scholarly journals Altered Vascular Endothelium-Dependent Responsiveness in Frail Elderly Patients Recovering from COVID-19 Pneumonia: Preliminary Evidence

2021 ◽  
Vol 10 (12) ◽  
pp. 2558
Author(s):  
Mara Paneroni ◽  
Evasio Pasini ◽  
Michele Vitacca ◽  
Simonetta Scalvini ◽  
Laura Comini ◽  
...  
Keyword(s):  
Blood Flow ◽  
Elderly Patients ◽  
Frail Elderly ◽  
Gas Analysis ◽  
Exercise Intolerance ◽  
Arterial Blood Gas ◽  
Markers Of Inflammation ◽  
Arterial Blood ◽  
Femoral Blood Flow ◽  
Femoral Blood

We evaluated vascular dysfunction with the single passive leg movement test (sPLM) in 22 frail elderly patients at 84 + 31 days after hospitalization for COVID-19 pneumonia, compared to 22 age-, sex- and comorbidity-matched controls (CTRL). At rest, all COVID-19 patients were in stable clinical condition without severe comorbidities. Patients (aged 72 ± 6 years, 73% male) had moderate disability (Barthel index score 77 ± 26), hypoxemia and normocapnia at arterial blood gas analysis and mild pulmonary restriction at spirometry. Values of circulating markers of inflammation (C-reactive protein: CRP; erythrocyte sedimentation rate: ESR) and coagulation (D-dimer) were: 27.13 ± 37.52 mg/dL, 64.24 ± 32.37 mm/1 h and 1043 ± 729 ng/mL, respectively. At rest, femoral artery diameter was similar in COVID-19 and CTRL (p = 0.16). On the contrary, COVID-19 infection deeply impacted blood velocity (p = 0.001) and femoral blood flow (p < 0.0001). After sPLM, peak femoral blood flow was dramatically reduced in COVID-19 compared to CTRL (p = 0.001), as was blood flow ∆peak (p = 0.05) and the area under the curve (p < 0.0001). This altered vascular responsiveness could be one of the unknown components of long COVID-19 syndrome leading to fatigue, changes in muscle metabolism and fibers’ composition, exercise intolerance and increased cardiovascular risk. Impact of specific treatments, such as exercise training, dietary supplements or drugs, should be evaluated.

scholarly journals Sex differences in leg vasodilation during graded knee extensor exercise in young adults

2007 ◽  
Vol 103 (5) ◽  
pp. 1583-1591 ◽  
Author(s):  
Beth A. Parker ◽  
Sandra L. Smithmyer ◽  
Justin A. Pelberg ◽  
Aaron D. Mishkin ◽  
Michael D. Herr ◽  
...  
Keyword(s):  
Blood Flow ◽  
Femoral Artery ◽  
Knee Extensor ◽  
Activity Levels ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Vasodilatory Response ◽  
Femoral Blood Flow ◽  
Femoral Blood ◽  
Response To Exercise

Limb vascular conductance responses to pharmacological and nonexercise vasodilator stimuli are generally augmented in women compared with men. In the present investigation, we tested the hypothesis that exercise-induced vasodilator responses are also greater in women than men. Sixteen women and 15 men (20–30 yr) with similar fitness and activity levels performed graded quadriceps exercise (supine, single-leg knee extensions, 40 contractions/min) to maximal exertion. Active limb hemodynamics (left common femoral artery diameter and volumetric blood flow), heart rate (ECG), and beat-to-beat mean arterial blood pressure (MAP; radial artery tonometry) were measured during each 3-min workload (4.8 and 8 W/stage for women and men, respectively). The hyperemic response to exercise (slope of femoral blood flow vs. workload) was greater ( P < 0.01) in women as was femoral blood flow at workloads >15 W. The leg vasodilatory response to exercise (slope of calculated femoral vascular conductance vs. absolute workload) was also greater in women than in men ( P < 0.01) because of the sex difference in hyperemia and the women's lower MAP (∼10–15 mmHg) at all workloads ( P < 0.05). The femoral artery dilated to a significantly greater extent in the women (∼0.5 mm) than in the men (∼0.1 mm) across all submaximal workloads. At maximal exertion, femoral vascular conductance was lower in the men (men, 18.0 ± 0.6 ml·min−1·mmHg−1; women, 22.6 ± 1.4 ml·min−1·mmHg−1; P < 0.01). Collectively, these findings suggest that the vasodilatory response to dynamic leg exercise is greater in young women vs. men.

scholarly journals Diaphragm function does not independently predict exercise intolerance in patients with precapillary pulmonary hypertension after adjustment for right ventricular function

