Redistribution Of Blood Flow Research Articles

The levels of oxidative stress markers in maternal and umbilical cord blood of pregnant women with diabetes mellitus in terms of blood flow redistribution in the fetal venous system

The levels of oxidative stress markers in maternal and umbilical cord blood of pregnant women with diabetes mellitus in terms of blood flow redistribution in the fetal venous system

One-year results from the REDUCER-I multi-center real-world clinical trial of the treatment of refractory angina with the coronary sinus Reducer

Abstract Background/Introduction Patients with refractory angina have chronic symptoms due to reversible ischemia which are inadequately controlled with optimal medical therapy or interventional treatments. These patients suffer from a poor quality of life and place a significant strain on the health care system due to their frequent rehospitalizations. The coronary sinus (CS) Reducer is a stainless-steel hour-glass shaped mesh stent that creates a focal narrowing in the lumen of the CS resulting in improved microvascular resistance and redistribution of myocardial blood flow. Purpose The COSIRA randomized controlled trial showed the Reducer is a safe and effective treatment for refractory angina with patients having significant improvements in Canadian Cardiovascular Society (CCS) class and other measures of quality of life. The REDUCER-I post-market study evaluated the long-term outcomes with the Reducer in a large and challenging ‘real-world’ cohort. Methods REDUCER-I is a multicenter, non-randomized study conducted across 26 medical centers in Europe. At one year, device effectiveness was assessed by improvement in CCS grade as compared to baseline and device safety was assessed by Major Adverse Cardiac Events (MACE). Secondary endpoints included six-minute walk tests, EQ-5D-5L tests, and Seattle Angina Questionnaires (SAQ). Subjects were followed at 30 days, 6 months, and annually through five years. Results The as-treated population includes a total of 371 patients who received a Reducer implant (78.7% (292/371) male, 47.2% (175/371) diabetic, 73.9% (274/371) post-revascularization). The one-year Kaplan-Meier overall MACE rate post-implant was 7.1% (95% CI [4.9, 10.4]). There were nine deaths within the first 365 days, one death was due to unknown causes and eight deaths were adjudicated to as not being device- or procedure-related. At 12 months, 70.0% (205/293) of patients improved by ≥1 CCS class. At baseline, 72.2% (232/363) of patients were CCS class III/IV and this proportion decreased to 18.1% (54/298) at 12 months (P<0.0001). The patients’ baseline six-minute walk distance was 327.5±116.1m which improved by a mean of 30.8±81.8m at 12 months (p<.0001). In the year prior to Reducer implant, 33.3% (88/264) of the patients had at least one visit to the emergency department compared to 11.7% (31/264) in the year after Reducer implant (p<.0001). The significant improvements in CCS class and SAQ-QoL were sustained through 3 years (Figure). Conclusion In this 12-month analysis of the REDUCER-I study, patients with refractory angina treated with the CS Reducer had low MACE rates and showed significant and sustained improvements in angina, QoL, functional capacity, and need for rehospitalization.

Physiological effects and safety of bed verticalization in patients with acute respiratory distress syndrome

BackgroundTrunk inclination in patients with Acute Respiratory Distress Syndrome (ARDS) in the supine position has gained scientific interest due to its effects on respiratory physiology, including mechanics, oxygenation, ventilation distribution, and efficiency. Changing from flat supine to semi-recumbent increases driving pressure due to decreased respiratory system compliance. Positional adjustments also deteriorate ventilatory efficiency for CO2 removal, particularly in COVID-19-associated ARDS (C-ARDS), indicating likely lung parenchyma overdistension. Tilting the trunk reduces chest wall compliance and, to a lesser extent, lung compliance and transpulmonary driving pressure, with significant hemodynamic and gas exchange implications.MethodsA prospective, pilot physiological study was conducted on early ARDS patients in two ICUs at CHU Clermont-Ferrand, France. The protocol involved 30-min step gradual verticalization from a 30° semi-seated position (baseline) to different levels of inclination (0°, 30°, 60°, and 90°), before returning to the baseline position. Measurements included tidal volume, positive end-expiratory pressure (PEEP), esophageal pressures, and pulmonary artery catheter data. The primary endpoint was the variation in transpulmonary driving pressure through the verticalization procedure.ResultsFrom May 2020 through January 2021, 30 patients were included. Transpulmonary driving pressure increased slightly from baseline (median and interquartile range [IQR], 9 [5–11] cmH2O) to the 90° position (10 [7–14] cmH2O; P < 10–2 for the overall effect of position in mixed model). End-expiratory lung volume increased with verticalization, in parallel to decreases in alveolar strain and increased arterial oxygenation. Verticalization was associated with decreased cardiac output and stroke volume, and increased norepinephrine doses and serum lactate levels, prompting interruption of the procedure in two patients. There were no other adverse events such as falls or equipment accidental removals.ConclusionsVerticalization to 90° is feasible in ARDS patients, improving EELV and oxygenation up to 30°, likely due to alveolar recruitment and blood flow redistribution. However, there is a risk of overdistension and hemodynamic instability beyond 30°, necessitating individualized bed angles based on clinical situations.Trial registration ClinicalTrials.gov registration number NCT04371016, April 24, 2020.

