Constriction Of Vessels Research Articles

Exploring Association of Anemia with Diabetic Foot Ulcer and its Impact on Disease Outcome in a Tertiary Care Hospital

Background: Both short-term and long-term complications are common in people with diabetes, making the disease quite difficult to manage. Among them development of foot ulcer is like a nightmare for diabetic patients. Foot deformities, impairment of microcirculation and concomitant neuropathy all add in the development of these ulcers, that are either delayed to heal or do not heal at all leading to amputation or in extreme cases even death. In addition to these major contributors, concomitant comorbidities like anemia may lead to development of an ulcer or effect it’s healing. If anemia identified and treated promptly may enhanced recovery of diabetic foot ulcer patients. We analyzed the effects of anemia on the prognosis of individuals with diabetic foot ulcers (DFUs). Methods: We prospectively followed 165 diabetic patients admitted to the hospital with DFU until they were either discharged or died. Patient's demographic data, characteristics of the ulcers, duration of diabetes, presence of comorbid conditions, need for blood transfusion and diabetic complications were all taken into account. The appropriate imaging and laboratory tests were conducted. The incidence of anemia and its effect on illness outcome in DFU patients were examined. Results: Anemia was found in 70% of patients with 38% required blood transfusion. The presence of gangrene, PAD, and an ulcer that had been present for more than a month prior to admission were all significant demographic and clinical predictors of anemia, [p0.008], [p0.00.1], [p0.001] respectively. Comorbidities like proteinuria [p0.003], moderate [p0.002] and severe [p0.00.1] constriction of the blood vessels, previous stroke [p0.012], kidney dysfunction [p0.002] were all significantly linked with anemia. Regarding effect of anemia on disease outcome delayed wound healing [p0.008], osteomyelitis [p0.005], amputation [p0.034] and mortality [p0.008] were all substantially correlated with anemia. Conclusion: Anemia was seen in majority of patients with DFU. Significant association was found between anemia and worse ulcer outcome in the form of delayed wound healing, osteomyelitis, mputation and mortality. Therefore, it needs to be identified and managed promptly, like other major risk factors such as infection, ischemia and pressure offloading, to promote earlier and complete healing. Keywords: Exploring, Association , Anemia, Diabetic Foot Ulcer , A Tertiary Care Hospital

Factors Affecting the Incidence of Hypertension in Menopause Using Literature Studies

ABSTRACT
 Introduction : Non Communicable Diseases (NCD) has become a health problem community both globally, nationally, regionally and even locally. World Health Organization (WHO) in 2015 reported that NCD killed 40 million people every year or equivalent of 70% of deaths worldwide. One of disease classified as non communicable which is dangerous namely hypertension. Hypertension is an important factor as a trigger for Non Communicable Diseases (NCD) such as heart disease, stoke, and others which is currently the number one cause of death scourge in the world. Menopause is one of the triggers for hypertension. Method : This study aims to analyze the factors that affected the incidence of hypertension in menopause. The study uses 4 databases namely E-resources, EBSCO, DOAJ, and Google Scholar using criteria inclusion and exclusion. Data analysis used descriptive method by summarizing research journals. There are 13 journals used. Results : From 13 articles, it was found several factors that cause hypertension in menopause such as age, physical activity, food / beverage intake, stress, and obesity. Conclusion : At menopause, there is a decrease in estrogen secretion resulting in constriction of blood vessels (vasoconstriction) which can cause blood pressure to rise. Henceforth, it is hoped that the community, especially families and respondents, will be able to know more about their health conditions, especially blood pressure so that they can check more frequently and also be able to maintain their lifestyle

A Novel Patient-Specific Computational Fluid Dynamics Study of the Activation of Primary Collateral Pathways in the Circle of Willis During Vasospasm.

