Compromised Blood Flow Research Articles

Anomalous origin of right coronary artery from left anterior descending coronary artery presenting with syncope – a case report

Introduction and importance: Non-dominant right coronary artery (RCA) is supposed to be benign as it does not result in large myocardial infarction. Still, in this case, non-dominant RCA from left anterior descending (LAD) artery not only produces ischemia but also results in incessant ventricular tachycardia, which is a life-threatening arrhythmia because of compromised blood flow. However, RCA is free of atherosclerotic plaque, which is the main cause of ischemia/infarction and subsequent arrhythmia. Case presentation: A 21-year-old male was admitted to the emergency cardiology ward of the National Institute of Cardiology following an episode of syncope. The patient reported a sudden loss of consciousness without preceding symptoms. Clinical discussion: The present case highlights the importance of a comprehensive evaluation and diagnosis in the management of syncope in young patients. The case presented here revealed a rare finding of a single coronary artery with a left main origin and an anomalous RCA emerging from the LAD artery. This is a very unusual presentation, with less than 50 occurrences recorded in the medical literature. This abnormality is classified as a single coronary artery anomaly (CAA), which means that the coronary arteries arise from a single coronary ostium within the aorta. Conclusion: In conclusion, CAA is an uncommon cause of SCA that can easily be overlooked without a systematic approach. In this report, we discuss the case of a patient who was discovered to have an anomalous RCA that branched off from the LAD artery.

Understanding perioperative risk determinants in carotid endarterectomy: the impact of compromised circle of Willis morphology on inter-hemispheric blood flow indices based on intraoperative internal carotid artery stump pulse pressure and backflow patterns.

Carotid artery stenosis (CAS) often requires surgical intervention through carotid endarterectomy (CEA) to prevent stroke. Accurate cerebrovascular risk assessments are crucial in CEA, as poor collateral circulation can lead to insufficient interhemispheric blood flow compensation, resulting in ischemic complications. Therefore, understanding perioperative risk determinants is vital. This study aims to determine the impact of compromised circle of Willis (CoW) morphology on inter-hemispheric blood flow, focusing on indices based on intraoperative internal carotid artery stump pulse pressure and backflow patterns. In 80 CAS patients who underwent CEA, preoperative CT angiography for CoW was conducted. Patients were categorized into five subgroups based on their CoW anatomy and three additional groups based on intraoperative internal carotid artery (ICA) stump backflow patterns evaluated by the surgeon. Continuous blood pressure signals, including systolic, diastolic, mean, and pulse pressure values, were recorded during the procedure. The relationship between CoW anatomical variants and the systolic and diastolic segments of the averaged pressure waveforms, particularly diastolic pressure decay, was analyzed. The correlation between CoW anatomy and stump backflow intensity was also examined. Significant variability in ICA stump backflow and pressure values was evident across CoW variants. Patients with compromised CoW morphology exhibited weaker backflow patterns and lower ICA stump pulse pressure values, consistent with impaired interhemispheric blood flow. Notably, ICA stump diastolic pressure decay was consistent across most CoW variant groups, indicating developed collateral circulation in cases with CoW anomalies. Thus, impaired CoW integrity is associated with compromised interhemispheric blood flow indices based on intraoperative ICA stump pulse pressure and backflow patterns during CEA. Integrating intraoperative pulse waveform analysis with preoperative CT angiography provides a more detailed assessment of cerebrovascular risk, guiding the selective use of shunts. This combined approach may improve surgical outcomes and patient safety by identifying patients at increased risk of perioperative neurological events due to CoW anomalies.

Using heart rate variability to predict neurological outcomes in preterm infants: a scoping review.