Elevated middle cerebral artery peak systolic velocity and risk of death in donor twin affected by twin-twin transfusion syndrome but not twin anemia-polycythemia sequence.

To determine the association between elevated (> 1.5 multiples of the median (MoM)) middle cerebral artery (MCA) peak systolic velocity (PSV) and fetal demise of the donor twin in pregnancies complicated by twin-twin transfusion syndrome (TTTS) in the absence of twin anemia-polycythemia sequence (TAPS). Secondary objectives were to evaluate if donor or recipient MCA-PSV is associated with a risk for their corresponding fetal death, and to compare the proportion of donor fetuses with low MCA pulsatility index (PI) among donor twins with high MCA-PSV and those with normal MCA-PSV to evaluate the contribution of blood-flow redistribution to the fetal brain in donor twins with high MCA-PSV. This prospective cohort study included TTTS cases that underwent laser surgery between 2011 and 2022 at a single center. TAPS cases were excluded from the study. Multivariable and Poisson regression analysis were performed to explore the association between isolated elevated donor MCA-PSV and fetal demise, adjusted for TTTS stage, selective fetal growth restriction (sFGR) and other confounders. Of 660 TTTS cases, donor MCA-PSV was not recorded in 48 (7.3%) cases. Of the remaining 612 patients, nine (1.5%) were lost to follow-up and 96 TAPS cases were excluded; thus, 507 cases were included in the study. High donor MCA-PSV was seen in 6.5% (33/507) of cases and was an independent risk factor for donor fetal demise (adjusted relative risk (aRR), 4.52 (95% CI, 2.72-7.50)), after adjusting for confounders. Regression analysis restricted to each Quintero TTTS stage demonstrated that high donor MCA-PSV was an independent risk factor for fetal demise of the donor in Quintero Stage II (aRR, 14.21 (95% CI, 1.09-186.2)) and Quintero Stage III (aRR, 3.41 (95% CI, 1.82-6.41)). Donor MCA-PSV in MoM was associated with fetal demise of the donor (area under the receiver-operating-characteristics curve (AUC), 0.69; P < 0.001), but recipient MCA-PSV in MoM was not associated with fetal demise of the recipient (AUC, 0.54; P = 0.44). A higher proportion of donor twins in the group with high MCA-PSV had a low MCA-PI compared to the group with normal MCA-PSV (33.3% vs 15.5%; P = 0.016). Elevated donor MCA-PSV without TAPS prior to laser surgery for TTTS is associated with a 4-fold increased risk for donor fetal demise, adjusted for sFGR, TTTS stage and other confounders. Doppler evaluation of donor MCA-PSV prior to laser surgery may help stratify TTTS staging to evaluate the risk of donor fetal demise. © 2024 International Society of Ultrasound in Obstetrics and Gynecology.

The role of umbilical-portal venous hemodynamics in fetal macrosomia pathogenesis in pregnancy complicated by diabetes mellitus

BACKGROUND: During pregnancy complicated by diabetes mellitus, the risks of developing fetal macrosomia and other perinatal complications increase. Redistribution of blood flow in the fetal umbilical-portal venous system may be an important but poorly understood compensatory mechanism that affects macrosomic fetal growth. AIM: The aim of this study was to determine the features of the fetal umbilical-portal venous hemodynamics in pregnant women with various types of diabetes mellitus and the absence of carbohydrate metabolism disorders, taking into account the gestational age and the macrosomic fetal growth. MATERIALS AND METHODS: In this prospective cohort study, 86 pregnant women with pregestational diabetes mellitus, 44 pregnant women with gestational diabetes mellitus and 58 patients without carbohydrate metabolism disorders underwent ultrasound examinations from 30+0 to 41+3 weeks of gestation. During ultrasound, we performed Doppler assessment of venous hemodynamic parameters in the vessels of the umbilical-portal venous system, with volumetric blood flow calculated for each vessel. Additionally, the total liver volumetric blood flow and ductus venosus shunt fraction were calculated. RESULTS: The presence of fetal macrosomia in patients from the pregestational diabetes mellitus group is associated with an increase in the volumetric blood flow of the umbilical vein by 89.5 ml/min (p = 0.003) and the left portal vein by 33.3 ml/min (p = 0.008), as well as the total volumetric blood flow of the fetal liver by 95.7 ml/min (p = 0.001) compared with normal-weight fetuses. At the same time, the ductus venosus shunt fraction decreased in macrosomic fetuses by 3.83% (p = 0.001). In the gestational diabetes mellitus and control groups, despite the tendency for these parameters to increase in fetuses with macrosomia, the differences did not reach statistical significance. With a left portal vein volume flow threshold of 94.51 ml/min, the sensitivity and specificity for predicting large births were 84.46 and 72.09%, respectively. CONCLUSIONS: Pregestational diabetes mellitus in the mother is associated with a priority redistribution of blood flow to the fetal liver and is accompanied by a decrease in the ductus venosus shunt fraction. The severity of these hemodynamic changes increases in the presence of fetal macrosomia, which confirms the role of liver perfusion in the regulation of fetal growth in uncomplicated pregnancy and maternal diabetes mellitus.