The Circle of Willis (CoW) is a redundant network of blood vessels that perfuses the brain. The ringlike anatomy mitigates the negative effects of stroke by activating collateral pathways that help maintain physiological perfusion. Previous studies have investigated the activation of these pathways during embolic stroke and internal carotid artery occlusion. However, the role of collateral pathways during cerebral vasospasm-an involuntary constriction of blood vessels after subarachnoid hemorrhage-is not well-documented. This study presents a novel technique to create patient-specific computational fluid dynamics (CFD) simulations of the Circle of Willis before and during vasospasm. Computed tomographic angiography (CTA) scans are segmented to model the vasculature, and transcranial Doppler ultrasound (TCD) measurements of blood flow velocity are applied as boundary conditions. Bayesian analysis leverages information about the uncertainty in the measurements of vessel diameters and velocities to find an optimized parameter set that satisfies mass conservation and that is applied in the final simulation. With this optimized parameter set, the diameters, velocities, and flow rates fall within typical literature values. Virtual angiograms modeled using passive scalar transport agree closely with clinical angiography. A sensitivity analysis quantifies the changes in collateral flow rates with respect to changes in the inlet and outlet flow rates. This analysis can be applied in the future to a cohort of patients to investigate the relationship between the locations and severities of vasospasm, the patient-to-patient anatomical variability in the Circle of Willis, and the activation of collateral pathways.

Vasorelaxant Effects of Syzygium samarangense (Blume) Merr. and L.M.Perry Extract Are Mediated by NO/cGMP Pathway in Isolated Rat Thoracic Aorta.

Syzygium samarangense (Blume) Merr. and L.M.Perry is utilized widely in traditional medicine. We have reported previously a wide array of pharmacological properties of its leaf extract, among them anti-inflammatory, antioxidant, hepatoprotective, antidiabetic, antiulcer, and antitrypanosomal activities. We also annotated its chemical composition using LC-MS/MS. Here, we continue our investigations and evaluate the vasorelaxant effects of the leaf extract on aortic rings isolated from rats and explore the possible underlying mechanisms. S. samarangense extract induced a concentration dependent relaxation of the phenylephrine-precontracted aorta in the rat model. However, this effect disappeared upon removing the functional endothelium. Pretreating the aortic tissues either with propranolol or NG-nitro-L-arginine methyl ester inhibited the relaxation induced by the extract; however, atropine did not affect the extract-induced vasodilation. Meanwhile, adenylate cyclase inhibitor, MDL; specific guanylate cyclase inhibitor, ODQ; high extracellular KCl; and indomethacin as cyclooxygenase inhibitor inhibited the extract-induced vasodilation. On the other hand, incubation of S. samarangense extract with aortae sections having their intact endothelium pre-constricted using phenylephrine or KCl in media free of Ca2+ showed no effect on the constriction of the aortae vessels induced by Ca2+. Taken together, the present study suggests that S. samarangense extract dilates isolated aortic rings via endothelium-dependent nitric oxide (NO)/cGMP signaling. The observed biological effects could be attributed to its rich secondary metabolites. The specific mechanisms of the active ingredients of S. samarangense extract await further investigations.

The role of angiotensin II and relaxin in vascular adaptation to pregnancy.

