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Obstetrical Pathophysiology of Cocaine
Published in Richard J. Konkol, George D. Olsen, Prenatal Cocaine Exposure, 2020
J. Christopher Glantz, James R. Woods
Pregnancy is not thought to be associated with altered adrenergic sensitivity in most studies, although the data are not entirely consistent. Systemic responses to infusions of norepinephrine were similar in pregnant and nonpregnant women in a study by Chesley et al.,119 and in vitro alpha adrenergic reactivity to norepinephrine does not differ in systemic vessels from pregnant and nonpregnant ewes.120 In a study by Barton et al., in which electromagnetic flow probes were used to measure uterine artery blood flow in pregnant and nonpregnant sheep, responses to infused epinephrine and norepinephrine were similar.121 In contrast, McLaughlin et al. studied sheep responses to sequential infusions of methoxamine, phenylephrine, and norepinephrine.122 Pregnancy was associated with decreased norepinephrine sensitivity, increased phenylephrine sensitivity, and no change in methoxamine sensitivity. The different responses may have been due to differences in reuptake properties among the three agonists, rather than due to differences in adrenergic receptor sensitivity.
Adrenergic Agonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Methoxamine activates α1 adrenoreceptors thereby causing vagally mediated bradycardia and vasoconstriction resulting in a prolonged rise in the blood pressure. Its use is in the treatment of hypotension occurring during surgery. This drug has contraindication in CAD and severe hypertension and can be used in caution after parenteral injection of ergot alkaloids, with congestive heart failure and hyperthyroidism (Brown et al., 1966, Florey, 2008). Methoxamine is administered by intravenous route and also by intramuscular route. Methoxamine intravenous administration gives its presser effect within 1–2 min whereas onset of activity of the intramuscular injection occurs within 15–20 min. Duration of activity of methoxamine via intravenous route is about 60 min while comparing to 90 min via the intramuscular route. Methoxamine undergoes dealkylation to form a metabolite O-dealkylated metabolite, 2-hydroxymethoxamine (Florey, 2008).
In Vivo and In Vitro Cardiac Preparations Used in Antiarrhythmic Assays
Published in John H. McNeill, Measurement of Cardiovascular Function, 2019
Rabbits. Rabbits are anesthetized initially with 5 mg/kg sodium meth-ohexital followed by 80 to 90 mg/kg chloralose over 20 min, supplemented as required.32 Ventilation initially is 10 ml/kg at 25 breaths/min and blood gases are maintained within physiological limits. Induction of torsade de pointes is sensitive to blood pH. Blood pressure and EKG leads II and V3 are recorded. Lead V3 gives the most characteristic EKG representation of torsade de pointes. Methoxamine is infused continuously at a dose of 70 nmol/kg/min (2 ml/kg/h) and the drug under test is infused over 10 min after starting methoxamine and doubled every 10 min. The end point is at least 5 consecutive undulating beats, starting with a characteristic “short-long-short” initiation sequence and an accompanying fall in blood pressure towards zero.
The nanomaterial-induced bystander effects reprogrammed macrophage immune function and metabolic profile
Published in Nanotoxicology, 2020
Peng Yuan, Xiangang Hu, Qixing Zhou
After coculture with A549 cells exposed to WS2 nanosheets for 24 h, the cell culture medium of differentiated THP-1 macrophages was removed, and the cells were washed twice with 1 mL of prewarmed PBS. Then, 1 mL of ice-cold 80:20 (v/v) methanol/water was immediately added, and the cells were scraped and collected in a 2-mL Eppendorf tube. The wells were washed again with an additional 1 mL of a methanol/water solution and combined with the previous solution. The metabolites were extracted using ice bath ultrasound (400 W, 30 min) followed by centrifugation (12 000 × g, 5 min, 4 °C). The supernatant was filtered through a 0.22-μm organic membrane filter, removed via nitrogen blowing, and lyophilized. Methoxamine hydrochloride (20 mg/mL, 50 μL) and N-methyl-N-(trimethylsilyl) trifluoroacetamide (80 μL) were added as derivatives. After derivatization, the samples (1 μL) were injected and analyzed using gas chromatography-mass spectrometry (GC-MS, 6890 N/5973, Agilent, USA). The metabolites were identified using full-scan monitoring with a detection slope of m/z 50-650, based on the National Institute of Standards and Technology (NIST) Mass Spectral Library in ChemStation software.
Moringa oleifera leaf extract induces vasorelaxation via endothelium-dependent hyperpolarization and calcium channel blockade in mesenteric arterial beds isolated from L-NAME hypertensive rats
Published in Clinical and Experimental Hypertension, 2020
Direk Aekthammarat, Patchareewan Pannangpetch, Panot Tangsucharit
Vascular smooth muscle contraction is initiated by an increase in cytosolic-free Ca2+ which promotes actin-myosin cross-bridge formation (4). The cellular mechanisms of vasoconstriction in the responses to an α1-adrenergic agonist and a depolarizing agent are different signaling pathways, but both of which converge to increase cytosolic Ca2+ concentration of vascular smooth muscle cells (26,27). Methoxamine is an α1-adrenergic agonist that raises the cytosolic Ca2+ concentration by two possible mechanisms: mobilizing Ca2+ from intracellular stores in sarcoplasmic reticulum via activating the G protein-coupled IP3 receptors, and enhancing extracellular Ca2+ entry through ROCCs and VOCCs (27). High K+ medium causes contraction through depolarizing of vascular smooth muscles which bypasses the G protein-coupled receptors leading to an increased Ca2+ entry through VOCCs (28). Since multiple mechanisms are probably involved in MOE-mediated relaxation, we investigated the important and dominant mechanisms that might be involved in endothelium-dependent and -independent pathways. Our initial investigations showed that MOE relaxed contraction of mesenteric arterial beds induced by methoxamine and high K+ in a dose-dependent manner. It could be hypothesized that MOE is able to induce vasorelaxation by interfering with a common signaling pathway of these contractile agents, such as membrane depolarization, extracellular Ca2+ entry and intracellular Ca2+ mobilization.
Attenuation of Retinal Endothelial Vasodilator Function in a Rat Model of Retinopathy of Prematurity
Published in Current Eye Research, 2019
Ayuki Nakano, Asami Mori, Shiho Arima, Daiki Asano, Akane Morita, Kenji Sakamoto, Tohru Nagamitsu, Tsutomu Nakahara
Retinal vasodilator responses were examined on P35 according to the procedures described previously.11,12 Briefly, control (n = 9) and ROP (n = 8) rats were anesthetized with sodium pentobarbital (50 mg/kg, i.p.; Nacalai Tesque). Following the loss of the corneal reflex, each animal was placed on a heating pad. We performed tracheotomy for artificial ventilation, and inserted catheters into the femoral veins for drug administration and into the left femoral artery for measuring arterial pressure and heart rate (HR). To minimize the influence of nerve activity and to capture fundus images at the same angle throughout experiment by preventing eye movements, the rats were treated with tetrodotoxin (TTX) (50 μg/kg, i.v.; Nacalai Tesque) under artificial ventilation with room air (stroke volume, 10 mL/kg; frequency, 80 strokes/min) using a rodent respirator. Both mean arterial pressure (MAP) and HR decreased after treatment with TTX; therefore, methoxamine (Sigma-Aldrich) was continuously infused into the jugular vein using a syringe pump (Model 1140–001, Harvard Apparatus, South Natick, MA, USA) to maintain adequate systemic circulation.