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Immediately after an experimental spinal cord injury (SCI) in rats, there is a large fall in mean arterial pressure (MAP) and heart rate (HR), followed by an abrupt increase in MAP. To better understand the mechanism involved in these early cardiovascular alterations, we tested the effect of treatment with ganglionic and sympathetic blockers in anesthetized rats subjected to T-5 SCI. Fall in MAP was partially diminished by propranolol and pentolinium, while increase in MAP was abolished by propranolol and pentolinium. Adrenalectomy did not diminish the fall in MAP and HR, however, the increase in MAP was significantly reduced. Likewise, propranolol and pentolinium completely abolished the effects in HR. These data suggest that the early cardiovascular alterations secondary to SCI results from an increased parasympathetic activity and a sympathetic withdrawal.
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Le propranolol est un médicament de choix pour de nombreuses maladies des nouveau-nés et des nourrissons, un groupe d’âge pour lequel les suspensions orales sont presque toujours requises. De nombreux patients adultes et âgés à qui l’on prescrit du propranolol sont également incapables d’avaler des formes pharmaceutiques solides. Au Canada, le propranolol n’est pas commercialisé sous forme liquide et les recettes actuelles pour les préparations extemporanées de ce médicament en suspension (1 mg/mL) sont limitées par des inquiétudes touchant le diabète sucré chez certaines sous-populations, le besoin d’une suspension plus concentrée chez les patients prenant de plus fortes doses et le long travail que nécessitent de telles préparations.
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Biodegradation of chiral pharmaceuticals in the environment can be enantioselective. Thus quantification of enantiomeric fractions during the biodegradation process is crucial for assessing the fate of chiral pollutants. This work presents the biodegradation of alprenolol and propranolol using an activated sludge inoculum, monitored by a validated enantioselective HPLC method with fluorescence detection. The enantioseparation was optimized using a vancomycin-based chiral stationary phase under polar ionic mode. The method was validated using a minimal salts medium inoculated with activated sludge as matrix. The method was selective and linear in the range of 10-800 ng/ml, with a R²>0.99. The accuracy ranged from 85.0 percent to 103 percent, the recovery ranged from 79.9 percent to 103 percent, and the precision measured by the relative standard deviation (RSD) was <7.18 percent for intra-batch and <5.39 percent for inter-batch assays. The limits of quantification and detection for all enantiomers were 10 ng/ml and 2.5 ng/ml, respectively. The method was successfully applied to follow the biodegradation of the target pharmaceuticals using an activated sludge inoculum during a fifteen days assay. The results indicated slightly higher biodegradation rates for the S-enantiomeric forms of both beta-blockers. The presence of another carbon source maintained the enantioselective degradation pattern while enhancing biodegradation extent up to fourteen percent.
A large heart rate (HR) increase at the onset of exercise has been linked to an increased risk for adverse cardiovascular events, including cardiac death. However, the relationship between changes in cardiac autonomic regulation induced by exercise onset and the confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, a retrospective analysis of the HR response to exercise onset was made in mongrel dogs with healed myocardial infarctions that were either susceptible (S, n = 131) or resistant (R, n = 114) to VF (induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise). The ECG was recorded, and time series analysis of HR variability (vagal activity index, the 0.24-1.04-Hz frequency component of R-R interval variability) was measured before and 30, 60, and 120 s after the onset of exercise (treadmill running). Exercise elicited significantly (ANOVA, P < 0.0001) greater increases in HR in susceptible dogs at all three times (e.g., at 60 s: R, 46.8 +/- 2.3 vs. S, 57.1 +/- 2.2 beats/min). However, the vagal activity index decreased to a similar extent in both groups of dogs (at 60 s: R, -2.8 +/- 0.1 vs. S, -3.0 +/- 0.2 ln ms2). Beta-adrenoceptor blockade (BB, propranolol 1.0 mg/kg iv) reduced the HR increase and eliminated the differences noted between the groups [at 60 s: R (n = 26), 40.4 +/- 3.2 vs. S (n = 31), 37.5 +/- 2.4 beats/min]. After BB, exercise once again elicited similar declines in vagal activity in both groups (at 60 s: R, -3.6 +/- 0.5 vs. S, -3.2 +/- 0.4 ln ms2). When considered together, these data suggest that at the onset of exercise HR increases to a greater extent in animals prone to VF compared with dogs resistant to this malignant arrhythmia due to an enhanced cardiac sympathetic activation in the susceptible dogs.
Effects of different drugs delivered by intra-brain or i.v. injections on blood pressure and heart rate were observed in rats.
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The myocardial performance index (MPI) is a Doppler-based measure of left ventricular (LV) function. It is noninvasive, independent of LV shape, and does not require dimensional measurements. However, it has never been validated in mice.