There is a pregnancy-induced vasodilation of blood vessels, which is known to have a protective effect on cardiovascular function and can be maintained postpartum. This review outlines the cardiovascular changes that occur in a healthy human and rodent pregnancy, as well as different pathways that are activated by angiotensin II and relaxin that result in blood vessel dilation. During pregnancy, systemic and uteroplacental blood flow increase to ensure an adequate blood supply that carries oxygen and nutrients from the mother to the fetus. This results in changes to the function of the maternal cardiovascular system. There is also a pregnancy-induced vasodilation of blood vessels, which is known to have a protective effect on cardiovascular health/function. Additionally, there is evidence that the effects of maternal vascular vasodilation are maintained post-partum, which may reduce the risk of developing high blood pressure in the next pregnancy and reduce cardiovascular risk later in life. At both non-pregnant and pregnant stages, vascular endothelial cells produce a number of vasodilators and vasoconstrictors, which transduce signals to the contractile vascular smooth muscle cells to control the dilation and constriction of blood vessels. These vascular cells are also targets of other vasoactive factors, including angiotensin II (Ang II) and relaxin. The binding of Ang II to its receptors activates different pathways to regulate the blood vessel vasoconstriction/vasodilation, and relaxin can interact with some of these pathways to induce vasodilation. Based on the available literature, this review outlines the cardiovascular changes that occur in a healthy human pregnancy, supplemented by studies in rodents. A specific focus is placed on vasodilation of blood vessels during pregnancy; the role of endothelial cells and endothelium-derived vasodilators will also be discussed. Additionally, different pathways that are activated by Ang II and relaxin that result in blood vessel dilation will also be reviewed.

Covid 19 vaccines and the misinterpretation of perceived side effects clarity on the safety of vaccines.

In the era of Covid 19 and mass vaccination programs, the anti-vaccination movement across the world is currently at an all-time high. Much of this anti-vaccination sentiment could be attributed to the alleged side effects that are perpetuated across social media from anti-vaccination groups. Fear mongering and misinformation being peddled by people with no scientific training to terrorise people into staying unvaccinated is not just causing people to remain susceptible to viral outbreaks, but could also be causing more side effects seen in the vaccination process. This brief review will offer data that may demonstrate that misinformation perpetuated by the anti-vaccination movement may be causing more deaths and side effects from any vaccine. A mini review of published literature has been conducted and found that mental stress clearly causes vasoconstriction and arterial constriction of the blood vessels. Therefore, if subjects are panicked, concerned, stressed or scared of the vaccination, their arteries will constrict and become smaller in and around the time of receiving the vaccine. This biological mechanism (the constriction of veins, arteries and vessels under mental stress) is the most likely cause for where there has been blood clots, strokes, heart attacks, dizziness, fainting, blurred vision, loss of smell and taste that may have been experienced shortly after vaccine administration. The extreme mental stress of the patient could most likely be attributed to the fear mongering and scare tactics used by various anti-vaccination groups. This paper does not aim to rule in or out every side effect seen, but it is highly likely that many apparent side effects seen shortly after a subject has received a vaccine could be the result of restricted or congested blood flow from blood vessel or arterial constriction caused by emotional distress or placebo based on fear around vaccines.

APIUM GRAVEOLENS L EXTRACT: Alternative Complementary Therapies to Decrease Hypertension

Hypertension is often mentioned as the silent killer because it is deadly without any symptoms. Along with the times, the world of health began to develop complementary therapies. Herbal medicines received considerable attention as complementary medicines in the world because of their cost-effectiveness, low toxicity, and therapeutic potential against various diseases. Apium graveolens L and several other plants have been recognized as plants who’s the pharmacological effects can treat diseases such as hypertension. The purpose of this research was to analyse the effect of Apium graveolens L Extract to decrease hypertension. The type of this research used quasi-experimental with pre-post test with control group design. The population in this research were all elderly people suffering from hypertension in Tambak Agung Village, Puri District, Mojokerto Regency. The samples were obtained by using the purposive sampling technique. With inclusion criteria, including: 1) Hypertensive patients, 2) Age 55 years old, 3) Blood pressure up to 140 mmHg / 90 mmHg, 4) Willing to be a respondent. The processed data was analyzed to determine the effect of Apium graveolens L Extract on decreasing hypertension in the elderly. The data were analyzed using a statistical test Paired sample test T-Test with SPSS 23 for windows. At the significance level <0.05, H0 is rejected or H1 is accepted, meaning that Apium graveolens L extract decreases hypertension in the elderly. Apium graveolens L extract effectively decrease blood pressure by regularly consuming it. Because the Apigenin content contained in Apium graveolens L (celery) can prevent constriction of blood vessels and Phthalides which can relax artery muscles or relax blood vessels.