Territory-Related Functional Connectivity Changes Associated with Verbal Memory Decline in Patients with Unilateral Asymptomatic Internal Carotid Stenosis.

Verbal memory decline is a common complaint of patients with severe asymptomatic stenosis of the internal carotid artery (aICS). Previous publications explored the associations between verbal memory decline and altered functional connectivity (FC) after aICS. Patients with severe aICS may show reduced perfusion in the ipsilateral territory and redistribution of cerebral blood flow to compensate for the deficient regions, including expansion of the posterior and contralateral ICA territories via the circle of Willis. However, aICS-related FC changes in anterior and posterior territories and the impact of the sides of stenosis were less explored. This study aims to investigate the altered FC in anterior and posterior circulation territories of patients with left or right unilateral aICS and its association with verbal memory decline. We enrolled 15 healthy controls (HCs), 22 patients with left aICS (aICSL), and 33 patients with right aICS (aICSR) to receive fMRI, Mini-Mental State Examination (MMSE), the Digit Span Test (DST), and the 12-item Chinese version of Verbal Learning Tests. We selected brain regions associated with verbal memory within anterior and posterior circulation territories. Territory-related FC alterations and verbal memory decline were identified by comparing the aICSL and aICSR groups with HC groups (P < .05, corrected for multiple comparisons), respectively. Furthermore, the association between altered FC and verbal memory decline was tested with the Pearson correlation analysis. Compared with HCs, patients with aICSL or aICSR had significant impairment in delayed recall of verbal memory. Decline in delayed recall of verbal memory was significantly associated with altered FC between the right cerebellum and right middle temporal pole in the posterior circulation territory (r = 0.40, P = .03) in the aICSR group and was significantly associated with altered FC between the right superior medial frontal gyrus and left lingual gyrus in the anterior circulation territory (r = 0.56, P = .01) in the aICSL group. Patients with aICSL and aICSR showed different patterns of FC alterations in both anterior and posterior circulation territories, which suggests that the side of aICS influences the compensatory mechanism for decline in delayed recall of verbal memory.

Echocardiographic assessment of cardiovascular physiology of preterm miniature piglets supported with a pumped artificial placenta system.

We evaluated fetal cardiovascular physiology and mode of cardiac failure in premature miniature piglets on a pumped artificial placenta (AP) circuit. Fetal pigs were cannulated via the umbilical vessels and transitioned to an AP circuit composed of a centrifugal pump and neonatal oxygenator and maintained in a fluid-filled biobag. Echocardiographic studies were conducted to measure ventricular function, umbilical blood flow, and fluid status. In utero scans were used as control data. AP fetuses (n=13; 102±4d gestational age [term 115d]; 616±139g [g]; survival 46.4±46.8h) were tachycardic and hypertensive with initially supraphysiologic circuit flows. Increased myocardial wall thickness was observed. Signs of fetal hydrops were present in all piglets. Global longitudinal strain (GLS) measurements increased in the left ventricle (LV) after transition to the circuit. Right ventricle (RV) and LV strain rate decreased early during AP support compared with in utero measurements but recovered toward the end of the experiment. Fetuses supported for >24h had similar RV GLS to in utero controls and significantly higher GLS compared to piglets surviving only up to 24h. Fetuses on a pump-supported AP circuit experienced an increase in afterload, and redistribution of blood flow between the AP and systemic circulations, associated with elevated end-diastolic filling pressures. This resulted in heart failure and hydrops. These preterm fetuses were unable to tolerate the hemodynamic changes associated with connection to the current AP circuit. To better mimic the physiology of the native placenta and preserve normal fetal cardiovascular physiology, further optimization of the circuit will be required.