Infants born preterm are at higher risk of neurological complications, including intraventricular haemorrhage and white matter injury. After discharge, these infants may experience adverse neurodevelopmental outcomes and exhibit lower educational attainment. Early detection of brain injury and accurate prediction of neurodevelopmental impairment would allow early intervention and support. Heart rate variability (HRV) describes the variation of time intervals between each subsequent heartbeat. HRV is controlled by the autonomic nervous system, which may be affected by hypoxia and compromised blood flow. While HRV has primarily been investigated in neonatal sepsis, the association between HRV, brain injury and neurodevelopmental outcomes in preterm infants is less established. The present scoping review examines the utility of HRV monitoring for predicting short-term and long-term neurological outcomes in preterm infants. Following systematic search of Medline, Embase, Web of Science and the Cochrane Library, 15 studies were included. Nine studies examined the relationship between HRV and brain injury, with all but two showed an association. Eight studies examined the relationship between HRV and long-term outcomes and all eight found an association. This scoping review suggests that decreased HRV in the neonatal period is associated with short- and long-term neurodevelopmental outcomes in preterm infants. IMPACT: Changes in heart rate variability correlate with the occurrence of intraventricular haemorrhage in preterm infants. A decrease in heart rate variability may precede the development of intraventricular haemorrhage. Alterations in heart rate variability correlate with long-term neurodevelopmental outcomes. Significant variability exists in metrics used in assessing heart rate variability.

Relationship Between Posterior Tibial Artery Blood Flow And Lower Leg Flexibility Among Collegiate Runners

Purpose: Understanding relationships between blood flow and muscle inflexibility in the lower leg can support improved healthcare competency. Sports medicine practitioners might use the reference ranges and knowledge of relationships among these variables to support effective health screenings among their competitive runners. These variables have been linked in other areas of the body where inflexibility in the pectoralis minor and scalene muscles have been associated with diminished blood flow to the upper limb. No studies, however, have examined the relationship between vascular and mobility characteristics in the lower legs of runners. Therefore, the purpose of this study was to examine the relationship between blood flow in the posterior tibial artery and ankle range of motion (ROM) among competitive runners. Methods: Blood flow in the posterior tibial artery and ankle ROM were measured bilaterally on twenty-five, asymptomatic collegiate track athletes (15 males, 10 females, age = 20.0±1.2 years, height = 171.5±10.2 cm, mass = 66.7±13.7 kg) using diagnostic ultrasound and standard goniometry, respectively. Pearson correlation analysis was used to analyze the relationship between blood flow in the posterior tibial artery and ROM of the ankle joint. Results: Findings revealed no significant relationship between blood flow in the dominant leg’s posterior tibial artery and dorsiflexion (r=.14, P=.52, CI95% = -0.27 – 0.51) or plantarflexion (r=-.32, P=.12, CI95% = -0.63 – 0.09) and no significant relationship between blood flow in the non-dominant leg’s posterior tibial artery and dorsiflexion (r=-.02, P=.93; CI95% = -0.41 – 0.38) or plantarflexion (r=-.02, P=.92; CI95% = -0.41 – 0.38). Conclusion: While muscle inflexibility is associated with compromised blood flow in other body regions, findings of this study demonstrated no relationship between the variables within the lower legs of a sample of competitive runners. Sports medicine practitioners should consider these findings in their efforts to predict, prevent, and manage potential vascular and musculoskeletal adaptations among clients/patients who are competitive runners.

Microscopical anatomy of the peripheral nervous system: An essential notion for understanding the pathophysiology of very early classic Guillain-Barré syndrome.

