scholarly journals Acute Beetroot Juice Ingestion Does Not Alter Renal Hemodynamics during Normoxia and Mild Hypercapnia in Healthy Young Adults

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1986
Author(s):  
Christopher L. Chapman ◽  
Zachary J. Schlader ◽  
Emma L. Reed ◽  
Morgan L. Worley ◽  
Blair D. Johnson

Arterial hypercapnia reduces renal perfusion. Beetroot juice (BRJ) increases nitric oxide bioavailability and may improve renal blood flow. We tested the hypothesis that acute consumption of BRJ attenuates both decreases in blood velocity and increases in vascular resistance in the renal and segmental arteries during acute hypercapnia. In fourteen healthy young adults, blood velocity and vascular resistance were measured with Doppler ultrasound in the renal and segmental arteries during five minutes of breathing a carbon dioxide gas mixture (CO2) before and three hours after consuming 500 mL of BRJ. There was no difference between pre- and post-BRJ consumption in the increase in the partial pressure of end-tidal CO2 during CO2 breathing (pre: +4 ± 1 mmHg; post: +4 ± 2 mmHg, p = 0.4281). Segmental artery blood velocity decreased during CO2 breathing in both pre- (by −1.8 ± 1.9 cm/s, p = 0.0193) and post-BRJ (by −2.1 ± 1.9 cm/s, p = 0.0079), but there were no differences between pre- and post-consumption (p = 0.7633). Segmental artery vascular resistance increased from room air baseline during CO2 at pre-BRJ consumption (by 0.4 ± 0.4 mmHg/cm/s, p = 0.0153) but not post-BRJ (p = 0.1336), with no differences between pre- and post-consumption (p = 0.7407). These findings indicate that BRJ consumption does not attenuate reductions in renal perfusion during acute mild hypercapnia in healthy young adults.

2020 ◽  
Vol 318 (4) ◽  
pp. R822-R827 ◽  
Author(s):  
Christopher L. Chapman ◽  
Zachary J. Schlader ◽  
Emma L. Reed ◽  
Morgan L. Worley ◽  
Blair D. Johnson

Profound increases (>15 mmHg) in arterial carbon dioxide (i.e., hypercapnia) reduce renal blood flow. However, a relatively brief and mild hypercapnia can occur in patients with sleep apnea or in those receiving supplemental oxygen therapy during an acute exacerbation of chronic obstructive pulmonary disease. We tested the hypothesis that a brief, mild hypercapnic exposure increases vascular resistance in the renal and segmental arteries. Blood velocity in 14 healthy adults (26 ± 4 yr; 7 women, 7 men) was measured in the renal and segmental arteries with Doppler ultrasound while subjects breathed room air (Air) and while they breathed a 3% CO2, 21% O2, 76% N2 gas mixture for 5 min (CO2). The end-tidal partial pressure of CO2 ([Formula: see text]) was measured via capnography. Mean arterial pressure (MAP) was measured beat to beat via the Penaz method. Vascular resistance in the renal and segmental arteries was calculated as MAP divided by blood velocity. [Formula: see text] increased with CO2 (Air: 45 ± 3, CO2: 48 ± 3 mmHg, P < 0.01), but there were no changes in MAP ( P = 0.77). CO2 decreased blood velocity in the renal (Air: 35.2 ± 8.1, CO2: 32.2 ± 7.3 cm/s, P < 0.01) and segmental (Air: 24.2 ± 5.1, CO2: 21.8 ± 4.2 cm/s, P < 0.01) arteries and increased vascular resistance in the renal (Air: 2.7 ± 0.9, CO2: 3.0 ± 0.9 mmHg·cm−1·s, P < 0.01) and segmental (Air: 3.9 ± 1.0, CO2: 4.4 ± 1.0 mmHg·cm−1·s, P < 0.01) arteries. These data provide evidence that the kidneys are hemodynamically responsive to a mild and acute hypercapnic stimulus in healthy humans.