Blood flow redistribution in the fetal umbilical-portal venous system in pregnancy complicated by diabetes mellitus

Blood flow redistribution in the fetal umbilical-portal venous system in pregnancy complicated by diabetes mellitus

A case of pulmonary endarterectomy in chronic thromboembolic pulmonary hypertension - a happily completed odyssey

Chronic thromboembolic pulmonary hypertension is a rare condition that is usually a consequence of prior acute pulmonary embolism. It is caused by persistent obstruction of pulmonary arteries by organized thrombi resulting in redistribution of blood flow and secondary pulmonary microvascular remodelling. Thus, pulmonary vascular resistance and pulmonary artery pressure are increased leading to right ventricle pressure overload, development of right heart failure and death. In eligible patients pulmonary endarterectomy is the standard of care and it can result in complete normalization of haemodynamics and right ventricular morphology and function. We present the case of a patient with chronic thromboembolic pulmonary hypertension with severe right ventricular dilation and dysfunction and refractory heart failure. After successful pulmonary endarterectomy we observed almost complete normalization of hemodynamics and restoration of right ventricular dimensions and function, as well as significant clinical improvement.

Skeletal muscle contractions attenuate the norepinephrine-related reduction in interstitial oxygen pressures in the rat spinotrapezius

Increased sympathetic nerve activity with exercise plays a key role in the control of arterial blood pressure and redistribution of blood flow. Within the microcirculation, elevated sympathetic outflow promotes the release of norepinephrine and smooth muscle contraction. Exercise-induced attenuation of sympathetic vasoconstriction (i.e., functional sympatholysis) is thus critical for active muscle oxygen delivery-utilization matching. However, the extent to which muscle contractions impact noradrenergic regulation of interstitial oxygen pressures (PO2is) is unknown. This is important because, as dictated by Fick’s law, PO2is provides the sole driving force for oxygen diffusion into the myocyte thereby supporting oxidative phosphorylation. PURPOSE: To determine the effects of norepinephrine administration on resting and contracting rat skeletal muscle PO2is. We tested the hypothesis that topical application (superfusion) of norepinephrine would result in blunted decreases in skeletal muscle PO2is during contractions compared to rest. METHODS: PO2is was determined via phosphorescence quenching in the exposed spinotrapezius muscle of anesthetized male Sprague-Dawley rats (n=7, 2-3 months old) at rest and during electrically-induced submaximal contractions (0.5 Hz, 3-6 V) for 6 minutes in response to norepinephrine superfusion (5x10−4 M). Functional sympatholysis was determined as the difference between the norepinephrine-induced changes in PO2is at rest and during the contraction steady-state (i.e., 2 min following the onset of muscle contractions) using (i) the absolute PO2is fall with norepinephrine (ΔPO2is), and (ii) the area under the PO2is curve plotted as a function of time (AUC). The tail (caudal) artery was cannulated for measurements of mean arterial pressure (MAP) and heart rate (HR). RESULTS: Consistent with our hypothesis, skeletal muscle contractions attenuated norepinephrine-evoked reductions in spinotrapezius interstitial oxygenation as evaluated by ΔPO2is (rest: -8.7±1.4, contractions: -4.3±1.1 mmHg, p&lt;0.05) and AUC (rest: 2246±368, contractions: 1066±273 mmHg·s, p&lt;0.05). Although MAP increased significantly with norepinephrine both at rest (+5±1%, p&lt;0.05) and during contractions (+8±1%, p&lt;0.05), this mild hypertensive response to norepinephrine was not different between conditions (p&gt;0.05). Norepinephrine superfusion did not affect HR at rest or during contractions (p&gt;0.05). CONCLUSIONS: That muscle contractions blunted the decrease in spinotrapezius PO2is with norepinephrine compared to the resting condition is consistent with functional sympatholysis. The latter serves to match active muscle O2 delivery-utilization in the face of elevated sympathetic nerve activity during exercise. The current results indicate that a novel combination of phosphorescence quenching (interstitial oxygenation, PO2is) and superfusion techniques may be used to evaluate functional sympatholysis in the intact rat spinotrapezius muscle. Showalter Research Trust, Purdue University. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Effects of Myocardial Infarction-induced Heart Failure on Diaphragm Arteriolar Vasorelaxation