The aim of this paper is to analyze the pathophysiological mechanisms acting in very early classic Guillain-Barré syndrome (GBS) (≤4 days of symptomatic onset). In this inaugural period, both in GBS and its animal model, experimental autoimmune neuritis, the outstanding pathological feature is inflammatory edema predominating in proximal nerve trunks, particularly spinal nerves, and possibly in preterminal nerve segments. Nerve trunks external to the subarachnoid angle possess epi- perineurium that is relatively inelastic and of low compliance. Here such edema can increase endoneurial fluid pressure that, when sufficiently critical, may stretch the perineurium and constrict transperineurial microcirculation, compromising blood flow and producing the potential for ischemic nerve injury, whose consequence is rapid partial or complete loss of nerve excitability. These histopathological features correlate well with electrophysiological and imaging findings reported in early GBS stages. Spinal nerve edema and ischemia help to understand the pattern of Wallerian-like degeneration observed in the axonal form of GBS, predominating in motor spinal roots at their exit from the dura matter (spinal nerves) with centrifugal distribution in more distant motor nerve trunks, and centripetal extension to the distal portion of intrathecal roots. The similarity of initial pathogenic mechanisms between demyelinating and axonal forms of GBS explains why an early increase of serum biomarkers of axonal damage is detected in both forms. In conclusion, knowledge of the microscopic anatomy of the peripheral nervous system is an essential step for a reliable understanding of pathophysiological mechanisms operating in the early phase of any classic GBS subtype.

PH-sensing GPR68 inhibits vascular smooth muscle cell proliferation through Rap1A.

Phenotypic transformation of vascular smooth muscle (VSM) from a contractile state to a synthetic, proliferative state is a hallmark of cardiovascular disease (CVD). In CVD, diseased tissue often becomes acidic from altered cellular metabolism secondary to compromised blood flow, yet the contribution of local acid/base imbalance to the disease process has been historically overlooked. In this study, we examined the regulatory impact of the pH-sensing G protein-coupled receptor GPR68 on vascular smooth muscle (VSM) proliferation in vivo and in vitro in wild-type (WT) and GPR68 knockout (KO) male and female mice. Arterial injury reduced GPR68 expression in WT vessels and exaggerated medial wall remodeling in GPR68 KO vessels. In vitro, KO VSM cells showed increased cell cycle progression and proliferation compared to WT VSM cells, and GPR68-inducing acidic exposure reduced proliferation in WT cells. mRNA and protein expression analyses revealed increased Rap1A in KO cells compared to WT cells, and RNA silencing of Rap1A reduced KO VSM cell proliferation. In sum, these findings support a growth-inhibitory capacity of pH-sensing GPR68 and suggest a mechanistic role for the small GTPase Rap1A in GPR68-mediated VSM growth control. These results shed light on GPR68 and its effector Rap1A as potential targets to combat pathologic phenotypic switching and proliferation in VSM.

Vascular Function and Ion Channels in Alzheimer's Disease.

This review paper explores the critical role of vascular ion channels in the regulation of cerebral artery function and examines the impact of Alzheimer's disease (AD) on these processes. Vascular ion channels are fundamental in controlling vascular tone, blood flow, and endothelial function in cerebral arteries. Dysfunction of these channels can lead to impaired cerebral autoregulation, contributing to cerebrovascular pathologies. AD, characterized by the accumulation of amyloid beta (Aβ) plaques and neurofibrillary tangles, has been increasingly linked to vascular abnormalities, including altered vascular ion channel activity. Here, we briefly review the role of vascular ion channels in cerebral blood flow control and neurovascular coupling. We then examine the vascular defects in AD, the current understanding of how AD pathology affects vascular ion channel function, and how these changes may lead to compromised cerebral blood flow and neurodegenerative processes. Finally, we provide future perspectives and conclusions. Understanding this topic is important as ion channels may be potential therapeutic targets for improving cerebrovascular health and mitigating AD progression.

Hypertension restricts leg blood flow and aggravates neuromuscular fatigue during human locomotion in males.