2020 ◽  
Vol 128 (3) ◽  
pp. 627-636 ◽  
Author(s):  
Christopher L. Chapman ◽  
Blair D. Johnson ◽  
David Hostler ◽  
Penelope C. Lema ◽  
Zachary J. Schlader

To optimize study design and data interpretation, there is a need to understand the reliability of Doppler ultrasound-derived measures of blood velocity (BV) measured in the renal and segmental arteries. Thus, this study tested the following two hypotheses: 1) renal and segmental artery BV measured over the current standard of three cardiac cycles have good agreement with measurements over nine cardiac cycles ( study 1); and 2) renal and segmental artery BV measurements have relatively poor day-to-day reliability ( study 2). In study 1, there was excellent agreement between measurements over three and nine cardiac cycles for BV in both the renal and segmental arteries, as evidenced by BV measurements that were not statistically different ( P ≥ 0.68), were highly consistent ( r ≥ 0.99, P < 0.01), had a coefficient of variation ≤2.5 ± 1.8%, and 97% (renal artery) and 92% (segmental artery) of the individual differences fell within the 95% limits of agreement. In study 2, there was relatively good day-to-day reliability in renal artery BV as evidenced by no differences between three separate days ( P ≥ 0.30), an intraclass correlation coefficient (ICC) of 0.92 (0.78, 0.98), and 7.4 ± 5.5% coefficient of variation. The day-to-day reliability was relatively poor in the segmental artery with an ICC of 0.77 (0.41, 0.93) and 9.0 ± 5.6% coefficient of variation. These findings support measuring renal and segmental artery hemodynamics over three cardiac cycles and the utility in reporting renal BV across days. However, because of the variation across days, hemodynamic responses in the segmental arteries should be reported as changes from baseline when making comparisons across multiple days. NEW & NOTEWORTHY The present study indicates that Doppler ultrasound-derived measures of renal and segmental artery hemodynamics over three cardiac cycles have excellent agreement with those over nine cardiac cycles. These findings support the current practice of measuring renal and segmental artery blood velocity over three cardiac cycles. This study also demonstrates that there is excellent day-to-day reliability for measures of renal artery blood velocity, which supports reporting absolute values of renal artery blood velocity across days. However, it was also found that the day-to-day reliability of segmental artery measurements is relatively poor. Thus, to account for this variability, we suggest that segmental artery hemodynamics be compared as relative changes from baseline across separate days.


1998 ◽  
Vol 16 (7) ◽  
pp. 1015-1022 ◽  
Author(s):  
David E. Anderson ◽  
Apsara Dhokalia ◽  
Daniel Parsons ◽  
Alexei Y. Bagrov

1988 ◽  
Vol 64 (4) ◽  
pp. 1451-1456 ◽  
Author(s):  
P. A. Easton ◽  
N. R. Anthonisen

We examined the interrelation between CO2 and the ventilatory response to moderate (80% arterial saturation) sustained hypoxia in normal young adults. On a background of continuous CO2-stimulated hyperventilation, hypoxia was introduced and sustained for 25 min. Initially, with the introduction of hypoxia onto hypercapnia, there was a brisk additional increase in inspiratory minute ventilation (VI) to 284% of resting VI, but the response was not sustained and hypoxic VI declined by 36% to a level intermediate between the initial increase and the preexisting hypercapnic hyperventilation. Through the continuous hypercapnia, the changes in hypoxic ventilation resulted from significant alterations in tidal volume (VT) and mean inspiratory flow (VT/TI) without changes in respiratory timing. In another experiment, sustained hypoxia was introduced on the usual background of room air, either with isocapnia or without maintenance of end-tidal CO2 (ETCO2) (poikilocapnic hypoxia). Regardless of the degree of maintenance of ETCO2, during 25 min of sustained hypoxia, VI showed an initial brisk increase and then declined by 35-40% of resting VI to a level intermediate between the initial response and resting room air VI. For both isocapnia and poikilocapnic conditions, the attenuation of VI was an expression of a diminished VT. Thus the decline in ventilation with sustained hypoxia occurred regardless of the background ETCO2, suggesting that the mechanism underlying the hypoxic decline is independent of CO2.