INTRODUCTION: Diaphragm atrophy and contractile dysfunction are prevalent in heart failure (HF), diminishing physical capacity and quality of life. The delivery of blood flow and oxygen necessary to support the metabolic demand of contractions is largely governed by the resistance vasculature (i.e., arterioles) with the endothelium playing a central role in arteriolar vasorelaxation. Adequate perfusion and blood flow distribution, and thus resistance vessel vasodilation, is a major determinate of diaphragm contractile function. While the mechanistic bases of HF-induced diaphragm dysfunction continue to be elucidated, the impact of HF on diaphragm vasomotor control has not been investigated. METHODS: Adult (6 mo) Sprague-Dawley rats (n=7) were divided into two groups: 1) Healthy Control (HC; n=4) and 2) MI-induced heart failure (HF; n=3). First-order arterioles (1A) from the medial costal diaphragm were isolated, cannulated, and pressurized at 90 cmH2O and allowed to equilibrate for 60 min to develop spontaneous tone. Thereafter, endothelium-dependent and -independent vasorelaxation responses to cumulative doses of acetylcholine (ACh; 10−9 to 10−4M) and sodium nitroprusside (SNP; 10−9 to 10−4M) were determined. RESULTS: There were no differences in spontaneous development (%) or maximal diameter (μm) between HC (20 ± 4%; 178 ± 11 μm) and HF (18 ± 2%; 184 ± 29 μm) diaphragm 1As ( P &gt; 0.05). Maximal ACh-mediated relaxation (%) was significantly reduced in HF rats compared to HC rats (52 ± 2 versus 68 ± 5%; P &lt; 0.05). Maximal endothelial-independent vasorelaxation with SNP, was not different between HC and HF rats (71 ± 3 versus 73 ± 1%; P &gt; 0.05). CONCLUSION: The preliminary data herein demonstrate that HF impaired endothelial function and vasomotor function in the medial costal diaphragm resistance vasculature. This suggests that, in HF, there may be a redistribution of blood flow to less effcient regions of the diaphragm (e.g., ventral costal) to sustain contractile function and compensate for the diminished medial costal vasomotor function demonstrated herein. Studies including a larger sample size are warranted to investigate the impact of HF on regional blood flow distribution and resistance vessel function in the diaphragm. Such investigations would yield novel mechanistic insights into HF-induced diaphragm dysfunction. National Institute of Aging 1R15AG078060, Ruth L. Kirschstein National Research Service Awards from the National Heart, Lung, and Blood Institute 1F31HL167618-01, and Sustained Momentum for Investigators with Laboratories Established (SMILE) Grants at Kansas State University. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Renal potassium regulation in a pig model of therapeutic hypothermia

Therapeutic hypothermia is increasingly utilized clinically to reduce tissue metabolism and protect against neurological damage in cases of cardiac arrest, traumatic brain injury or perinatal hypoxic ischemia. With even mild exposure to hypothermia, hypokalemia develops purportedly due to transcellular potassium shifts resulting in decreased circulating potassium levels. Renal dysfunction with body temperature cooling has also been postulated to potentially contribute to development of sustained hypokalemia. In this study, we used a pig model of controlled acute hypothermia without confounding hypotension and hypoxemia, to test the hypothesis that renal handling of potassium remains intact in hypothermia and is not the cause of decreased circulating plasma potassium seen with body cooling. Anesthetized, mechanically ventilated Duroc cross young pigs (n=25, body weight = 10.0 ± 0.4 kg, male or female) were catheterized for hemodynamic monitoring, regional blood flow assessment via colored microspheres, and urine collection. After baseline values were obtained, pigs were divided into a control normothermia group (n=12) with body temperature maintained at 38.4 ± 0.1 oC or a hypothermia group (n=13) with core body temperature cooled to 34.5 ± 0.1 oC and hypothermia sustained for 2 hours. Hypothermia reduced tissue metabolism as indicated by a decrease in oxygen consumption (VO2= 5.2 ± 0.2 ml/kg in normothermia vs 3.7 ± 0.3 ml/kg in hypothermia. Mean arterial pressure (68± 3 mm Hg) and cardiac output (199 ± 21 ml/min/kg) were not different between groups. Even with the short duration of cold exposure, plasma potassium was lower (p&lt;0.05) within 2 hours of hypothermia (4.1 ± 0.1 mEq/L) vs control (4.8 ± 0.1 mEq/L). Cold exposure caused redistribution of blood flow to the small intestines from other internal organs. Renal blood flow tended to decrease with cold, but glomerular filtration rate was suffcient to maintain urine flow, sodium excretion and free water clearance. Potassium clearance, however, was lower (p&lt;0.05) in hypothermia (0.70 ± 0.07 ml/min/kg) than in normothermia (1.04 ± 0.07 ml/min/kg), with lower potassium excretion (hypothermia = 2997 ± 331 mEq/min vs control = 4784 ± 393 mEq/min, p&lt;0.05) and fractional excretion of potassium. Reduced renal potassium excretion is consistent with renal compensation for lower circulating potassium induced by hypothermia. Interestingly, with relatively higher blood flow to the small intestines compared to decreased blood flow of other internal organs, potassium secretion in the early colon may contribute to further potassium wasting in hypothermia. The rapid initiation of decreased potassium circulating levels with hypothermia supports the thesis of temperature sensitive cell membrane potassium channels affecting extracellular to intracellular shifts of potassium. Results of this study indicate that renal potassium regulation is maintained in hypothermia and functions to decrease urinary potassium loss in the face of hypokalemia. The views expressed are those of the authors and do not necessarily reflect the offcial policy or position of the Defense Health Agency, Department of the Army, Department of Defense, or the U.S. Government. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Experimental and theoretical model of microvascular network remodeling and blood flow redistribution following minimally invasive microvessel laser ablation.