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Jens Spiesshoefer ◽  
Simon Herkenrath ◽  
Michael Mohr ◽  
Winfired Randerath ◽  
Izabela Tuleta ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Gas Analysis ◽  
Exercise Intolerance ◽  
Diaphragm Dysfunction ◽  
Arterial Blood Gas ◽  
Exercise Limitation ◽  
Amino Terminal ◽  
Arterial Blood ◽  
Diaphragm Function

Abstract Background: Several determinants of exercise intolerance in patients with precapillary pulmonary hypertension (PH) due to pulmonary arterial hypertension and/or chronic thromboembolic PH (CTEPH) have been suggested, including diaphragm dysfunction. However, these have rarely been evaluated in a multimodal manner. Methods: Forty-three patients with PH (age 58 ± 17 years, 30% male) and 43 age- and gender-matched controls (age 54 ± 13 years, 30% male) underwent diaphragm function (excursion and thickening) assessment by ultrasound, standard spirometry, arterial blood gas analysis, echocardiographic assessment of pulmonary artery pressure (PAP), assay of amino-terminal pro-brain natriuretic peptide (NT-proBNP) levels, and cardiac magnetic resonance (CMR) imaging to evaluate right ventricular systolic ejection fraction (RVEF). Exercise capacity was determined using the 6-min walk distance (6MWD). Results: Excursion velocity during a sniff maneuver (SniffV, 4.5 ± 1.7 vs. 6.8 ± 2.3 cm/s, P&lt;0.01) and diaphragm thickening ratio (DTR, 1.7 ± 0.5 vs. 2.8 ± 0.8, P&lt;0.01) were significantly lower in PH patients versus controls. PH patients with worse exercise tolerance (6MWD &lt;377 vs. ≥377 m) were characterized by worse SniffV, worse DTR, and higher NT-pro-BNP levels as well as by lower arterial carbon dioxide levels and RVEF, which were all univariate predictors of exercise limitation. On multivariate analysis, the only independent predictors of exercise limitation were RVEF (r = 0.47, P=0.001) and NT-proBNP (r = −0.27, P=0.047). Conclusion: Patients with PH showed diaphragm dysfunction, especially as exercise intolerance progressed. However, diaphragm dysfunction does not independently contribute to exercise intolerance, beyond what can be explained from right heart failure.

The ontogeny of hemodynamic responses to prolonged umbilical cord occlusion in fetal sheep

2007 ◽  
Vol 103 (4) ◽  
pp. 1311-1317 ◽  
Author(s):  
Guido Wassink ◽  
Laura Bennet ◽  
Lindsea C. Booth ◽  
Ellen C. Jensen ◽  
Bert Wibbens ◽  
...  
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Rapid Onset ◽  
Hemodynamic Responses ◽  
Fetal Sheep ◽  
Eeg Activity ◽  
Progressive Development ◽  
Arterial Blood ◽  
Femoral Blood Flow ◽  
Femoral Blood

There is evidence that preterm fetuses have blunted chemoreflex-mediated responses to hypoxia. However, the preterm fetus has much lower aerobic requirements than at term, and so moderate hypoxia may not be sufficient to elicit maximal chemoreflex responses; there are only limited quantitative data on the ontogeny of chemoreflex and hemodynamic responses to severe asphyxia. Chronically instrumented fetal sheep at 0.6 ( n = 12), 0.7 ( n = 12), and 0.85 ( n = 8) of gestational age (GA; term = 147 days) were exposed to 30, 25, or 15 min of complete umbilical cord occlusion, respectively. At all ages, occlusion was associated with early onset of bradycardia, profoundly reduced femoral blood flow and conductance, and hypertension. The 0.6-GA fetuses showed a significantly slower and lesser fall in femoral blood flow and conductance compared with the 0.85-GA group, with a correspondingly reduced relative rise in mean arterial blood pressure. As occlusion continued, the initial adaptation was followed by loss of peripheral vasoconstriction and progressive development of hypotension in all groups. The 0.85-GA fetuses showed significantly more sustained reduction in femoral conductance but also more rapid onset of hypotension than either of the younger groups. Electroencephalographic (EEG) activity was suppressed during occlusion in all groups, but the degree of suppression was less at 0.6 GA than at term. In conclusion, the near-midgestation fetus shows attenuated initial (chemoreflex) peripheral vasomotor responses to severe asphyxia compared with more mature fetuses but more sustained hemodynamic adaptation and reduced suppression of EEG activity during continued occlusion of the umbilical cord.