Vascular Reactions of the Diving Reflex in Men and Women Carrying Different ADRA1A Genotypes.

The diving reflex is an oxygen-saving mechanism which is accompanied by apnea, reflex bradycardia development, peripheral vasoconstriction, spleen erythrocyte release, and selective redistribution of blood flow to the organs most vulnerable to lack of oxygen, such as the brain, heart, and lungs. However, this is a poorly studied form of hypoxia, with a knowledge gap on physiological and biochemical adaptation mechanisms. The reflective sympathetic constriction of the resistive vessels is realized via ADRA1A. It has been shown that ADRA1A SNP (p.Arg347Cys; rs1048101) is associated with changes in tonus in vessel walls. Moreover, the Cys347 allele has been shown to regulate systolic blood pressure. The aim of this work was to evaluate whether the ADRA1A polymorphism affected the pulmonary vascular reactions in men and women in response to the diving reflex. Men (n = 52) and women (n = 50) untrained in diving aged 18 to 25 were recruited into the study. The vascular reactions and blood flow were examined by integrated rheography and rheography of the pulmonary artery. Peripheral blood circulation was registered by plethysmography. The ADRA1A gene polymorphism (p.Arg347Cys; rs1048101) was determined by PCR-RFLP. In both men and women, reflective pulmonary vasodilation did occur in response to the diving reflex, but in women this vasodilation was more pronounced and was accompanied by a higher filling of the lungs with blood.. Additionally, ADRA1A SNP (p.Arg347Cys; rs1048101) is associated with sex. Interestingly, women with the Arg347 allele demonstrated the highest vasodilation of the lung vessels. Therefore, our data may help to indicate women with the most prominent adaptive reactions to the diving reflex. Our data also indicate that women and men with the Cys allele of the ADRA1A gene polymorphism have the highest risk of developing lung hypertension in response to the diving reflex. The diving reflex is an oxygen-saving mechanism which is accompanied by apnea, reflex bradycardia development, peripheral vasoconstriction, spleen erythrocyte release, and selective redistribution of blood flow to the organs most vulnerable to lack of oxygen, such as the brain, heart, and lungs. However, this is a poorly studied form of hypoxia, with a knowledge gap on physiological and biochemical adaptation mechanisms.

Direct Oral Anticoagulants (DOACs) for Therapeutic Targeting of Thrombin, a Key Mediator of Cerebrovascular and Neuronal Dysfunction in Alzheimer's Disease.

Although preclinical research and observer studies on patients with atrial fibrillation concluded that direct oral anticoagulants (DOACs) can protect against dementia like Alzheimer’s disease (AD), clinical investigation towards therapeutical approval is still pending. DOACs target pathological thrombin, which is, like toxic tau and amyloid-ß proteins (Aß), an early hallmark of AD. Especially in hippocampal and neocortical areas, the release of parenchymal Aß into the blood induces thrombin and proinflammatory bradykinin synthesis by activating factor XII of the contact system. Thrombin promotes platelet aggregation and catalyzes conversion of fibrinogen to fibrin, leading to degradation-resistant, Aß-containing fibrin clots. Together with oligomeric Aß, these clots trigger vessel constriction and cerebral amyloid angiopathy (CAA) with vessel occlusion and hemorrhages, leading to vascular and blood–brain barrier (BBB) dysfunction. As consequences, brain blood flow, perfusion, and supply with oxygen (hypoxia) and nutrients decrease. In parenchymal tissue, hypoxia stimulates Aß synthesis, leading to Aß accumulation, which is further enhanced by BBB-impaired perivascular Aß clearance. Aß trigger neuronal damage and promote tau pathologies. BBB dysfunction enables thrombin and fibrin(ogen) to migrate into parenchymal tissue and to activate glial cells. Inflammation and continued Aß production are the results. Synapses and neurons die, and cognitive abilities are lost. DOACs block thrombin by inhibiting its activity (dabigatran) or production (FXa-inhibitors, e.g., apixaban, rivaroxaban). Therefore, DOAC use could preserve vascular integrity and brain perfusion and, thereby, could counteract vascular-driven neuronal and cognitive decline in AD. A conception for clinical investigation is presented, focused on DOAC treatment of patients with diagnosed AD in early-stage and low risk of major bleeding.