Overly dense microvascular networks are treated by selective reduction of vascular elements. Inappropriate manipulation of microvessels could result in loss of host tissue function or a worsening of the clinical problem. Here, experimental, and computational models were developed to induce blood flow changes via selective artery and vein laser ablation and study the compensatory collateral flow redistribution and vessel diameter remodeling. The microvasculature was imaged non-invasively by bright-field and multi-photon laser microscopy, and optical coherencetomography pre-ablation and up to 30 days post-ablation. A theoretical model of network remodeling was developed to compute blood flow and intravascular pressure and identify vessels most susceptible to changes in flow direction. The skin microvascular remodeling patterns were consistent among the five specimens studied. Significant remodeling occurred at various time points, beginning as early as days 1-3 and continuing beyond day 20. The remodeling patterns included collateral development, venous and arterial reopening, and both outward and inward remodeling, with variations in the time frames for each mouse. In a representative specimen, immediately post-ablation, the average artery and vein diameters increased by 14% and 23%, respectively. At day 20 post-ablation, the maximum increases in arterial and venous diameters were 2.5× and 3.3×, respectively. By day 30, the average artery diameter remained 11% increased whereas the vein diameters returned to near pre-ablation values. Some arteries regenerated across the ablation sites via endothelial cell migration, while veins either reconnected or rerouted flow around the ablation site, likely depending on local pressure driving forces. In the intact network, the theoretical model predicts that the vessels that act as collaterals after flow disruption are those most sensitive to distant changes in pressure. The model results correlate with the post-ablation microvascular remodeling patterns.

Pulmonary hypertension impairs vasomotor function in rat diaphragm arterioles

Pulmonary hypertension (PH) is a chronic, progressive condition in which respiratory muscle dysfunction is a primary contributor to exercise intolerance and dyspnea in patients. Contractile function, blood flow distribution, and the hyperemic response are altered in the diaphragm with PH, and we sought to determine whether this may be attributed, in part, to impaired vasoreactivity of the resistance vasculature. We hypothesized that there would be blunted endothelium-dependent vasodilation and impaired myogenic responsiveness in arterioles from the diaphragm of PH rats. Female Sprague-Dawley rats were randomized into healthy control (HC, n = 9) and monocrotaline-induced PH rats (MCT, n = 9). Endothelium-dependent and -independent vasodilation and myogenic responses were assessed in first-order arterioles (1As) from the medial costal diaphragm in vitro. There was a significant reduction in endothelium-dependent (via acetylcholine; HC, 78 ± 15% vs. MCT, 47 ± 17%; P < 0.05) and -independent (via sodium nitroprusside; HC, 89 ± 10% vs. MCT, 66 ± 10%; P < 0.05) vasodilation in 1As from MCT rats. MCT-induced PH also diminished myogenic constriction (P < 0.05) but did not alter passive pressure responses. The diaphragmatic weakness, impaired hyperemia, and blood flow redistribution associated with PH may be due, in part, to diaphragm vascular dysfunction and thus compromised oxygen delivery which occurs through both endothelium-dependent and -independent mechanisms.

Causes and management of urinary system problems in children on long-term home invasive mechanical ventilation.

Many ventilator-dependent children have comorbid conditions including urinary tract disorders. We aimed to present a focused review of the literature describing the causes and management of urinary system problems in children with long-term home mechanical ventilation. We performed a literature search in PubMed/MEDLINE, Scopus, and Web of Science with keywords "children," "home mechanical ventilation," "urinary system," "urinary tract," "neurogenic bladder," "clean intermittent catheterization," "urinary tract infection," "urolithiasis," and "acute kidney injury." We included original articles, reviews, guidelines, and case reports published in English. Ventilator-dependent children may have neurogenic bladder/bowel dysfunction which renders them prone to urinary tract infection, high bladder pressure, vesicoureteral reflux, hydronephrosis, and renal dysfunction. These children require bladder catheterization, medications affecting parasympathetic/sympathetic nervous systems, or surgical procedures to prevent urinary infections, and to maintain continence and renal functions. However, bladder catheterization or surgical procedures like augmentation cystoplasty may also be complicated with urinary infections, urolithiasis, or urethral strictures. Urolithiasis frequency is also increased due to immobilization-related hypercalciuria, hypocitraturia caused by antiepileptic drugs, urinary stasis, and urinary infections. On the other hand, mechanical ventilation can impair renal function by reduction of cardiac output, redistribution of intrarenal blood flow and stimulation of sympathetic and hormonal pathways. Children requiring long-term invasive home mechanical ventilation may have other comorbid conditions, including urinary system diseases, which become manifest as these patients are being kept alive due to the advances in ventilation strategies. These children must be carefully observed for urological complications and managed accordingly to prevent kidney injury.