Central command contributes to increased blood flow in the noncontracting muscle at the start of one-legged dynamic exercise in humans

2012 ◽  
Vol 112 (12) ◽  
pp. 1961-1974 ◽  
Author(s):  
Kei Ishii ◽  
Nan Liang ◽  
Anna Oue ◽  
Ai Hirasawa ◽  
Kohei Sato ◽  
...  
Keyword(s):  
Blood Flow ◽  
Voluntary Exercise ◽  
Tissue Blood Flow ◽  
Central Command ◽  
Arterial Blood ◽  
Femoral Blood Flow ◽  
Muscle Mechanoreflex ◽  
Femoral Blood ◽  
The Right ◽  
Exercise In Humans

Whether neurogenic vasodilatation contributes to exercise hyperemia is still controversial. Blood flow to noncontracting muscle, however, is chiefly regulated by a neural mechanism. Although vasodilatation in the nonexercising limb was shown at the onset of exercise, it was unclear whether central command or muscle mechanoreflex is responsible for the vasodilatation. To clarify this, using voluntary one-legged cycling with the right leg in humans, we measured the relative changes in concentrations of oxygenated-hemoglobin (Oxy-Hb) of the noncontracting vastus lateralis (VL) muscle with near-infrared spectroscopy as an index of tissue blood flow and femoral blood flow to the nonexercising leg. Oxy-Hb in the noncontracting VL and femoral blood flow increased ( P < 0.05) at the start period of voluntary one-legged cycling without accompanying a rise in arterial blood pressure. In contrast, no increases in Oxy-Hb and femoral blood flow were detected at the start period of passive one-legged cycling, suggesting that muscle mechanoreflex cannot explain the initial vasodilatation of the noncontracting muscle during voluntary one-legged cycling. Motor imagery of the voluntary one-legged cycling increased Oxy-Hb of not only the right but also the left VL. Furthermore, an increase in Oxy-Hb of the contracting VL, which was observed at the start period of voluntary one-legged cycling, had the same time course and magnitude as the increase in Oxy-Hb of the noncontracting muscle. Thus it is concluded that the centrally induced vasodilator signal is equally transmitted to the bilateral VL muscles, not only during imagery of exercise but also at the start period of voluntary exercise in humans.

Acute on chronic exposure to endotoxin is associated with enhanced chemoreflex responses in preterm fetal sheep

2013 ◽  
Vol 304 (10) ◽  
pp. R799-R803 ◽  
Author(s):  
Lindsea C. Booth ◽  
Paul P. Drury ◽  
Cameron Muir ◽  
Ellen C. Jensen ◽  
Alistair J. Gunn ◽  
...  
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Chronic Exposure ◽  
Fetal Sheep ◽  
Hypoxic Injury ◽  
Arterial Blood ◽  
Femoral Blood Flow ◽  
Dose Infusion ◽  
Initial Hypothesis ◽  
Femoral Blood

There is increasing evidence that exposure to infection can sensitize the fetus to subsequent hypoxic injury. However, it is unclear whether this involves compromise of the fetal cardiovascular adaptation to acute asphyxia. Chronically instrumented 103-day-old (0.7 gestational age, term is 147 days) fetal sheep in utero were randomized to receive either gram-negative lipopolysaccharide (LPS) as a continuous low-dose infusion for 120 h plus boluses of 1 μg LPS at 48, 72, and 96 h with asphyxia at 102 h (i.e., 6 h after the final LPS bolus) induced by umbilical cord occlusion for 15 min (LPS treated, n = 8), or the same volume of saline plus occlusion (saline treated, n = 7). Fetuses were killed 5 days after occlusion. LPS was associated with a more rapid fall in fetal heart rate at the onset of occlusion ( P < 0.05) and with minimally lower values during occlusion ( P < 0.05). The LPS-treated fetuses had lower fetal mean arterial blood pressure (BP) and greater carotid artery blood flow (CaBF) before occlusion ( P < 0.05) but showed an increase in BP and fall in CaBF to similar values as saline controls during occlusion. There were no differences between the groups in femoral blood flow before or during occlusion. Contrary to our initial hypothesis, acute on chronic exposure to LPS was associated with more rapid cardiovascular adaptation to umbilical cord occlusion.

Pulmonary effects of intravenous atropine induce ventilation perfusion mismatch

2014 ◽  
Vol 92 (5) ◽  
pp. 399-404 ◽  
Author(s):  
Romolo J. Gaspari ◽  
David Paydarfar
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Blood Flow ◽  
Gas Analysis ◽  
Pulmonary Gas Exchange ◽  
Blood Gas ◽  
Arterial Blood Gas ◽  
Anticholinergic Medications ◽  
Arterial Blood ◽  
Intravenous Atropine