2020 ◽  
Vol 120 (7) ◽  
pp. 1637-1649
Author(s):  
Leena N. Shoemaker ◽  
Luke C. Wilson ◽  
Samuel J. E. Lucas ◽  
Liana Machado ◽  
James D. Cotter

2019 ◽  
Vol 127 (4) ◽  
pp. 974-983 ◽  
Author(s):  
Christopher L. Chapman ◽  
Julia M. Benati ◽  
Blair D. Johnson ◽  
Nicole T. Vargas ◽  
Penelope C. Lema ◽  
...  

High environmental temperatures are associated with increased risk of acute kidney injury, which may be related to reductions in renal blood flow. The susceptibility of the kidneys may be increased because of heat stress-induced changes in renal vascular resistance (RVR) to sympathetic activation. We tested the hypotheses that, compared with normothermia, increases in RVR during the cold pressor test (CPT, a sympathoexcitatory maneuver) are attenuated during passive heating and exacerbated after cooling recovery. Twenty-four healthy adults (22 ± 2 yr; 12 women, 12 men) completed CPTs at normothermic baseline, after passive heating to a rise in core temperature of ~1.2°C, and after cooling recovery when core temperature returned to ~0.2°C above normothermic baseline. Blood velocity was measured by Doppler ultrasound in the distal segment of the right renal artery (Renal, n = 24 during thermal stress, n = 12 during CPTs) or the middle portion of a segmental artery (Segmental, n = 12). RVR was calculated as mean arterial pressure divided by renal or segmental blood velocity. RVR increased at the end of CPT during normothermic baseline in both arteries (Renal: by 1.0 ± 1.0 mmHg·cm−1·s, Segmental: by 2.2 ± 1.2 mmHg·cm−1·s, P ≤ 0.03), and these increases were abolished with passive heating ( P ≥ 0.76). At the end of cooling recovery, RVR in both arteries to the CPT was restored to that of normothermic baseline ( P ≤ 0.17). These data show that increases in RVR to sympathetic activation during passive heating are attenuated and return to that of normothermic baseline after cooling recovery. NEW & NOTEWORTHY Our data indicate that increases in renal vascular resistance to the cold pressor test (i.e., sympathetic activation) are attenuated during passive heating, but at the end of cooling recovery this response returns to that of normothermic baseline. Importantly, hemodynamic responses were assessed in arteries going to (renal artery) and within (segmental artery) the kidney, which has not been previously examined in the same study during thermal and/or sympathetic stressors.


2021 ◽  
Vol 10 (4) ◽  
pp. 561
Author(s):  
Aliyah Snyder ◽  
Christopher Sheridan ◽  
Alexandra Tanner ◽  
Kevin Bickart ◽  
Molly Sullan ◽  
...  

Dysregulation of the autonomic nervous system (ANS) may play an important role in the development and maintenance of persistent post-concussive symptoms (PPCS). Post-injury breathing dysfunction, which is influenced by the ANS, has not been well-studied in youth. This study evaluated cardiorespiratory functioning at baseline in youth patients with PPCS and examined the relationship of cardiorespiratory variables with neurobehavioral outcomes. Participants were between the ages of 13–25 in two groups: (1) Patients with PPCS (concussion within the past 2–16 months; n = 13) and (2) non-injured controls (n = 12). Capnometry was used to obtain end-tidal CO2 (EtCO2), oxygen saturation (SaO2), respiration rate (RR), and pulse rate (PR) at seated rest. PPCS participants exhibited a reduced mean value of EtCO2 in exhaled breath (M = 36.3 mmHg, SD = 2.86 mmHg) and an altered inter-correlation between EtCO2 and RR compared to controls. Neurobehavioral outcomes including depression, severity of self-reported concussion symptoms, cognitive catastrophizing, and psychomotor processing speed were correlated with cardiorespiratory variables when the groups were combined. Overall, results from this study suggest that breathing dynamics may be altered in youth with PPCS and that cardiorespiratory outcomes could be related to a dimension of neurobehavioral outcomes associated with poorer recovery from concussion.


1990 ◽  
Vol 5 (1) ◽  
pp. 42-46 ◽  
Author(s):  
Arnaldo Dubin ◽  
Carlos Silva ◽  
Gladys Calvo ◽  
Javier Valli ◽  
Osvaldo Fariña ◽  
...  

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