Towards effects from stent implantation into coronary bifurcation stenosis: experiment and simulation

Coronary artery disease is a widespread cause of death and disability in the population. Angioplasty of the coronary arteries is one of the most common methods of eliminating the cause of ischemia – stenosis of the coronary arteries. As a result of stent installation, a change in the angle of vascular bifurcation occurs usually, as well as a redistribution of volumetric blood flow in the coronary artery system. Considering the high variability of the branching angioarchitecture of these arteries, as well as the structure of their environment, the problem of predicting the specific redistribution of blood flow in these arteries remains unsolved; the main ways of its implementation are computational and experimental hemodynamics. Material and methods. This paper uses an experimental approach to explore the effect of stent placement in a model of coronary artery stenosis, and also provides an analysis of the current level of awareness of the scientific community on this issue. Results and discussion. The experiment showed that the throughput of the model increases by 14 % compared to the model with stenosis, and the redistribution of flows in the model depends not on diameters but on the anatomy of a particular vascular network. The data of the performed mathematical modeling are generally consistent with the results of the experiment before stent installation, when the coronary tree consists of several load-bearing branches, but have quantitative differences for the distal branches of the coronary artery model in the presence of an installed stent. Conclusions. The results of the work can be used to accumulate an experimental data array on the restructuring of blood flow during angioplasty, and can also be used to verify the numerical hemodynamics of the coronary arteries during the virtual installation of a stent in them to resolve stenosis.

Lower limb blood flow occlusion increases systemic pressor response without increasing brachial arterial blood flow redistribution in women.

This study was conducted to investigate the systemic hemodynamic and vascular changes in women during and after two commonly used clinical blood flow restriction (BFR) pressures at rest. There are minimal data regarding the independent effects of BFR on hemodynamic and systemic vascular changes due to pressor response, particularly among women. Therefore, this study investigated BFR-induced alterations in pressor response and systemic flow redistribution at rest during two commonly used pressures (50% and 80% limb occlusion pressure [LOP]). Fifteen women (22.1 ± 4.2 years) completed two randomised sessions involving 8-min of bilateral, lower limb restriction at 50% or 80% LOP followed by 8-min of recovery post-deflation. Changes in vascular (arterial diameter [DIA], time-averaged mean velocity [TAMV], volume flow [VF], and area) and hemodynamic (heart rate [HR] and blood pressure) measures over time (pre-, during, post-occlusion) and by session (50% vs. 80% LOP) were tested using repeated measures analysis of variance. Repeated measures correlations (rrm) quantified common intraindividual associations between BFR-induced hemodynamic and vascular responses. HR increased from baseline during 50% LOP and remained elevated during recovery (p < 0.05). HR increased from baseline during 80% LOP, while tibial VF and TAMV decreased (p < 0.03 for all). HR and TAMV values returned to baseline during recovery, while brachial artery VF decreased (p < 0.05). Changes in HR, brachial VF, and brachial TAMV were similar between 50% and 80% LOP (rrm = 0.32-0.70, p < 0.05 for all). At 80% LOP, changes in HR were positively correlated with brachial VF (rrm = 0.38) and TAMV (rrm = 0.43) and negatively correlated with tibial VF (rrm = -0.36) and TAMV (rrm = -0.30) (p < 0.05 for all). Results suggest that BFR at 80% LOP elicits an acute systemic pressor reflex without concomitant increases in brachial arterial flow, while 50% LOP elicits a subdued response.

