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The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Blood is transported away from the heart via arteries, the largest of which is the aorta. Arteries become progressively smaller the further they are from the heart, finally becoming very small vessels known as arterioles. Arterioles feed into capillaries in the capillary bed of all body tissues. Whilst arterioles are very small, capillaries are microscopic, with very thin walls. It is at the capillary bed that the exchange of nutrients and oxygen occurs, from the blood to the tissues, and waste products are exchanged to the blood from the tissues. Blood leaves the capillary bed via small venules that join with others to become veins, the largest of which are the superior vena cava (SVC) and the inferior vena cava (IVC). Veins transport blood to the heart.
The Design of Receptor-Binding Radiotracers
Published in Lelio G. Colombetti, Principles of Radiopharmacology, 2019
William C. Eckelman, Raymond E. Gibson, Waclaw J. Rzeszotarski, Victor Jiang, J. Krijn Mazaitis, Chang Paik, Toru Komai, Richard C. Reba
The distribution of a radiotracer is controlled by many factors. After IV injection, the material is distributed throughout the body on the basis of the fractional cardiac output received by each organ. The liver and kidney have the highest blood flow at rest and therefore would receive the highest dose of radiopharmaceutical in the first pass.52 The type of capillary within the organ is another important factor; most capillary beds have relatively large intercellular pores. Consequently, even the most polar drugs can readily leave the vascular pool. The one exception to this is the continuous endothelium, which acts as a blood brain barrier. In addition to passing through the pores of the capillary wall, lipid-soluble drugs dissolve in the cellular membrane and thus may pass rapidly through the endothelial cells of the capillaries and into tissue cells. The important factors in capillary cell transport and in tissue cell membrane transport are (1) size, (2) lipid solubility, and (3) pKa, if acids or bases are present.53 There are a number of other cellular membrane transport mechanisms including: (1) simple diffusion as found for anions crossing the erythrocyte membrane; (2) filtration as seen in the renal glomeruli; (3) active transport mechanisms, as exemplified by rose bengal uptake in the parenchymal cells of the liver; and (4) pinocytosis of macromolecules.
The Dermal Microvascular Unit: Relationship to Immunological Processes and Dermal Dendrocytes
Published in Brian J. Nickoloff, Dermal Immune System, 2019
The microanatomical features and the 3-D organization of the microcirculation described above clarify how the microvasculature participates in a variety of physiologic and pathologic states. The resistance vessels of the skin involved in reactive vasoconstriction and vasodilation are represented by the arterioles of the lower plexus and the ascending segments with their immediate branches that give rise to the upper plexus. The precapillary sphincter is placed at the distal end of these branches, thereby controlling tissue perfusion through the dermal capillary beds and the capillary loops in the dermal papillae. The upper plexus, which is situated 2 mm below the skin surface, is the major site of thermoregulation. The resistance vessels and the precapillary sphincters regulate the volume of blood in the upper plexus from which heat is radiated. The smooth muscle sphincters of the terminal arterioles appear to be the sites of the pulsatile vasomotor activity detected by laser Doppler flowmetry.10,15 This vasomotion facilitates tissue perfusion through the capillary beds.
Novel transdermal curcumin therapeutic preserves endothelial barrier function in a high-dose LPS rat model
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
William H. Nugent, Danuel A. Carr, Joel Friedman, Bjorn K. Song
Sepsis—a driver of systemic inflammatory response syndrome—accounts for 20% of global deaths annually [1]. Despite a complex and multifaceted pathology triggered and perpetuated by widespread innate immune activity, the true “motor of sepsis” is recognised as microvascular dysfunction [2], which stems from endothelial barrier breakdown [3]. While inflammation is a necessary component of homeostatic restoration following infection and injury, the process disrupts normal vascular function [4,5]. Microvessels dilate and their endothelial linings—the endothelial surface layer (ESL/glycocalyx) in contact with the blood—become porous permitting the extravasation of fluids, solutes, neutrophils, and macrophages. Locally, so-called “leaky vessels” have a minor impact on circulatory volume, but can lead to circulatory failure when dysregulated at a systemic level. The damaged endothelium also becomes prothrombotic, increasing red blood cell aggregation to create pockets of microvascular ischaemia [6]. Coupled with hypovolemia, capillary beds become ischaemic causing organ damage, which is proximate to severe morbidity and mortality in sepsis [7].
Neurologic conditions in Hereditary Hemorrhagic Telangiectasia with pulmonary arteriovenous malformations: Database study
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2023
Chester Lau, Joel Agarwal, Ben Vandermeer, W. Ted Allison, Thomas Jeerakathil, Dilini Vethanayagam
An estimated 35–40% of HHT subjects have pulmonary arteriovenous malformations (PAVMs), consisting of abnormal connections between the feeding artery(ies) and draining vein(s).9 These fragile and dilated vessels allow blood contents from the pulmonary circulation to bypass capillary beds and travel toward the systemic circulation, preventing gas exchange.9,12 PAVMs result in the physiologic consequence of intrapulmonary right-to-left shunt (RLS), causing air and/or particulate emboli to traverse through the bloodstream into the cerebral vessels.13 This may lead to a plethora of neurological conditions, including migraines, seizures, ischemic (embolic) stroke, transient ischemic attack (TIA) and cerebral abscess.14 These neurologic conditions may also be dependent on PAVM shunt grade.9,13,15–17 Other clinical features of PAVMs include clubbing, dyspnea and hypoxemia; however, many patients with PAVMs are asymptomatic.12
The Association of Acute Cerebrospinal Fluid Pressure Reduction with Choroidal Thickness
Published in Current Eye Research, 2021
Xiangxiang Liu, Mohamed M. Khodeiry, Danting Lin, Yunxiao Sun, Caixia Lin, Wei Feng, Jing Li, Yaxing Wang, Qing Zhang, Kai Cao, Jiawei Wang, Ningli Wang
To the best of our knowledge, no studies have examined subfoveal choroidal thickness after CSFP reduction. A previous population-based study found that SFCT was associated with CSFP.14 These results consist of the present data. Additionally, we extended previous findings suggesting a significant association between CSFP and the ratio of SMVL thickness to total choroidal thickness. Histologically, choroidal blood drains into the intracranial cavernous sinus through the vortex veins and the superior venous plexus, and these anatomical features indicate that CSFP may influence the choroidal thickness.1 The choriocapillaris is a specialized capillary bed with the greatest density of capillaries that arises from the arterioles in Sattler’s layer.1,15 In addition, the extravascular tissue in the medium vessel layer contains collagen and elastic fibres, etc.16 These structural features make the small to medium vessel layer more flexible than other regions in response to pressure changes, indicating that the SMVL is more sensitive to pressure alterations. Furthermore, the primary function of the choroid, especially the choriocapillaris, is supplying oxygen and nutrients to the retina, so attenuation of the SMVL may be correlated with decreased choroidal circulation and may produce a relatively ischemic environment, leading to retinal dysfunction.