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Effects of Antithrombotic and Results of Drug Screening
Published in Josef Hladovec, Antithrombotic Drugs in Thrombosis Models, 2020
All these data supported the use of our models for testing adrenolytics as they particularly stress the role of endothelial function in thrombogenesis. Endothelial cells are known to possess both beta2- and alpha2-adrenergic receptors as well as receptors for propranol- ol.491–493 addition, they contain enzymes of catecholamine metabolism.494, 495 Epinephrine has been shown to injure endothelial cells under an electron microscope by Sunaga et al.496 The influence of adrenolytics may be based on the membrane-stabilizing effects of some adrenomimetic and adrenolytic drugs.497, 498 An endothelial factor has been shown to inhibit the influx of calcium ions into the smooth muscles of the vessel wall, and in this way, an intact endothelium may modulate the alpha-adrenergic receptor stimulated contractions.466
Gender Issues in Brain Injury
Published in Mark R. Lovell, Ruben J. Echemendia, Jeffrey T. Barth, Michael W. Collins, Traumatic Brain Injury in Sports, 2020
Roof and colleagues (1993) measured cerebral edema following cerebral contusion in rats. Normally cycling females exhibited less edema than males, and pseudopregnant females were virtually spared from post-injury edema. The presence of estrogen was not necessary for this effect. It was postulated that progesterone may improve the blood-brain barrier function post-injury either by influencing ion transport via Na+, K+-ATPase (Chaplin, Free, & Goldstein, 1981), by influencing the astroglial-inducer or the endothelial-effector cell components of the blood-brain barrier (Wolff, Laterra, & Goldstein, 1992) or by inhibition of vessel growth associated with leaky blood-brain barrier function following brain injury (Plum, Alvord, & Posner, 1963). A second study by Roof and colleagues (1994) demonstrated that progesterone injections following posttraumatic medial frontal contusive injury reduced edema and were equally effective in female and male rats. Progesterone is postulated to be a free radical scavenger (Betz & Coester, 1990; Olson, Poor, & Beck, 1988) and may act to reduce peroxidative damage. It appears to have a membrane stabilizing effect that reduces damage caused by lipid peroxidation. It may also provide neuroprotection by suppressing neuronal hyperexcitability (Roof & Hall, 2000). Thus, treatment may limit tissue breakdown and edema formation limiting secondary damage and cognitive sequelae.
Interaction of Drugs of Dependence With Receptors
Published in S.J. Mulé, Henry Brill, Chemical and Biological Aspects of Drug Dependence, 2019
These findings suggested a theoretical basis for mescaline activity5 involving the ability of the drug to destabilize membranes during its passage through the CNS. The ability of chlorpromazine to block the psychotomimetic effects of mescaline is attributed to the powerful membrane-stabilizing effects of the neuroleptic at low doses.4,5,83
Tempol (4-hydroxy tempo) protects mice from cisplatin-induced acute kidney injury via modulation of expression of aquaporins and kidney injury molecule-1
Published in Drug and Chemical Toxicology, 2022
Mohd Amir Afjal, Poonam Goswami, Shahzad Ahmad, Sadaf Dabeer, Juheb Akhter, Mohd Salman, Anuradha Mangla, Sheikh Raisuddin
Tempol is a pharmaceutical compound of interest. It is a membrane-permeable radical scavenger with SOD mimetic activity and other antioxidant activities such as anti-lipid peroxidation (LPO) (Ahmed et al. 2014, Youn et al. 2016). Most of the antioxidants have membrane stabilizing effect, as they prevent LPO as the first order of defense. LPO has cascading effect not only on cell membrane but also on cellular functions and intracellular homeostatis. Antioxidants also augment cell membrane integrity. AQPs are membrane proteins and therefore an antioxidant by way of its protective effect on cell membrane/LPO is likely to protect AQPs. AVP is reported to regulate AQP (He and Yang 2019). It has been shown that tempol prevents renal proximal tubular cell apoptosis, and inhibits mitochondrial dysfunction, DNA damage and inflammation (Ahmed et al. 2014, Youn et al. 2016, Soni et al. 2018, Afjal et al. 2019). In this study, we explored effect of tempol on AQP and AVP expression in case of CP-induced AKI in mice. Tempol pretreatment showed a significant restoration in mRNA expression of AQP1, AQP2, AQP3, AQP4, AVP and KIM-1 in mice which also helped in AQP accumulation at the apical membrane of mouse kidney. This may be one of the factors which might have resulted in protection afforded by tempol to AVP/AQPs. However, more confirmatory studies are required to conclusively prove this relationship.
Toxicity of chloroquine and hydroxychloroquine following therapeutic use or overdose
Published in Clinical Toxicology, 2021
Cassandra Doyno, Diana M. Sobieraj, William L. Baker
The effect of chloroquine and hydroxychloroquine on cardiac conduction has garnered considerable interest in recent years [40]. In vivo studies and feline models show chloroquine blocks the inward rectifying potassium current, sodium current, and L-type calcium current [41,42]. These membrane-stabilizing effects can lead to QRS interval widening, atrioventricular nodal conduction slowing or blockade, and QT interval prolongation. Appreciably higher drug concentrations may be required to exert these physiologic effects than those observed with routine chloroquine or hydroxychloroquine use [34]. A healthy-volunteer study by Mzayek et al. [43] showed prolongation of the Bazett-corrected QT interval by 16 ms (95% confidence interval 9–23 ms) 4 h after a single chloroquine 600 mg dose. Case reports of corrected QT interval prolongation using lower hydroxychloroquine doses exist [44], although are often complicated by pre-existing conduction abnormalities or co-administration of QT-prolonging medications [45]; the latter will be discussed later in this review. A systematic review of clinical trials for malaria treatment revealed rare reports of electrocardiographic abnormalities or ventricular arrhythmias with chloroquine use [40]. The World Health Organization came to the conclusion in its 2016 report evaluating the cardiotoxicity of antimalarials that drug-induced torsades des pointes and life-threatening ventricular tachyarrhythmias are very rare events [46].
Diallyl sulfide alleviates cyclophosphamide-induced nephropathic encephalopathy in rats
Published in Toxicology Mechanisms and Methods, 2020
Shereen M. Galal, Heba H. Mansour, Abeer A. Elkhoely
Administration of CP induced hyper-kalemia, hyper-natraemia and hypercalcemia. Concordant with our results, previous report postulated that, CP-induced injury in the renal vasculature, which includes urine sediment abnormalities, electrolyte imbalances, filtration surface area alterations, mesangial cells contraction and leading to a reduction in the glomerular filtration rate (Singh et al. 2014). On the other hand, the changes in the levels of sodium, potassium and calcium in CP group might be ascribed to damage of cellular integrity, suppression of Na+/k + ATPase function as result of lipid peroxidation production, energy depletion and fluctuations in ratio of extracellular and intracellular volume (Alnumair et al. 2012). In the cell, ATPase are strictly coupled with the plasma membrane and contribute to the energy dependent transport of sodium, potassium and calcium translocation. This electrolyte changes might be due to the direct action of CP on the kidney and not on the urinary tract (Arafa 2009). Our data show that DAS did not induce any variation on electrolytes levels. On the other hand, DAS administration prior CP induced significant decrease in serum sodium, potassium and calcium levels. This may be due to the ability of DAS to regulate the electrolyte levels via prevention of sulfhydryl-group of the ATPases from oxidative damage via the inhibition of peroxidation of membrane lipids demonstrating the membrane stabilizing effects of DAS (Chung 2006). The prevention of electrolyte imbalances may lead to lessening the adverse action during the administration of anticancer drugs (Liamis et al. 2016).