Canine Smooth Muscle Contraction Model.

Smooth muscle is found extensively in the human body, including in blood vessels, airways, the gastrointestinal tract, and the urinary bladder. Although the contractile proteins of smooth muscle are very similar to those of striated muscle, smooth muscle's contractile mechanism has not been studied as extensively as those for cardiac and skeletal muscle. Previous studies developed a lumped model of muscle contraction and applied it to cardiac muscle and to skeletal muscle. In this study, this model is used to quantitatively describe the contractile properties of canine smooth muscle, using data from the literature. Results show that a single equation relating muscle force to muscle length and time, and a single set of model parameters, is able to describe smooth muscle's passive and active isometric forces, isometric twitch contractions, isotonic contractions, and an inverse force-velocity relation. The latter arises from the model without assumption of a particular force-velocity curve embodied as a contractile element. This new constitutive relation may be used to describe smooth muscle within larger physiological models, for instance to describe blood vessel constriction or urinary bladder function.

Regulation of blood vessels by ATP in the ventral medullary surface in a rat model of Parkinson’s disease

Parkinson’s disease (PD) patients often experience impairment of autonomic and respiratory functions. These include conditions such as orthostatic hypotension and sleep apnea, which are highly correlated with dysfunctional central chemoreception. Blood flow is a fundamental determinant of tissue CO2/H+, yet the extent to which blood flow regulation within chemoreceptor regions contributes to respiratory behavior during neurological disease remains unknown. Here, we tested the hypothesis that 6-hydroxydopamine injection to inducing a known model of PD results in dysfunctional vascular homeostasis, biochemical dysregulation, and glial morphology of the ventral medullary surface (VMS). We show that hypercapnia (FiCO2 = 10%) induced elevated VMS pial vessel constriction in PD animals through a P2-receptor dependent mechanism. Similarly, we found a greater CO2-induced vascular constriction after ARL67156 (an ectonucleotidase inhibitor) in control and PD-induced animals. In addition, we also report that weighted gene correlational network analysis of the proteomic data showed a protein expression module differentially represented between both groups. This module showed that gene ontology enrichment for components of the ATP machinery were reduced in our PD-model compared to control animals. Altogether, our data indicate that dysfunction in purinergic signaling, potentially through altered ATP bioavailability in the VMS region, may compromise the RTN neuroglial vascular unit in a PD animal model.

Toward Better Posture: A Wearable Back Posture Alerting Device

Back pain is the leading cause of disability worldwide, preventing many people from engaging in work or other everyday activities. Good posture entails training your body to develop a habit that exerts the least amount of pressure on supporting ligaments and muscles; however, posture is not consciously maintained. Instead, muscle groups automatically support and enable flexing the spine, meaning efforts to consciously improve posture will ultimately fail. Over time, muscles develop habits that can put extra strain on the back and make correcting posture difficult. The greatest contributor to postural problems is poor everyday postural habits, common in a work environment that requires long hours of sitting or standing. Harmful consequences of poor posture include misalignment of the spine, back pain, sore muscles, improper lung function, blood vessel constrictions, improper gait, and proneness to injury. Reversing bad posture should be tackled as soon as the problem is identified, and having an easily accessible posture monitoring device would be useful in preventing long-term detrimental effects of bad posture. In this project, I developed and tested a wearable garment that monitors, evaluates, and communicates real-time sensory feedback of back posture.