Atropine is used for a number of medical conditions, predominantly for its cardiovascular effects. Cholinergic nerves that innervate pulmonary smooth muscle, glands, and vasculature may be affected by anticholinergic medications. We hypothesized that atropine causes alterations in pulmonary gas exchange. We conducted a prospective interventional study with detailed physiologic recordings in anesthetized, spontaneously breathing rats (n = 8). Animals breathing a normoxic gas mixture titrated to a partial arterial pressure of oxygen of 110–120 were exposed to an escalating dose of intravenous atropine (0.001, 0.01, 0.1, 5.0, and 20.0 mg/kg body mass). Arterial blood gas measurements were recorded every 2 min (×5) at baseline, and following each of the 5 doses of atropine. In addition, the animals regional pulmonary blood flow was measured using neutron-activated microspheres. Oxygenation decreased immediately following intravenous administration of atropine, despite a small increase in the volume of inspired air with no change in respiratory rate. Arterial blood gas analysis showed an increase in pulmonary dysfunction, characterized by a widening of the alveolar–arteriole gradient (p < 0.003 all groups except for the lowest dose of atropine). The microsphere data demonstrates an abrupt and marked heterogeneity of pulmonary blood flow following atropine treatment. In conclusion, atropine was found to decrease pulmonary gas exchange in a dose-dependent fashion in this rat model.

Circulatory effects of moderately and severely increased intracranial pressure in the dog

1972 ◽  
Vol 36 (6) ◽  
pp. 721-727 ◽  
Author(s):  
Norberto C. Gonzalez ◽  
John Overman ◽  
John A. Maxwell
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Peripheral Resistance ◽  
Arterial Blood ◽  
Femoral Blood Flow ◽  
Femoral Blood

✓ Anesthetized dogs were subjected to elevated intracranial pressure (ICP) of 60 and 100 mm Hg. At 60 mm Hg, decreases in heart rate and arterial blood pressure were observed associated with an increase in femoral blood flow that suggested vasodilation in the somatic areas. Cardiac output showed little change. Subsequent elevation of ICP to 100 mm Hg was followed by an increase in arterial blood pressure; cardiac output increased, and femoral flow increased still further. Since resistance to flow did not change, the hypertension was thought to be due to an increase in flow rather than peripheral resistance. An increase in heart rate was associated with the elevation in cardiac output; the fact that femoral blood flow increased proportionately more than cardiac output suggested a redistribution of blood flow. The changes in peripheral blood flow and in cardiac output were associated with a decrease in the arteriovenous oxygen (A–VO2) difference. No signs of tissue hypoxia were observed; specifically there was no significant change in the lactate-to-pyruvate ratio; the changes in A–VO2 difference were correlated with changes in flow and the product of the two variables, namely, oxygen consumption, remained unchanged. The data show that experimental elevation of ICP restricted to moderate levels is followed by hemodynamic changes suggesting peripheral vasodilation, and that when an increase in blood pressure then occurs, it is due to an increase in blood flow despite the decrease in peripheral resistance.

scholarly journals Human muscle length-dependent changes in blood flow

2012 ◽  
Vol 112 (4) ◽  
pp. 560-565 ◽  
Author(s):  
John McDaniel ◽  
Stephen J. Ives ◽  
Russell S. Richardson
Keyword(s):  
Blood Flow ◽  
Knee Joint ◽  
Joint Angle ◽  
Muscle Blood Flow ◽  
Muscle Length ◽  
Limb Blood Flow ◽  
Knee Joint Angle ◽  
Femoral Blood Flow ◽  
Femoral Blood ◽  
Cyclic Changes

Although a multitude of factors that influence skeletal muscle blood flow have been extensively investigated, the influence of muscle length on limb blood flow has received little attention. Thus the purpose of this investigation was to determine if cyclic changes in muscle length influence resting blood flow. Nine healthy men (28 ± 4 yr of age) underwent a passive knee extension protocol during which the subjects' knee joint was passively extended and flexed through 100–180° knee joint angle at a rate of 1 cycle per 30 s. Femoral blood flow, cardiac output (CO), heart rate (HR), stroke volume (SV), and mean arterial pressure (MAP) were continuously recorded during the entire protocol. These measurements revealed that slow passive changes in knee joint angle did not have a significant influence on HR, SV, MAP, or CO; however, net femoral blood flow demonstrated a curvilinear increase with knee joint angle ( r2 = 0.98) such that blood flow increased by ∼90% (125 ml/min) across the 80° range of motion. This net change in blood flow was due to a constant antegrade blood flow across knee joint angle and negative relationship between retrograde blood flow and knee joint angle ( r2 = 0.98). Thus, despite the absence of central hemodynamic changes and local metabolic factors, blood flow to the leg was altered by changes in muscle length. Therefore, when designing research protocols, researchers need to be cognizant of the fact that joint angle, and ultimately muscle length, influence limb blood flow.

Sign in / Sign up

Export Citation Format

Share Document