Abstract TP178: Impact of Fetal PCA on Ipsilateral Carotid Artery Stiffness: Results From Northern Manhattan Stroke Study (NOMAS)

Introduction: The wall stress is the major contributor of arterial stiffness, which is well-known risk factor for cardiovascular diseases. The interindividual variability of the Circle of Willis affects blood flow redistribution intracranially. The fetal posterior cerebral artery (fPCA) is associated with larger carotid arteries due to increased brain territory supplied by the anterior circulation. Thus, an fPCA increases blood flow in the ipsilateral carotid artery and could plausibly increase ipsilateral carotid artery stiffness. Methods: We included participants from the multi-ethnic community-based Northern Manhattan Stroke Study (NOMAS) cohort with available time-of-flight MRA. High-resolution B-mode ultrasound of the right common carotid artery (CCA) evaluated markers of arterial stiffness, including diastolic diameter (DD), strain (systolic diameter - DD/DD), cIMT (carotid intima-media thickness), and stiffness (systolic blood pressure - diastolic blood pressure/strain). We used multivariable regression analyses to calculate odds ratios and beta values, examining the association of fPCA and markers of stiffness. Results: Among 1,210 NOMAS (mean age 70 ± 9 years, 61% women, 66% Hispanic) participants with available MRA, 151 (12.5%) participants had a right fPCA, and 129 (10.7%) had a left fPCA. In models adjusted for demographics, vascular risk factors, and height, right fPCA was associated with a higher ipsilateral CCA diastolic diameter (B = 0.31, p=0.001) and strain (B=0.04, p=0.02). Notably, no similar association was found between the left fPCA and contralateral carotid measures (Table 1). Conclusion: A fetal PCA associated with ipsilateral markers of cervical carotid stiffness. This research provides valuable insight into the changes in demands resulting from the variability of the circle of Willis and the extracranial correspondence of such demand.

NO Deficiency Compromises Inter- and Intrahemispheric Blood Flow Adaptation to Unilateral Carotid Artery Occlusion.

Carotid artery stenosis (CAS) affects approximately 5-7.5% of older adults and is recognized as a significant risk factor for vascular cognitive impairment (VCI). The impact of CAS on cerebral blood flow (CBF) within the ipsilateral hemisphere relies on the adaptive capabilities of the cerebral microcirculation. In this study, we aimed to test the hypothesis that the impaired availability of nitric oxide (NO) compromises CBF homeostasis after unilateral carotid artery occlusion (CAO). To investigate this, three mouse models exhibiting compromised production of NO were tested: NOS1 knockout, NOS1/3 double knockout, and mice treated with the NO synthesis inhibitor L-NAME. Regional CBF changes following CAO were evaluated using laser-speckle contrast imaging (LSCI). Our findings demonstrated that NOS1 knockout, NOS1/3 double knockout, and L-NAME-treated mice exhibited impaired CBF adaptation to CAO. Furthermore, genetic deficiency of one or two NO synthase isoforms increased the tortuosity of pial collaterals connecting the frontoparietal and temporal regions. In conclusion, our study highlights the significant contribution of NO production to the functional adaptation of cerebrocortical microcirculation to unilateral CAO. We propose that impaired bioavailability of NO contributes to the impaired CBF homeostasis by altering inter- and intrahemispheric blood flow redistribution after unilateral disruption of carotid artery flow.

Cardiac Adaptation and Preferential Streaming in Fetuses with Multiple Nuchal Cords.

The echocardiographic monitoring of a fetus with multiple nuchal cords around the fetal neck is important as it may result in cardiac remodeling and preferential streaming, thus affecting the condition of the fetus. The main aim of our study was to assess whether the collision of the umbilical cord around the fetal neck can lead to discrepancies in the size of the pulmonary artery and the aorta in the three-vessel view and to an increase in the size of the heart, which may result from the compression of the carotid arteries caused by the umbilical cord wrapping around the fetal neck. A total number of 854 patients were included in this study and divided into three groups. Group A (control group) included 716 fetuses (84%) without the umbilical cord around the fetal neck. Group B (study group B) included 102 fetuses (12%) with one coil of the umbilical cord around the fetal neck. Group C (study group C) included 32 fetuses (4%) with two coils of the umbilical cord around the fetal neck. The range of the gestational age of the patients considered for this study was 27-40.2 weeks based on the ultrasound biometry and was not statistically different between the analyzed groups A, B and C (p > 0.05). The Pa/Ao index was calculated by dividing the value of the width of the pulmonary artery (in mm) to the width of the aorta (in mm) measured in the ultrasound three-vessel view. We found that fetuses that the fetuses with one and two coils of the umbilical cord around the neck showed significantly higher values of the width of the pulmonary trunk with the unchanged value of the aorta width. Therefore, we also observed significantly higher values of the ratio of the pulmonary trunk to the aorta for the fetuses wrapped with the umbilical cord around the neck compared with the control group without the umbilical cord around the neck (. Moreover, in the fetuses with one and two coils of the umbilical cord around the fetal neck, an increased amount of amniotic fluid was observed, whereas larger dimensions of CTAR in the fetuses with two coils of the umbilical cord around the neck were present (p < 0.05). The wrapping of the fetus with the umbilical cord around the fetal neck may induce the redistribution of blood flow, leading to fetal heart enlargement and disproportion and may be the cause of polyhydramnios.