Common Shared Pathogenic Aspects of Small Vessels in Heart and Brain Disease

Small-vessel disease (SVD), also known as microvascular endothelial dysfunction, is a disorder with negative consequences for various organs such as the heart and brain. Impaired dilatation and constriction of small vessels in the heart lead to reduced blood flow and ischemia independently of coronary artery disease (CAD) and are associated with major cardiac events. SVD is usually a silent form of subcortical vascular burden in the brain with various clinical manifestations, such as silent-lacunar-ischemic events and confluent white-matter hyperintensities. Imaging techniques are the main help for clinicians to diagnose cardiac and brain SVD correctly. Markers of inflammation, such as C-reactive protein, tumor-necrosis-factor α, and interleukin 6, provide insight into the disease and markers that negatively influence nitric-oxide bioavailability and promote oxidative stress. Unfortunately, the therapeutic approach against SVD is still not well-defined. In the last decades, various antioxidants, oxidative stress inhibitors, and superoxide scavengers have been the target of extensive investigations due to their potential therapeutic effect, but with unsatisfactory results. In clinical practice, traditional anti-ischemic and risk-reduction therapies for CAD are currently in use for SVD treatment.

Capillary model tracks blood flow in healthy and diseased networks

3D model of retina capillary networks provides insight on flow of blood cells, impacts of constricted vessels

Highly Diluted Antibodies to eNOS Restore Endothelium Function in Aortic Rings From Hypertensive Rats.

BackgroundNitric oxide (NO) as a vaso- and cardio-protective agent could reduce vasomotor dysfunction in different cardiovascular diseases. One of the current therapeutics targeted at NO availability in the vascular wall are highly diluted antibodies to endothelial NO-synthase (eNOS). This drug has previously shown its endothelium-protective effect and effectiveness in reducing hypertension. Current study was dedicated to evaluate the direct impact of highly diluted antibodies to eNOS on the vessel constriction and dilation ex vivo.MethodsFor that purpose, we used thoracic aortas dissected from spontaneously hypertensive (SHR) rats. Endothelium-dependent relaxation in the presence of highly diluted antibodies to eNOS (1 mL) was examined after phenylephrine-induced pre-constriction of the aorta rings in response to gradually increased acetylcholine concentration (1 nM to 10 µM).ResultsHighly diluted antibodies to eNOS enhanced acetylcholine-induced relaxation in a statistically significant manner. Moreover, it was demonstrated that observed effect was similar to perindopril, a well-known angiotensin-converting-enzyme inhibitor, which works through relaxing and widening blood vessels.ConclusionsOur findings indicate that highly diluted antibodies to eNOS restored impaired endothelium function, as demonstrated by increased relaxation of SHR rats aorta rings. The revealed results suggest beneficial effect of highly diluted antibodies to eNOS to ameliorate hypertension and related diseases.

Compromised Blood Flow in the Optic Nerve Head after Systemic Administration of Aldosterone in Rats: A Possible Rat Model of Retinal Ganglion Cell Loss

PurposeTo investigate the optic nerve head (ONH) blood flow, retinal vessel diameters, and retinal ganglion cell (RGC) loss after systemic administration of aldosterone in rats.MethodsAldosterone (80 µg/kg/day) or vehicle was administered using an osmotic minipump in Brown Norway rats. The mean blur rate in the vessel (MV) and tissue (MT) regions and retinal vessel diameters in the ONH were measured by laser speckle flowgraphy before and 1, 2, and 4 weeks after administration of aldosterone or vehicle. Intraocular pressure (IOP), blood pressure, and heart rate were recorded. The retrogradely labeled RGCs were counted in the retinal flatmounts prepared 5 weeks after treatment.ResultsThe MV and MT in the aldosterone group significantly decreased at 2 and 4 weeks (MV: 2 weeks, p = 0.001, 4 weeks, p < 0.001; MT: 2 weeks, p = 0.02, 4 weeks, p = 0.03). The artery and vein diameters significantly decreased at 1, 2, and 4 weeks in the aldosterone group (all p < 0.001). The MV, MT, and vessel diameters remained unchanged in the vehicle group. Other parameters did not change over time in either group. RGC counts were significantly lower in the aldosterone group than in the vehicle group (p < 0.001).ConclusionsONH blood flow decreased following retinal vessel constriction without changes in IOP or blood pressure in a possible rat model of RGC loss by systemic administration of aldosterone.