Patients with hypertension (HTN) are characterized by exaggerated vascular resistance and mean arterial pressure (MAP) and a compromised leg blood flow (QL) response to exercise recruiting a small muscle mass. However, the impact of hypertension on peripheral hemodynamics and the development of neuromuscular fatigue during locomotor activities, which critically depends on QL, remain unknown. Eight HTN (143 ± 11 mmHg/95 ± 6 mmHg; 45 ± 13 yr) and eight matched (age and activity) controls (120 ± 6 mmHg/77 ± 7 mmHg; CTRL) performed constant-load cycling exercise at 25, 50, and 75 W (for 4 min each) and at 165 ± 41 W (for 5 min). Exercise-induced locomotor muscle fatigue was quantified as the pre- to postexercise change in quadriceps twitch-torque (ΔQtw, peripheral fatigue) and voluntary activation (ΔVA%, central fatigue). QL (Doppler ultrasound) and leg vascular conductance (LVC) were determined during cycling at 25, 50, and 75 W. Heart rate and ventilatory responses were recorded during all intensities. MAP during exercise was, on average, ∼21 mmHg higher (P = 0.002) and LVC ∼39% lower (P = 0.001) in HTN compared with CTRL. QL was consistently between 20 and 30% lower (P = 0.004), and heart rate was significantly higher in HTN. Exercise-induced peripheral (ΔQtw: -53 ± 19% vs. -25 ± 23%) and central (ΔVA%: -7 ± 5% vs. -3 ± 2%) fatigue was significantly greater in HTN compared with CTRL. In addition to an exaggerated MAP, LVC and QL were lower during exercise in HTN compared with CTRL. Given the critical role of QL in determining the development of neuromuscular fatigue, these hemodynamic impairments likely accounted for the faster development of neuromuscular fatigue characterizing hypertensive individuals during locomotor exercise. NEW & NOTEWORTHY The impact of primary hypertension on the cardiovascular and neuromuscular fatigue response to locomotor exercise is unknown. We compared central and peripheral hemodynamics and the development of central and peripheral fatigue during cycling exercise in patients with stage I/II hypertension and age- and activity-matched healthy individuals. In addition to a significantly elevated blood pressure, hypertensive patients were, compared with their nonhypertensive counterparts, also characterized by considerable leg blood flow limitations and impaired neuromuscular fatigue resistance.

Designing a personalized thermo-mechanically optimized liner for transfemoral prosthetics

Elastomeric interphases (liners) protect the residual limb and distribute mass bearing to the prosthetic socket. However, discomfort due to excessive sweat and heat in the residual limb is the most relevant factor that negatively affects the quality of life in transfemoral prosthetics users. Additionally, a warm and humid environment and the non-uniform mass distribution can compromise blood flow in the residual limb; these factors favor the development of skin lesions, the dropout rate of prosthetic use, and subsequent amputations. Previous mathematical models that predict skin temperature distribution based on Pennes' model and explain the Fourier and non-Fourier thermic response are available. However, these models require knowledge of difficult parameters to obtain in conditions that lead to amputation. Therefore, the current study aims to propose an experimentally based method to design a personalized liner with areas of different diffusivity rates by using perforations according to thermal needs, preserving the mechanical properties of the liner. After thermal and mechanical characterization, we elaborated a personalized plane liner according to the thermal expression of the anterior thigh using infrared analysis. We tested the liner to probe its ability to dissipate heat.

Unraveling the intricate physiological processes dysregulated in CHD-affected and Dan-Lou tablet-treated individuals

Coronary heart disease (CHD), a multifactorial cardiovascular condition, arises from the accumulation of atherosclerotic plaque in the coronary arteries, resulting in compromised blood flow to the heart and complications such as angina, myocardial infarction, or heart failure. Addressing global prevalence, risk factors, and genetics is crucial for effective management. The current study aims to identify molecular biomarkers for CHD by scrutinizing the expression patterns of differentially expressed genes (DEGs), utilizing various bioinformatic tools. In this investigation, a total of 24 samples underwent examination using the GEO2R tool. These included eight samples from individuals before treatment (GSM5434123–30), eight samples from patients after Dan-Lou tablet treatment (GSM5434131–38), and eight samples from healthy control subjects (GSM5434139–46). A suite of bioinformatics tools was used to detect enriched genes within the network, namely, Cytoscape (v3.10.1) and Molecular Complex Detection (MCODE). Functional analysis of the DEGs was conducted via clusterProfiler, a R-based package, and ClueGO. 182 and 174 DEGs corresponding to untreated and treated patient sample groups were functionally annotated for gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) terms. ARF6 gene dysregulation was implicated in the myeloid cell apoptotic process (GO:0033028), regulation of actin cytoskeleton (hsa:04810), and other vital cellular functions. The myeloid cell apoptotic process (GO:0033028) was also observed to be regulated by the differential expression of the STAT5B gene. Additionally, STAT5B was found to be associated with the regulation of erythrocyte differentiation (GO:0045646). Providing targeted therapy based on the patient's idiosyncratic gene expression profiles could lead to the curing of various disorders in the near future.

