The immune and lymphatic systems, infection and sepsis
Ian Peate, Helen Dutton in Acute Nursing Care, 2014
Circulation. The cardiovascular system should be assessed for the following clinical signs: tachycardia, with or with out associated myocardial ischaemia (chest pain);profound hypotension and dizziness due to peripheral vasodilation;clammy, sweaty skin, flushed or pale skin depending on the reaction. Remembering the processes for the inflammatory response, there will be increased capillary permeability leading to the sequestering of fluids in the tissues giving rise to swelling and oedema. If left untreated, the patient may go on to develop cardiac arrest.
Injuries Due to Burns and Cold
Ian Greaves, Keith Porter, Jeff Garner in Trauma Care Manual, 2021
The inflammatory process associated with burn injury evolves during the 8–24 hours after the burn and can cause further local and systemic injury. There is increased capillary permeability with fluid loss from the intravascular space. The magnitude of the inflammatory response is related to the extent of the tissue injury and is most easily expressed as the percentage of the total body surface area (% TBSA) that is burnt. Superficial burns cause only erythema with no significant capillary leakage. In burns greater than approximately 20% TBSA, the inflammatory mediators affect the whole body and patients may develop a systemic inflammatory response syndrome (SIRS)3 over several hours, with significant intravascular fluid loss and the potential for the development of hypovolaemic shock.4 Other causes of hypovolaemia, for example, from associated traumatic injuries from jumping to escape a fire, should be excluded before attributing hypovolaemia solely to the burn injury.
Treatment of Anti-Phospholipid Antibody Mediated Fetal Loss: The Case for Corticosteroid Therapy
E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson in Phospholipid-Binding Antibodies, 2020
Corticosteroid therapy has been shown in SLE to improve renal histology where it exerts an anti-inflammatory effect by way of the micro vasculature, neutrophils and other white cells. Therapy decreases capillary permeability and blood flow. Endothelial swelling and the passage of immune complexes across the basement membrane are reduced. It is also considered to inhibit histamine release, to exert prostaglandin-like and anticomplementary activity and to stabilize lysozomal membranes. Prednisone in high dosage suppresses the histological activity as measured by repeated renal biopsy.39 Corticosteroid therapy also has a direct suppressive effect on B lymphocyte responsiveness and the ability to synthesize antibodies.40
The lethal effects and determinants of microcystin-LR on heart: a mini review
Published in Toxin Reviews, 2021
Muwaffak Alosman, Linghui Cao, Isaac Yaw Massey, Fei Yang
Researchers such as Milutinovic et al. (2006) considered that the outcome of hypovolemic shock as extensive and may cause tissue damage that ultimately leads to death as a result of MC intoxication. The production of high levels of MC leads to an intensive amount of protein in blood capillaries hence necessitating a significant increase in peripheral pressure. An increase in blood pressure is responsible for the increase of glomerular pressure which consequently affects the health of human and animals. Interference in blood flow is as a result of toxin-treated group. Therefore, there is an increase in vascular permeability due to capillary injuries that are caused by increased blood flow. Direct permeability is caused by endothelial injury and the alteration in blood flow (Best et al. 2001). An experimental study done by Qiu et al. (2009) indicated that rats exposed to MC-LR at a lethal dose experienced a decrease in blood pressure, which suggested a basic dysfunction of the normal compensatory responses vasculature and heart to hypotension. In the meantime, the observed decrease in both stroke volume and cardiac output in the rats exposed to lethal doses of MC-LR pointed at the proposition that MCs impede the heart's blood pumping role.
Pro-inflammatory cytokines as potential predictors for intradialytic hypotension
Published in Renal Failure, 2021
Jinbo Yu, Xiaohong Chen, Yang Li, Yaqiong Wang, Xuesen Cao, Zhonghua Liu, Bo Shen, Jianzhou Zou, Xiaoqiang Ding
Association between fluid overload (FO) and inflammation was revealed in MHD patients [25–27]. Inflammation might theoretically contribute to FO because of hypoalbuminemia. Hypoalbuminemia can lead to vascular volume migration to the interstitial chamber, which hinders fluid removal during dialysis [28]. However, FO itself can also reduce serum albumin levels by dilution, as serum albumin levels increased after excessive ultrafiltration [29]. Inflammation may also result in interstitial fluid accumulation by increasing capillary permeability. FO may also bring about inflammation by endotoxin fragment passing through a congested intestinal wall or visceral ischemia [30,31]. As volume overload, hypoalbuminemia and malnutrition are common predictors of IDH. We presumed that inflammatory markers might play a part in the onset of IDH. Serum TNF-α and IL-1β were observed elevated in the IDH group (p < 0.001).
Comparative pharmacokinetics of quercitrin, astragalin, afzelin and taxifolin in plasma after oral administration of Polygonum orientale inflorescence in sham-operated and myocardial ischemia–reperfusion injury rats
Published in Xenobiotica, 2020
Lin Zheng, Yueting Li, Zuying Zhou, Wenying Xiang, Zipeng Gong, Siying Chen, Yonglin Wang, Aimin Wang, Yanyu Lan, Yongjun Li, Yong Huang
The main reason is that the ischemic body causes the elimination of metabolites to slow down (Dong et al., 2016). Moreover, the vascular response is a central part of the inflammatory response, and inflammation can lead to an increase in tissue vasodilation and capillary permeability (Gao et al., 2013). As such, another possibility is microvascular dysfunction caused by myocardial ischemia–reperfusion injury (MIRI), including increased vascular permeability, endothelial cell inflammation, vasodilation, vasoconstriction factors and an imbalance between coagulation activation and the complement system (Li, 2014; Chai & Yu, 2014; Elizabeth & Charles, 2008; Gao et al., 2013; Yang et al., 2006). Accordingly, the higher values of AUC(0–t), MRT(0–t), AUC(0–∞) and MRT(0–∞), with decreased CL, in the MIRI model rats may have possibly resulted from a decrease in the elimination of quercitrin, astragalin, afzelin and taxifolin.
Related Knowledge Centers
- Cell Junction
- Inflammation
- Junctional Epithelium
- Leukocyte Extravasation
- Endothelium
- Connective Tissue
- Lymphocyte
- Neutrophil
- Blood Vessel
- Vasodilation