A B S T R A C T The effects of phosphorus depletion on cardiac muscle function in six awake dogs were evaluated with surgically implanted transducers to serially measure ascending aortic root blood flow and high fidelity left ventricular pressure. After the animals recovered from surgery, phosphorus depletion was induced by feeding them a synthetic phosphorusdeficient diet plus aluminum carbonate gel for 35 days, followed by the same diet with phosphorus supplementation for 21 days. In addition to the cardiac studies, sequential measurements of phosphorus content in skeletal muscle and phosphorus in serum were obtained to ascertain the level of phosphorus depletion.Serum inorganic phosphorus concentration (mg/100 ml) decreased from 5.1±0.1 on day 0 to 0.9±0.1 on day 35 (P < 0.01), and total muscle phosphorus (content mmol/100 g fat-free dry weight) decreased from 28.0 ±0.2 on day 0 to 22.6±0.5 on day 35 (P < 0.01). During the period of phosphorus depletion, there was no significant change in heart rate; however, stroke volume (milliliter) and peak blood flow velocity (centimeter per second) declined from 24±2 to 17±2 (P < 0.01) and 121±12 to 98±7 (P <0.01), respectively. Maximum ascending aortic blood flow acceleration (centimeter per second square) and maximum left ventricular time rate of change of pressure (mm Hg per second) also decreased from 4,630±313 to 3,817+346 (P < 0.01) and 2,582+347 to 2,120±297 (P < 0.01) during phosphorus depletion. After repletion all values returned to control values.These results indicate that moderate diet-induced phosphorus depletion can depress myocardial perfor-
Increases in neuronal metabolic demand are typically matched by a proportional increase in brain blood flow. This neurovascular coupling (NVC) response is impaired with healthy aging and in Alzheimer's disease and has been attributed to an imbalance of reactive oxygen species (ROS) relative to endogenous antioxidant defenses (oxidative stress) in animal models; however, the role of ROS on NVC in healthy humans is not completely understood. High levels of ROS in the vasculature impairs endothelium‐dependent vasodilatation whereas smaller amounts of ROS in neurons may be necessary for NVC. Therefore, we aimed to investigate the effect of an acute antioxidant infusion (vitamin C; VTC) on NVC and shear‐mediated dilation of the internal carotid artery (ICA) in healthy adults. We hypothesized that, compared with control (saline), acute infusion of the antioxidant VTC would augment NVC in healthy adults. Seven healthy adults (2 males/5 females, age: 38 ± 24 years; BMI: 24.0 ± 3.5 kg/m2; blood pressure (BP): 104 ± 8/62 ± 5 mmHg) participated in this randomized, double‐blind placebo‐controlled intervention. Participants received a 20‐minute priming bolus infusion of either saline or 0.06 g ascorbic acid per kg fat‐free mass (FFM), followed by a drip‐infusion of either saline or 0.02 g ascorbic acid per kg FFM. Middle cerebral artery blood flow velocity (MCAv) was measured using transcranial Doppler (TCD) ultrasound (Spencer Technologies, Redmond, WA) at an average insonation depth of 48.0 ± 6.0 mm. Cerebrovascular conductance (CVC) was calculated as mean MCAV divided by beat‐beat mean arterial pressure (FINAPRES NOVA, Enschede, Netherlands). NVC was assessed as the percent change (from baseline) in CVC (CVC%Δ) during an incrementally difficult cognitive challenge (N‐back task) after acute infusion of VTC vs. saline. Shear‐mediated vasodilation of the ICA to a transient (30 second) hypercapnia stimulus was also assessed at each time point as a measure of vascular function independent of neuronal demand. To quantify the NVC response, post infusion CVC and performance at each stage of the N‐back test were analyzed using a 2×2 repeated measures ANOVA with treatment (saline vs. VTC) and stage of the N‐back test as factors. Post‐infusion vasodilation of the ICA to transient hypercapnia was analyzed between treatment conditions using a paired t‐test. Data are presented as mean ± SD. Post‐infusion CVC%Δ was blunted at all levels of the N‐Back task after the infusion of VTC vs. saline (0‐Back: −3.94 ± 7.23% vs. 0.95 ± 3.23%; 1‐Back,: −4.16 ± 8.15% vs. 2.23 ± 4.72%; 2‐Back: −4.83 ± 14.94% vs. 4.79 ± 6.13%; Treatment effect: P = 0.045; F‐statistic (1,18) = 4.66). While there were no significant differences between stages, the number of correct responses decreased as the difficulty of the test increased. No significant differences in the ICA response to transient hypercapnia were observed after infusion of VTC vs. saline (4.08 ± 1.44% vs. 4.62 ± 0.76%; P = 0.54). These data suggest that ROS may be necessary to elicit an appropriate NVC response in healthy adults.Support or Funding InformationThis work was supported by a pilot grant through the Center of Biomedical Research Excellence in Cardiovascular Health P20GM113125.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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