Idiopathic Atypical Hemolytic Uremic Syndrome: A Case Report

Thrombotic microangiopathies (TMAs) are a spectrum of disorders characterized by hemolytic anemia, thrombocytopenia, and formation of microthrombi in blood vessels, resulting in tissue injury due to compromised blood flow. This classical presentation of TMA is characterized by varying degrees of microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and ischemic damage to the brain, kidneys, heart, lungs and GI tract. TMA can be classified into different types based upon the etiology and pathogenesis like thrombotic thrombocytopenic purpura (TTP), Complement mediated TMA (atypical Hemolytic uremic syndrome [aHUS]), infection associated TMA (shiga toxin producing E.coli, streptococcus pneumoniae) secondary to systemic causes like malignancy, autoimmune diseases and medications. In this article, we discuss a case of a female diagnosed with aHUS with acute kidney injury complicated by hypertension and severe anemia. As aHUS is known to be associated with high mortality and morbidity, prompt recognition of aHUS is crucial for efficient treatment. Here we have discussed the clinical presentation, histopathological hallmarks, and the diagnostic approach for TMA.

Systematic review and meta-analysis: Evaluating the influence of intrahepatic cholestasis of pregnancy on obstetric and neonatal outcomes.

Intrahepatic cholestasis of pregnancy (ICP) is a serious liver conditions that negatively impacts obstetric and neonatal outcomes. Elevated levels of bile acid, particularly glycine conjugate, may compromise blood flow and cause functional hypoxia-ischemia. This meta-analysis aims to assess the association between ICP and key pregnancy outcomes including emergency caesarian sections (C-sections), preeclampsia, hemorrhage, preterm birth, small for gestational age, admission rate to neonatal intensive care union (NICU), gestational age, and stillbirth. Literature search across five databases (PubMed, Embase, Web of Science) was done to detect relevant studies published up until June 2023. Meta-analysis of the identified studies was done using a random-effects model, and the results presented as Odds ratio (OR). A literature search identified 662 studies. Of them, 21 met the inclusion criteria. There was a significant association between ICP and odds of C-section (OR: 1.42, p <0.001), preeclampsia (OR: 2.64, p <0.001), NICU admission (OR: 2.1, p <0.001), and pre-term birth (OR: 2.64, p <0.001). ICP was not associated with postpartum hemmorhage (OR: 1.31, p = 0.13), small for gestational age (OR: 0.87, p = 0.07), stillbirth (OR: 1.49, p = 0.29). Our results confirm the adverse effects of ICP on co-existing pregnancy complications, obstetric and neonatal outcomes. ICP in associated with severe complications including increased rates of preeclampsia, emergency C-sections, preterm births, l gestational periods and higher rates of NICU admissions. These results may assist healthcare professionals in formulating comprehensive care guidelines for expectant mothers and newborns.

Anti-oxidative and anti-inflammatory effects of Ginkgo biloba extract (EGb761) on hindlimb skeletal muscle ischemia-reperfusion injury in rats.

