Explore chapters and articles related to this topic
Cellular and Molecular Mechanisms of Ischemic Acute Renal Failure and Repair
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Joseph V. Bonventre, Ralph Witzgall
Heterogeneity of blood flow plays an important role in the pathophysiology of ischemic renal failure. Differences in the distribution of blood flow likely plays an important role in the heterogeneous nature of the tubule lesions seen with ischemia (Oliver, et al., 1951). Vascular congestion in the outer medulla (Mason, et al., 1989) and decreased blood flow (Vetterlein, et al., 1986) to this region is a feature of experimental ischemic acute renal failure in rats. This vascular congestion may be the result at least in part of swelling of endothelial or tubular epithelial cells, resulting in interference with flow through the vasa recta and further compromise of blood flow.
Historical Perspectives
Published in Mark R. Lovell, Ruben J. Echemendia, Jeffrey T. Barth, Michael W. Collins, Traumatic Brain Injury in Sports, 2020
Scott D. Bender, Jeffrey T. Barth, James Irby
Though the exact pathophysiology of SIS is poorly understood, available evidence suggests that the first impact results in subclinical edema and increased intracranial pressure (ICP), which make the brain susceptible to further injury. Significant ICP following the second impact impairs blood flow and causes severe tissue damage (“malignant cerebral edema”). Recent studies suggest that the reduction in blood flow is due to autoregulatory dysfunction and consequent vascular congestion (Alves & Polin, 1996). It appears that the vasoconstriction associated with Ca2+ influx near the site of injury is specifically responsible for the reduced blood flow (Wojtys et al., 1999).
Diseases of the Nervous System
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Snake venoms contain a complex mixture of toxic proteins which act on several organs with ensuing neurotoxicity or hemolysis.589 Snake neurotoxins are rapidly absorbed from subcutaneous tissues and distributed throughout the body, with high concentration at the motor end plates, where the primary action manifests. Scorpion venoms or scorpamines are lethal neurotoxins. They contain small basic proteins and hyaluronidase which increase capillary permeability. The mechanism of action of these toxins resides in the presence of disulfide bridges and lysine residues.71,168,411 Certain spider’s bites cause a variety of signs, ranging from local pain and necrosis to systemic hemolysis and nervous system dysfunction. Tarantulas secrete occasionally toxic venom, but the most toxic is the black widow spider, Lactrodectus mactans, which causes frequent and severe neurologic dysfunction.,71,589 Bee stings can exert nervous system actions. Severe anaphylactic reactions are accompanied by cerebral edema and vascular congestion. Widespread demyelination can exert effects on the peripheral and central nervous system. A relationship has been reported between the action of bee stings and local mononeuropathies.508
Investigating the fate and toxicity of green synthesized gold nanoparticles in albino mice
Published in Drug Development and Industrial Pharmacy, 2023
Nosaibah Akkam, Alaa A. A. Aljabali, Yazan Akkam, Osama Abo Alrob, Bahaa Al-Trad, Hiba Alzoubi, Murtaza M. Tambuwala, Khalid M. Al-Batayneh
Histological examinations were performed on mouse tissue to investigate the effects of AuNPs. Figures 10–12 display histological images of mouse tissue after intraperitoneal administration of 50 nm AuNPs, as a single dose and daily dose. The following tissue changes were observed: Spleen: in the single-dose group, the architecture remained intact with mild congestion in the red pulp and mild white pulp follicular hyperplasia (Figure 11(A)). In the daily dose group, the architecture appeared mildly distorted with marked follicular hyperplasia in the white pulp (Figure 12(A)). Liver: the liver architecture was preserved in both the single and daily dose groups (Figures 11(B) and 12(B)). Scattered inflammatory foci containing lymphocytes were observed in the daily dose group (Figure 12(B)). Kidney: mild vascular congestion and tubular cell swelling were observed in the single-dose group (Figure 11(C)). The daily dose group exhibited moderate vascular congestion, interstitial chronic inflammatory foci, and proximal tubular atrophy (Figure 12(C)). Heart: the general architecture of the heart appeared similar in all groups (Figures 11(D) and 12(D)). Moderate vascular congestion was observed in the daily dose group (Figure 12(D)). These findings provide insights into the histological changes induced by AuNPs in the examined organs.
Mechanisms of COVID-19-induced cerebellitis
Published in Current Medical Research and Opinion, 2022
Mohammad Banazadeh, Sepehr Olangian-Tehrani, Melika Sharifi, Mohammadreza Malek-Ahmadi, Farhad Nikzad, Nooria Doozandeh-Nargesi, Alireza Mohammadi, Gary J. Stephens, Mohammad Shabani
COVID-19 affects the function and morphology of many organs and body tissues, including lungs, kidneys, heart, liver, and brain62. Several studies have reported hypoxic alterations and neuronal loss in the hippocampus, cerebral cortex, and cerebellar Purkinje cell layer, despite no signs of major thrombi or acute stroke63–65. However, some studies reported atherosclerosis and microhemorrhages in brain specimens62,66,67. Other histopathological findings include progressed myelin loss, terminal hypoxic-ischemic injury typified by necrotic neurons in the hippocampus and cerebellum, perivascular cellular infiltrates, with differing levels of axonal damage being observed62,64. The study of Bryce and coworkers66 reported that only one patient showed signs of a remarkably large cerebral artery territory infarct, and three patients demonstrated minor and sparse peripheral and deep parenchymal ischemic infarcts, while others were hemorrhagic. In addition to these microhemorrhages, some vascular congestion that worsens vascular damage and reperfusion injury has been reported62,65.
Effect of Chrysin on Endoplasmic Reticulum Stress in a Rat Model of Testicular Torsion
Published in Journal of Investigative Surgery, 2022
Ilke Onur Kazaz, Selim Demir, Gokcen Kerimoglu, Fatih Colak, Nihal Turkmen Alemdar, Ahmet Ugur Akman, Ozan Can Cekuc, Ahmet Mentese
Histological Johnsen scores were shown in Table 2, and images of testicular tissues of the groups were shown in Figure 1. Although I/R application significantly decreased the Johnsen score compared with control group (p = 0.0001), CHS treatment improved the Johnsen score close to the control group value (p = 0.0001). In addition, there was no statistically significant difference between the control group and the T/D + CHS group in terms of Johnsen scores (p > 0.05). When Figure 1 is examined, it was observed that seminiferous tubule and peritubular tissue structures was regular and there were many spermatozoa in the lumen of the seminiferous tubule in the control group (A). In T/D group, it was observed that the seminiferous tubule structure was significantly deteriorated, and there were separations and distinct vacuolizations in the epithelium lining the tubule. Hemorrhage, edema and vascular congestion findings were obtained in the peritubular tissue (B). In T/D + CHS group similar to the control group, the seminiferous tubule and peritubular tissue structures were regular and there were many spermatozoa in the seminiferous tubule lumen. Only, mild edema was observed in the peritubular tissue (C).