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A new approach based on miniemulsion polymerization is demonstrated for synthesis of molecularly imprinted nanoparticles (MIP-NP; 30-150 nm) with "monoclonal" binding behavior. The performance of the MIP nanoparticles is characterized with partial filling capillary electrochromatography, for the analysis of rac-propranolol, where (S)-propranolol is used as a template. In contrast to previous HPLC and CEC methods based on the use of MIPs, there is no apparent tailing for the enantiomer peaks, and baseline separation with 25,000-60,000 plate number is achieved. These effects are attributed to reduction of the MIP site heterogeneity by means of peripheral location of the core cross-linked NP and to MIP-binding sites with the same ordered radial orientation. This new MIP approach is based on the substitution of the functional monomers with a surfactant monomer, sodium N-undecenoyl glycinate (SUG) for improved inclusion in the MIP-NP structure and to the use of a miniemulsion in the MIP-NP synthesis. The feasibility of working primarily with aqueous electrolytes (10 mM phosphate with a 20% acetonitrile at pH 7) is attributable to the micellar character of the MIP-NPs, provided by the inclusion of the SUG monomers in the structure. To our knowledge this is the first example of "monoclonal" MIP-NPs incorporated in CEC separations of drug enantiomers.
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We present evidence that stimulation of the human beta-3 adrenergic receptor (AR), expressed in Chinese hamster ovary/K1 cells, specifically activates the mitogen-activated protein kinases extracellular signal-regulated kinase (ERK)1 and 2, but not JNK or p38. The extent and kinetics of the ERK stimulation by the beta-3 AR are identical with those of the endogenic insulin receptor. However, insulin augments cellular proliferation, whereas beta-3 AR agonists inhibit proliferation due to the production of cyclic AMP. The pharmacological profile of the ERK activation by the beta-3 AR differs significantly from its activation of adenylyl cyclase. The order of potency and intrinsic activities of both natural ligands, norepinephrine and epinephrine, is inversed between both signaling pathways. In addition, BRL 37344 and propranolol, ligands that act as agonists in the stimulation of cyclase, act as antagonists for ERK activation. The activation of ERK1/2 is sensitive to pertussis toxin, suggesting that the beta-3 AR, in addition to its interaction with Gs, can couple to Gi/o. Furthermore, the activation of ERK by the beta-3 AR is sensitive to PD98059, wortmannin, and LY294002, indicating a crucial role for mitogen-activated protein kinase kinase and phosphatidylinositol-3 kinase (PI3K), respectively. A beta-3 AR-mediated stimulation of PI3K is confirmed by the observation that the selective agonist CGP 12177A specifically activates protein kinase B. As was observed for the activation of ERK, the activation of protein kinase B is inhibited by preincubation with pertussis toxin and PI3K inhibitors, suggesting that both are a consequence of a Gi/o-mediated activation of PI3K.
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The organic cation transporter 2 (OCT2, SLC22A2) plays an important role for renal drug elimination. Recent clinical studies indicate an impact of the frequent nonsynonymous c.808G>T (p.270Ala>Ser) polymorphism on renal clearance of metformin and the extent of the metformin-cimetidine interaction. The role of this polymorphism for renal disposition of endogenous compounds and drugs other than metformin has not been investigated. In addition, it is unclear whether the observed genotype dependence of an OCT2-mediated drug-drug interaction might occur also with other OCT inhibitors. To address these issues, we generated human embryonic kidney cells stably expressing wild-type OCT2 or the p.270Ala>Ser variant. No differences in protein expression levels and membrane incorporation pattern were observed between the two cell lines. The p.270Ala>Ser variant significantly impaired uptake kinetics of 1-methyl-4-phenylpyridinium, dopamine, norepinephrine, and propranolol. V(max) values were significantly reduced for uptake of all four compounds mediated by the p.270Ala>Ser variant compared with wild-type OCT2. In addition, a significant difference in the affinity to wild-type and mutant OCT2 was observed for dopamine (K(m) dopamine: 932 +/- 77 versus 1285 +/- 132 microM). Moreover, out of a set of 27 compounds p.270Ala>Ser OCT2 was significantly less sensitive to inhibition by cimetidine, flurazepam, metformin, mexiletine, propranolol, and verapamil than wild-type OCT2 (e.g., for propranolol: IC(50) wild type versus p.270Ala>Ser 189 versus 895 microM, P < 0.001). Our results indicate that the common OCT2 c.808G>T single nucleotide polymorphism significantly alters uptake of endogenous compounds and drugs. Moreover, for selected compounds the extent of OCT2-mediated drug interactions could depend on OCT2 c.808G>T genotype.
This study was comprised of a literature review and interventional case report. Two (2) patients with nonresolving or recurrent CSCR were commenced on a trial of oral propranolol 40 mg twice a day and followed up at monthly intervals. Visual acuity, metamorphopsia, and central retinal thickness quantified by ocular coherence tomography (OCT) were recorded at baseline and follow-up visits.
The potential treatment with beta-blockers of patients with pancreatic cancer or other malignancies should be further evaluated as an adjuvant anti-neoplastic agent in clinical trials.
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Antigen-specific T-cell lines were generated in the presence of recombinant human IL-2 and tetanus with or without varying concentrations of (R)- and (S)-isomers of albuterol alone or in combination. Parallel lines were generated in the presence of propranolol. Cells were briefly pulsed with PHA and evaluated for proliferation, apoptosis, and cytokine secretion.