In posterior spine surgery, retractors exert pressure on paraspinal muscles, elevating intramuscular pressure and compromising blood flow, potentially causing muscle injury during ischemia-reperfusion. Ginkgo biloba extract (EGb 761), known for its antioxidant and free radical scavenging properties and its role in treating cerebrovascular diseases, is investigated for its protective effects against muscle ischemia-reperfusion injury invitro and invivo. Animals were randomly divided into the control group, receiving normal saline, and experimental groups, receiving varying doses of EGb761 (25/50/100/200 mg/kg). A 2-h hind limb tourniquet-induced ischemia was followed by reperfusion. Blood samples collected pre-ischemia and 24 h post-reperfusion, along with muscle tissue samples after 24 h, demonstrated that EGb761 at 1000 μg/mL effectively inhibited IL-6 and TNF-α secretion in RAW 264.7 cells without cytotoxicity. EGb761 significantly reduced nitric oxide (NO) and malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and increased glutathione (GSH) levels compared to the control after 24 h. Muscle tissue sections revealed more severe damage in the control group, indicating EGb761's potential in mitigating inflammatory responses and oxidative stress during ischemia-reperfusion injury, effectively protecting against muscle damage.

INCIDENCE OF BRADYCARDIA IN INFANTS UNDERGOING INTUBATION WITH OR WITHOUT ATROPINE

Bradycardia is a life-threatening arrhythmia that endangers life by compromising blood flow to the brain. During intubation, its prevention is life-saving—the benefit of atropine in preventing bradycardia before intubation is controversial in the literature. Objective: The objective of the study was to find and compare the incidence of bradycardia with and without atropine. Methods: This single-centre randomised controlled trial was conducted at a tertiary care pediatric emergency department for six months. After applying inclusion and exclusion criteria, children were divided into two groups. Group 1 was given atropine before intubation, and group 2 was not. The overall incidence of bradycardia in subgroups was noted, along with the number of attempts and intubation time. Data was analysed using SPSS 26.0. Results: 86 patents were included in the study, with 43 in both groups. The mean age of the participants was 69.02+109.10 days. 48 (55.8%) were males and 38 (44.2%) were females. The incidence of bradycardia was 7% (6 Patients), with no statistically significant difference in both the groups (p-value was greater than 0.05). The number of attempts for intubation and intubation duration was also neither associated with bradycardia nor with atropine use. (p-value&gt; 0.05).Conclusion: There is a higher incidence of bradycardia during intubation in children, with no significant difference in its occurrence with the use of atropine.

Ultrafast gelling bioadhesive based on blood plasma and gelatin for wound closure and healing

Tissue adhesives offer a plethora of advantages in achieving efficient wound closure over conventional sutures and staples. Such materials are of great value, especially in cases where suturing could potentially damage tissues or compromise blood flow or in cases of hard-to-reach areas. Besides providing wound closure, the tissue adhesives must also facilitate wound healing. Previously, plasma-based tissue adhesives and similar bioinspired strategies have been utilized to aid in wound healing. Still, their application is constrained by factors such as high cost, diminished biocompatibility, prolonged gelation times, inadequate swelling, quick resorption, as well as short-term and inconsistent efficacy. To address these limitations, we report the development of a highly biocompatible and ultrafast-gelling tissue adhesive hydrogels. Freeze-dried platelet-rich plasma, heat-denatured freeze-dried platelet-poor plasma, and gelatin were utilized as the base matrix. Gelation was initiated by adding tetrakis hydroxymethyl phosphonium chloride. The fabricated gels displayed rapid gelation (3–4 s), low swelling, increased proliferation, and migration against L929 cells and had porcine skin tissue adhesion strength similar to that of plasma-based commercial glue (Tisseel®).

Reevaluating the epinephrine myth: A comprehensive review.

