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The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The cerebral blood vessels and the blood contained within them take up approximately 10 per cent of the space within the skull. Blood vessel diameter affects the amount of space that the blood vessels occupy within the brain. Blood vessels may dilate due to increased blood volume or because of metabolic factors influencing blood vessel tone, for example, pH, PaO2, and PaCO2. Hypoxia, hypercapnia and acidosis cause vasodilation of blood vessels, increasing ICP. The reverse is also true: hypocapnia and alkalosis cause vasoconstriction, reducing cerebral blood flow. As a result of these effects on the cerebral blood vessels, the partial pressure of carbon dioxide in arterial blood gas (PaCO2) is monitored closely and maintained within normal limits between 4.6–6kPa for optimal cerebral blood flow (Carney et al. 2016).
Conclusion
Published in Jay A. Goldstein, Chronic Fatigue Syndromes, 2020
IL-1 beta leads to induction of nitric oxide synthase which synthesizes nitric oxide (NO) from L-arginine with tetrahydrobiopterin (BH4), flavin adenine dinucleotide (FAD), and flavin mononucleotide (FMN) as necessary co-factors. NO is released continuously in varying amounts to regulate blood vessel tone as a vasodilator. Local changes in expression of NO synthase may be produced by alterations in the balance of cytokines such as IL-1, which induce NO synthase, and those such as TGF-beta 50 and IL-10 51 which inhibit induction. Such inhibitory factors may be involved in the decrease in regional cerebral blood flow which we usually observe in CFS patients after exercise. NO is also thought to be a mediator of slow synaptic transmission and is thought to be important in memory and learning processes. IL-10 has a high homology to a product of EBV called BCRF-1 52 and it has been speculated that EBV has appropriated this gene from the human genome. IL-10 inhibits the synthesis of cytokines by TH1 cells, a member of a pair of mutually inhibitory subsets of T-cells. TH1 cells inhibit TH2 cells, which produce IL-4 and IL-5 which lead to some of the major manifestations of allergy. IL-10 production may bias an immune response towards allergy. 53
Neuronal Mechanisms of Cutaneous Blood Flow
Published in Geoffrey Burnstock, Susan G. Griffith, Nonadrenergic Innervation of Blood Vessels, 2019
Fred Lembeck, Margarethe Holzbauer
Among the neuropeptides involved in the regulation of the blood vessel tone, SP has been investigated in most detail. It is present in approximately 30 regions of the mammalian central nervous system and in the intestinal tract (for review see References 21 and 22). It also occurs in a certain group of nonmyelinated sensory nerve fibers which are involved in the control of cutaneous blood vessels. Like all primary sensory neurons, these SP-containing neurons are pseudounipolar neurons; their perikarya lie in the spinal ganglia23 or in corresponding ganglia of the cranial nerves.24 As nociceptive impulses are transmitted via the central endings of SP neurons in the brain, they are classified as pain fibers. Release of SP from the central endings of these neurons is an important link in the “damage report” to the brain.25
Uric acid can enhance MAPK pathway-mediated proliferation in rat primary vascular smooth muscle cells via controlling of mitochondria and caspase-dependent cell death
Published in Journal of Receptors and Signal Transduction, 2022
Segün Doğru, Ekrem Yaşar, Akın Yeşilkaya
VSMCs are the main functions of blood vessel tone diameter, blood pressure, regulation of blood flow, and contractile function by contractile proteins located in the medial layer of the vasculature. They are highly specialized cells with lower proliferation and apoptosis levels. In pathological conditions such as hypertension and atherosclerosis, VSMCs lose their contractile properties. This situation is explained by a different phenotypic change by increasing cellular proliferation and migration rates [44–49]. In vitro and in vivo studies have also revealed that uric acid has a role in cardiovascular diseases by causing vascular structural changes related to proliferative, oxidative, inflammation effects [23,27,50–56]. These studies show that uric acid has proliferative or apoptotic effect on VSMCs, but this effect on VSMCs remains a paradox, especially in hyperuricemic conditions.
Metabolomics analysis for diagnosis and biomarker discovery of transthyretin amyloidosis
Published in Amyloid, 2021
Malin Olsson, Urban Hellman, Jonas Wixner, Intissar Anan
Tryptophan has been suggested to be involved in numerous neurodegenerative diseases such as Alzheimer’s disease and ALS [22]. Tryptophan is an essential amino acid and is metabolised by at least two major pathways, the serotonin and kynurenine pathways [23]. Serotonin plays a role in gastrointestinal regulation and is a modulator of blood vessel tone. Nyhlin et al. [24] showed a decrease in serotonin-producing cells in the gastrointestinal tract in patients with ATTRV30M. The decrease in tryptophan in this study suggests that tryptophan could be involved in autonomic dysfunction seen in patients with ATTRV30M. Hatano et al. [25] suggested that the decrease in tryptophan levels may be linked to differences in the serotonin pathway, but not in the kynurenine pathway. This study showed that the kynurenine pathway is likewise affected, as a decreased kynurenine levels in ATTRV30M patients was detected. Dysregulation of this pathway may have a neurotoxic effect [26] which could be involved in the neuropathy affecting ATTR patients.
Endothelial function in patients with atrial fibrillation
Published in Annals of Medicine, 2020
Ahsan A. Khan, Graham N. Thomas, Gregory Y. H. Lip, Alena Shantsila
The endothelium is considered a dynamic organ [7]. It constitutes several unique functions in vascular biology by responding to various hormones, neurotransmitters, vasoactive factors and processes which then affect blood vessel tone (vasomotion) and haemostasis (thrombosis, platelet aggregation and inflammation) [7]. The endothelium releases several vasoactive factors, which are either vasodilatory such as NO, prostacyclin (PGI2) and endothelium-derived hyperpolarizing factor (EDHF) or vasoconstrictive factors such as thromboxane (TXA2) and endothelin-1 (ET-1) [11]. The balanced production of these vasoactive factors is atheroprotective, whereas disrupted production of these factors leads to endothelial dysfunction. Endothelial dysfunction is a hallmark of vascular diseases and has been shown to predict future adverse cardiovascular events such as cardiac death, myocardial infarction, unstable angina and stroke. It is also present in inflammatory disease processes, such as rheumatoid arthritis or systemic lupus erythematosus (Figure 1) [12]. Endothelial dysfunction presents a final common pathway or “barometer” of the combined impact of traditional atherosclerotic risk factors; thus assessment of endothelial dysfunction in humans presents an attractive option for determination of risk associated with thrombogenesis and combined risk factor impact on atherogenesis [13].