The Critical Role of Spreading Depolarizations in Early Brain Injury: Consensus and Contention

BackgroundWhen a patient arrives in the emergency department following a stroke, a traumatic brain injury, or sudden cardiac arrest, there is no therapeutic drug available to help protect their jeopardized neurons. One crucial reason is that we have not identified the molecular mechanisms leading to electrical failure, neuronal swelling, and blood vessel constriction in newly injured gray matter. All three result from a process termed spreading depolarization (SD). Because we only partially understand SD, we lack molecular targets and biomarkers to help neurons survive after losing their blood flow and then undergoing recurrent SD.MethodsIn this review, we introduce SD as a single or recurring event, generated in gray matter following lost blood flow, which compromises the Na+/K+ pump. Electrical recovery from each SD event requires so much energy that neurons often die over minutes and hours following initial injury, independent of extracellular glutamate.ResultsWe discuss how SD has been investigated with various pitfalls in numerous experimental preparations, how overtaxing the Na+/K+ ATPase elicits SD. Elevated K+ or glutamate are unlikely natural activators of SD. We then turn to the properties of SD itself, focusing on its initiation and propagation as well as on computer modeling.ConclusionsFinally, we summarize points of consensus and contention among the authors as well as where SD research may be heading. In an accompanying review, we critique the role of the glutamate excitotoxicity theory, how it has shaped SD research, and its questionable importance to the study of early brain injury as compared with SD theory.

Raynaud's Phenomenon: Reviewing the Pathophysiology and Management Strategies.

Raynaud’s phenomenon (RP) is a multifactorial vasospastic disorder characterized by a transient, recurrent, and reversible constriction of peripheral blood vessels. RP is documented to affect up to 5% of the general population, but variation in its prevalence is commonly recognized owing to many factors, including varied definitions, gender, genetics, hormones, and region. Furthermore, RP may be idiopathic or be a clinical manifestation of an underlying illness. Patients with RP classically describe a triphasic discoloration of the affected area, beginning with pallor, followed by cyanosis, and finally ending with erythema. This change in color spares the thumb and is often associated with pain. Each attack may persist from several minutes to hours.Moreover, the transient cessation of blood flow in RP is postulated to be mediated by neural and vascular mechanisms. Both structural and functional alterations observed in the blood vessels contribute to the vascular abnormalities documented in RP. However, functional impairment serves as a primary contributor to the pathophysiology of primary Raynaud’s. Substances like endothelin-1, angiotensin, and angiopoietin-2 play a significant role in the vessel-mediated pathophysiology of RP. The role of nitric oxide in the development of this phenomenon is still complex. Neural abnormalities resulting in RP are recognized as either being concerned with central mechanisms or peripheral mechanisms. CNS involvement in RP may be suggested by the fact that emotional distress and low temperature serve as major triggers for an attack, but recent observations have highlighted the importance of locally produced factors in this regard as well. Impaired vasodilation, increased vasoconstriction, and several intravascular abnormalities have been documented as potential contributors to the development of this disorder. RP has also been observed to occur as a side effect of various drugs.Recent advances in understanding the mechanism of RP have yielded better pharmacological therapies. However, general lifestyle modifications along with other nonpharmacological interventions remain first-line in the management of these patients. Calcium channel blockers, alpha-1 adrenoreceptor antagonists, angiotensin-converting enzyme inhibitors, nitric oxide, prostaglandin analogs, and phosphodiesterase inhibitors are some of the common classes of drugs that have been found to be therapeutically significant in the management of RP. Additionally, anxiety management, measures to avoid colder temperatures, and smoking cessation, along with other simple modifications, have proven to be effective non-drug strategies in patients experiencing milder symptoms.