The combination of local anesthetic drugs with epinephrine has conventionally been contraindicated in acral regions due to concerns of potential necrosis caused by compromised blood flow. However, this belief has been challenged since 2001, when studies demonstrated the safety and effectiveness of the combination. This review aims to analyze reported cases of acral area necrosis following the use of local anesthesia with epinephrine since 2001. A thorough search was conducted on PubMed and Google Scholar using specific keywords to identify articles reporting acral area necrosis caused using local anesthesia and epinephrine. Our search yielded eight publications describing a total of 13 cases of ischemic events in acral areas. These cases involved finger necrosis (five cases), scrotal skin necrosis (two cases), and eyelid necrosis (six cases), following the injection of a combination of epinephrine and lignocaine. The majority of affected patients were female who underwent surgical intervention and reconstruction. The use of epinephrine in local anesthesia offers significant advantages and is generally safe for acral areas. However, the risk of necrosis cannot be entirely eliminated, particularly in patients with compromised vascular function. Adhering to proper guidelines and selecting suitable patients can help mitigate the risk. Phentolamine serves as a potential rescue agent if vascular compromise occurs. Precautionary measures must be taken when using this combination in high-risk patients.

Microvascular development and remodeling

Skeletal fragility is an important complication of Type 1 Diabetes (T1D), particularly among older adults. Microvascular disease (MVD) has been linked to worse bone health in T1D, suggesting a potential direct pathophysiologic link between vascular disease and bone deficits. However, bone vascular control has not been explored in the context of T1D. Thus, this preliminary work investigates key mechanisms of regulation of the bone vasculature in older adults with T1D. Myogenic vasoconstriction and reactive hyperemia of tibial blood flow were assessed in older healthy adults (n=9, 65 ± 7 yrs) and older adults with T1D (n=10, 63 ± 6 yrs). Myogenic vasoconstriction was assessed in response to leg dependency (two levels of increased arterial transmural pressure obtained by lowering the leg below heart level) and reactive hyperemia was assessed in response to lower leg arterial occlusion via thigh cuff inflation. The initial peak reactive hyperemic response was considered a surrogate of myogenic vasodilation. For both stimuli, tibial blood flow was assessed via NIRS as total hemoglobin (tHb) and whole leg blood flow velocity (LBF) in the popliteal artery of the same leg was measured via Doppler ultrasound. Data are presented as mean±standard error. In response to leg dependency, with increased perfusion pressure, older adults had a tendency for smaller declines in LBF (L1: -3.85 ± 2.01 cm/s; L2: -6.22 ± 4.19 cm/s) compared to older adults with T1D (L1: -6.14 ±2.24 cm/s; L2: -10.4 ± 1.90 cm/s; group p=0.06, level p=0.07). Tibial tHb did not decline in older adults (L1: 1.16 ± 7.27 M; L2: 9.11 ± 13.8 M), but decreased progressively in those with T1D (L1: - 3.40 ± 2.79 M, L2: -6.14 ± 2.24 M, group p&lt;0.01, group*level p=0.07), indicating pronounced tibial myogenic vasoconstriction. In response to reactive hyperemia, LBF increased rapidly with cuff release in both groups (older adults: 50.8 ±22.7cm/s; T1D: 40.0 ± 13.4cm/s). Despite similar responses in LBF, tibial tHb surpassed baseline values in older adults (1.50 ± 5.35M), whereas tibial tHb did not reach baseline values within 5 min post cuff release in T1D (-2.85 ± 5.09M, p=0.09), indicating impaired tibial myogenic vasodilation. Interestingly, older adults with T1D and MVD (n=5) had a stronger tendency for greater tibial myogenic vasoconstriction at both levels and significantly impaired reactive hyperemic response compared to those with no MVD (n=5). Our preliminary results indicate that older adults with T1D have greater myogenic vasoconstriction and impaired reactive hyperemic responses that appear to be worse in the presence of MVD. Alterations in myogenic control act to compromise blood flow regulation, restricting blood flow to bone, and potentially contributing to diabetes-inducted skeletal fragility. NIH NIDDK R01 DK124710. 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.

