17 mm Hg. TAPSE/PASP quartiles showed a dose-response relationship with survival. This remained significant (HR for lowest quartile vs highest quartile=2.21, 95% CI 1.07 to 4.57, p=0.03) after adjusting for age, atrial fibrillation, LVEF, stroke volume index, Society of Thoracic Surgeons Predicted Risk of Mortality.ConclusionBaseline TAPSE/PASP ratio is associated with all-cause mortality in TAVI patients as it evaluates RV systolic performance at a given degree of afterload. Incorporation of right-side unit into the risk stratification may improve optimal selection of patients for TAVI.

Systolic Pressure Variation as a Guide to Fluid Therapy in Patients with Sepsis-induced Hypotension 

1998 ◽  
Vol 89 (6) ◽  
pp. 1313-1321 ◽  
Author(s):  
Benoit Tavernier ◽  
Olivier Makhotine ◽  
Gilles Lebuffe ◽  
Jacques Dupont ◽  
Philippe Scherpereel
Keyword(s):  
Pulmonary Artery ◽  
Systolic Pressure ◽  
Stroke Volume Index ◽  
Pulmonary Artery Occlusion Pressure ◽  
Artery Occlusion ◽  
Pressure Variation ◽  
Volume Index ◽  
Occlusion Pressure ◽  
Area Index ◽  
Systolic Pressure Variation

Background Monitoring left ventricular preload is critical to achieve adequate fluid resuscitation in patients with hypotension and sepsis. This prospective study tested the correlation of the pulmonary artery occlusion pressure, the left ventricular end-diastolic area index measured by transesophageal echocardiography, the arterial systolic pressure variation (the difference between maximal and minimal systolic blood pressure values during one mechanical breath), and its delta down (dDown) component (= apneic - minimum systolic blood pressure) with the response of cardiac output to volume expansion during sepsis. Methods Preload parameters were measured at baseline and during graded volume expansion (increments of 500 ml) in 15 patients with sepsis-induced hypotension who required mechanical ventilation. Each volume-loading step (VLS) was classified as a responder (increase in stroke volume index &gt; or = 15%) or a nonresponder. Successive VLSs were performed until a nonresponder VLS was obtained. Results Thirty-five VLSs (21 responders) were performed. Fluid loading caused an overall significant increase in pulmonary artery occlusion pressure and end-diastolic area index, and a significant decrease in systolic pressure variation and delta down (P &lt; 0.01). There was a significant difference between responder and nonresponder VLSs in end-diastolic area index, systolic pressure variation, and dDown, but not in pulmonary artery occlusion pressure. Receiver-operator curve analysis showed that dDown was a more accurate indicator of the response of stroke volume index to volume loading than end-diastolic area index and pulmonary artery occlusion pressure. A dDown component of more than 5 mmHg indicated that the stroke volume index would increase in response to a subsequent fluid challenge (positive and negative predictive values: 95% and 93%, respectively). Conclusion The dDown component of the systolic pressure variation is a sensitive indicator of the response of cardiac output to volume infusion in patient with sepsis-induced hypotension who require mechanical ventilation.

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 The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021 ◽  
Vol 22 (9) ◽  
pp. 4980
Author(s):  
Inés Roger ◽  
Javier Milara ◽  
Paula Montero ◽  
Julio Cortijo
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Vascular Remodeling ◽  
Pulmonary Arteries ◽  
Clinical Manifestations ◽  
Different Types ◽  
Artery Remodeling ◽  
Stat Pathway ◽  
Pulmonary Artery Remodeling

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular, and cellular processes involved in PH. Chronic inflammation contributes to pulmonary artery remodeling and PH, among other vascular disorders, and many inflammatory mediators signal through the JAK/STAT pathway. Recent evidence indicates that the JAK/STAT pathway is overactivated in the pulmonary arteries of patients with PH of different types. In addition, different profibrotic cytokines such as IL-6, IL-13, and IL-11 and growth factors such as PDGF, VEGF, and TGFβ1 are activators of the JAK/STAT pathway and inducers of pulmonary remodeling, thus participating in the development of PH. The understanding of the participation and modulation of the JAK/STAT pathway in PH could be an attractive strategy for developing future treatments. There have been no studies to date focused on the JAK/STAT pathway and PH. In this review, we focus on the analysis of the expression and distribution of different JAK/STAT isoforms in the pulmonary arteries of patients with different types of PH. Furthermore, molecular canonical and noncanonical JAK/STAT pathway transactivation will be discussed in the context of vascular remodeling and PH. The consequences of JAK/STAT activation for endothelial cells and pulmonary artery smooth muscle cells’ proliferation, migration, senescence, and transformation into mesenchymal/myofibroblast cells will be described and discussed, together with different promising drugs targeting the JAK/STAT pathway in vitro and in vivo.

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)

scholarly journals Adventitial Alterations Are the Main Features in Pulmonary Artery Remodeling due to Long-Term Chronic Intermittent Hypobaric Hypoxia in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Julio Brito ◽  
Patricia Siques ◽  
Silvia M. Arribas ◽  
Angel L. López de Pablo ◽  
M. Carmen González ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Inflammatory Cells ◽  
Cell Number ◽  
Hypoxic Conditions ◽  
Artery Remodeling ◽  
Medial Hypertrophy ◽  
The Right ◽  
Pulmonary Artery Remodeling

Long-term chronic intermittent exposure to altitude hypoxia is a labor phenomenon requiring further research. Using a rat model, we examined whether this type of exposure differed from chronic exposure in terms of pulmonary artery remodeling and other features. Rats were subjected to chronic hypoxia (CH,n=9) and long-term intermittent hypoxia (CIH2x2; 2 days of hypoxia/2 days of normoxia,n=10) in a chamber (428 Torr, 4,600 m of altitude) for 46 days and compared to rats under normoxia (NX,n=10). Body weight, hematocrit, and right ventricle ratio were measured. Pulmonary artery remodeling was assessed using confocal microscopy of tissues stained with a nuclear dye (DAPI) and CD11b antibody. Both hypoxic conditions exhibited increased hematocrit and hypertrophy of the right ventricle, tunica adventitia, and tunica media, with no changes in lumen size. The medial hypertrophy area (larger in CH) depicted a significant increase in smooth muscle cell number. Additionally, CIH2x2 increased the adventitial hypertrophy area, with an increased cellularity and a larger prevalence of clustered inflammatory cells. In conclusion, CIH2x2 elicits milder effects on pulmonary artery medial layer muscularization and subsequent right ventricular hypertrophy than CH. However, CIH2x2 induces greater and characteristic alterations of the adventitial layer.

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.

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