Does Oxidative Stress Management Help Alleviation of COVID-19 Symptoms in Patients Experiencing Diabetes?

Severe acute respiratory syndrome (SARS)-CoV-2 virus causes novel coronavirus disease 2019 (COVID-19) with other comorbidities such as diabetes. Diabetes is the most common cause of diabetic nephropathy, which is attributed to hyperglycemia. COVID-19 produces severe complications in people with diabetes mellitus. This article explains how SARS-CoV-2 causes more significant kidney damage in diabetic patients. Importantly, COVID-19 and diabetes share inflammatory pathways of disease progression. SARS-CoV-2 binding with ACE-2 causes depletion of ACE-2 (angiotensin-converting enzyme 2) from blood vessels, and subsequently, angiotensin-II interacts with angiotensin receptor-1 from vascular membranes that produce NADPH (nicotinamide adenine dinucleotide hydrogen phosphate) oxidase, oxidative stress, and constriction of blood vessels. Since diabetes and COVID-19 can create oxidative stress, we hypothesize that COVID-19 with comorbidities such as diabetes can synergistically increase oxidative stress leading to end-stage renal failure and death. Antioxidants may therefore prevent renal damage-induced death by inhibiting oxidative damage and thus can help protect people from COVID-19 related comorbidities. A few clinical trials indicated how effective the antioxidant therapy is against improving COVID-19 symptoms, based on a limited number of patients who experienced COVID-19. In this review, we tried to understand how effective antioxidants (such as vitamin D and flavonoids) can act as food supplements or therapeutics against COVID-19 with diabetes as comorbidity based on recently available clinical, preclinical, or in silico studies.

Hemoglobin Precipitation: An Index of In Vitro Vasoconstrictive Activities of Methanol Leaf Extracts of Croton megalocarpus Hutch and Lantana camara Linn.

The function of innate hemostasis aids the body in bleeding control, preventing the loss of excessive amounts of blood following low-degree injuries. However, injuries of a higher degree may require extrinsic intervention to stop life-threatening blood loss. Astringent agents' actions result in mechanical constriction of small blood vessels and shrinkage of body tissues, thereby stopping blood loss. This enhances the primary phase of hemostasis, where vasoconstriction is the main mechanism at play during the initial response to injury. The effects of plant extracts on protein precipitation have been linked to blood vessel vasoconstriction. Traditionally, the leaves of Croton megalocarpus Hutch and Lantana camara Linn plants are used by communities living in Makueni County, Kenya, for peripheral bleeding control. However, the effects of extracts of both plants on hemoglobin precipitation have not been evaluated scientifically. In the current study, the activities of methanol extracts of C. megalocarpus (H.) and L. camara (L.) on blood protein precipitation were investigated. The leaves were harvested, cleaned, air-dried, milled, and extracted in absolute methanol before being concentrated into dry powders. A qualitative phytochemical screen revealed the presence of terpenoids, steroids, tannins, phenols, flavonoids, reducing sugars, cardiac glycosides, and carbohydrates in the methanol extract of C. megalocarpus (H.). The methanol extracts of L. camara (L.) contained cardiac glycosides, saponins, tannins, phenols, terpenoids, reducing sugars, and carbohydrates. The hemoglobin precipitation ability of various concentrations of extracts using mice samples was presented as relative astringency following the tannic acid external standard method. Methanol extracts C. megalocarpus (H.) and L. camara (L.) had significantly higher relative astringency compared with the normal control, indicating a protein precipitating activity. The relative astringency observed in both plant extracts is linked to the activity of tannins, phenols, flavonoids, and saponins detected during preliminary phytochemical screening.