NURSES ROLES IN THE MANAGEMENT OF PRESSURE INJURY

Pressure injury, also referred to as pressure ulcers or bedsores, are debilitating wounds that develop when prolonged pressure is applied to the skin, resulting in localized tissue damage and compromised blood flow. These injuries often occur in areas where bony prominence come into contact with surfaces such as beds, chairs, or medical devices. The National Pressure Injury Advisory Panel (NPIAP) defines pressure injury as "localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction." This definition highlights the multi-factorial nature of pressure injury development, which can involve not only pressure but also shear forces and friction. The importance of managing pressure injury cannot be overstated, as they pose significant health risks and can lead to serious complications if left untreated.More importantly, pressure injury can impair mobility, hinder rehabilitation efforts, and prolong hospitalization, resulting in increased healthcare costs and diminished quality of life. Pressure injury is the third most expensive disorder after cardiovascular diseases and cancer (Agrawal &amp; Chauhan, 2012 as cited in Nkor M.M.,2022). Objectives : the objectives of this study includes , identification of various risk factors influencing the development of pressure injury, outlining assessment techniques for pressure injury, standardized tools used for pressure injury assessment, stages of pressure injury, nursing interventions for pressure injury and evidence base wound care techniques for various stages. Summary: In summary, pressure injuries remain a significant healthcare challenge, particularly for individuals with limited mobility or underlying health conditions. Effective prevention, assessment, and management of pressure injuries require a multifaceted approach that incorporates evidence-based practices, interdisciplinary collaboration, and patient-centered care.

OVERVIEW OF THE LIPID ABNORMALITIES IN THE HEART FAILURE

A complicated clinical disease known as heart failure (HF) comes on by anatomical or functional anomalies in the heart that compromise blood flow. This review article presents a comprehensive examination of the role of lipid profiles in the HF. It specifically focuses on the serum levels of traditional lipid parameters, such as total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in the development and progression of the HF. To conduct this review, several databases such as Google Scholar, PubMed, and Science Direct were utilized. Specific keywords used in the search include “heart failure”, “lipid profile”, “triglycerides”, “total cholesterol”, “high-density lipoprotein cholesterol”, and “low-density lipoprotein cholesterol”. The language for clinical investigations included in this review were limited to those set to English. The findings suggest that lower levels of TG may be associated with elevated pulmonary artery pressure, tricuspid regurgitation, and increased dimensions of the right side of the heart. These associations indicate impaired liver function due to right-sided HF in the chronic HF patients. Dysfunctional HDL-C is believed to contribute to the occurrence and advancement of HF. Additionally, serum TC levels have been identified as a potential prognostic factor in individuals with advanced HF. On the other hand, lower LDL-C levels seem to indicate worse prognosis for HF patients. However, further research is required to determine the precise mechanisms by which these lipid profiles influence the development and progression of the HF.

Whole exome sequencing of placental chorangioma

IntroductionPlacental chorangioma is a benign non-trophoblastic vascular proliferation of the placental chorion favored to represent hamartoma-like or hyperplastic capillary lesions. As the exact pathophysiology has not been established, we investigated the molecular characteristics of placental chorangiomas using exploratory whole exome sequencing. MethodsThree cases were retrospectively selected and whole exome sequencing was performed on macrodissected lesions. DNA extraction, DNA quantification, library preparation and sequencing were performed with IDT xGen™ Exome Hybridization Panel v2 for library capture. Sequencing data was analyzed with an in-house bioinformatics pipeline for single-nucleotide variants and insertions/deletions. ResultsAll neonates were delivered at term and had birth weights ranging from 11th-35th percentile for gestational age. All mothers presented with hypertensive disorder during pregnancy. Chorangiomas ranged from 0.7 cm to 5.1 cm and were well-circumscribed near the fetal surface. Case 1 showed a background of chorangiosis and acute subchorionitis, while case 2 had foci of chronic lymphocytic villitis. Whole exome sequencing did not reveal any significant pathologic variants. DiscussionsThe absence of molecular alteration in placental chorangioma is likely indicative of the reactive/non-neoplastic nature of this lesion. The presence of compromised blood flow in the form of hypertensive disorders in our cases may be one of its underlying pathophysiologic mechanisms.