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Journal of Optometry 2019We tested the hypothesis that changes in accommodation after instillation of Phenylephrine Hydrochloride (PHCl) observed in some studies could be caused by changes in...
PURPOSE
We tested the hypothesis that changes in accommodation after instillation of Phenylephrine Hydrochloride (PHCl) observed in some studies could be caused by changes in optics.
METHODS
We performed two experiments to test the effects of PHCl on static and on dynamic accommodation in 8 and 6 subjects, respectively. Objective wavefront measurements were recorded of the static accommodation response to a stimulus at different distances or dynamic accommodation response to a sinusoidally moving stimulus (between 1 and 3 D of accommodative demand at 0.2Hz). The responses were characterized using two methods: one that takes into account the mydriatic optical effects on the accommodation produced by higher-order aberrations of the eye and another that takes into account only power changes paraxially due to the action of the ciliary muscle and regardless of the pupil size.
RESULTS
When mydriatic optical effects were taken into account, differences in responses before and after PHCl instillation were 0.51±0.53 D, and 0.12±0.15, for static and dynamic accommodation, respectively, and were statistically significant (p<0.039). When mydriatic optical effects were not taken into account, the differences in responses before and after PHCl instillation were -0.20±0.51 D, and -0.05±0.14, for static and dynamic accommodation, respectively, and were not statistically significant (p>0.313).
CONCLUSIONS
The mydriatic effect of the PHCl causes optical changes in the eye that can reduce the objective and subjective measurement of accommodation.
Topics: Accommodation, Ocular; Adult; Ciliary Body; Female; Humans; Male; Mydriatics; Phenylephrine
PubMed: 29602687
DOI: 10.1016/j.optom.2018.01.005 -
Journal of the American Veterinary... Apr 2013To compare the outcome of horses with nephrosplenic entrapment of the large colon (NSELC) that were treated nonsurgically by IV administration of phenylephrine and...
Comparison of phenylephrine administration and exercise versus phenylephrine administration and a rolling procedure for the correction of nephrosplenic entrapment of the large colon in horses: 88 cases (2004-2010).
OBJECTIVE
To compare the outcome of horses with nephrosplenic entrapment of the large colon (NSELC) that were treated nonsurgically by IV administration of phenylephrine and exercise with that of horses treated by IV administration of phenylephrine and a rolling procedure under general anesthesia.
DESIGN
Retrospective case series.
ANIMALS
88 horses with NSELC.
PROCEDURES
Horses examined between 2004 and 2010 because of acute abdominal pain that had NSELC on the basis of findings on abdominal palpation per rectum, abdominal ultrasonography, or both were included. Medical records were reviewed to obtain information on treatment (IV administration of phenylephrine and exercise vs IV administration of phenylephrine and a rolling procedure) and outcome.
RESULTS
Overall, 85% (75/88) of horses with NSELC responded to exercise or rolling under general anesthesia. The success rate of rolling under general anesthesia (42/50 [84%]) was significantly higher than the success rate of exercise after IV administration of phenylephrine (24/38 [63.2%]). Resolution of NSELC was achieved by rolling under general anesthesia in 8 of 14 horses that initially failed to resolve with exercise.
CONCLUSIONS AND CLINICAL RELEVANCE
A rolling procedure performed under general anesthesia had a higher success rate than exercise after IV phenylephrine administration for resolution of NSELC in horses, suggesting that rolling could be considered as the initial medical treatment. The rolling procedure may be labor intensive and should only be attempted in a surgical facility in the event that exploratory laparotomy is required.
Topics: Anesthesia, General; Animals; Colon; Horse Diseases; Horses; Intestinal Obstruction; Phenylephrine; Physical Conditioning, Animal; Retrospective Studies; Sympathomimetics
PubMed: 23547680
DOI: 10.2460/javma.242.8.1146 -
Anesthesiology Jul 1997
Review
Topics: Administration, Inhalation; Adult; Cardiotonic Agents; Humans; Nitric Oxide; Phenylephrine; Respiratory Distress Syndrome
PubMed: 9232127
DOI: 10.1097/00000542-199707000-00001 -
Investigative Ophthalmology & Visual... Oct 2021Phenylephrine has been shown to affect intraocular pressure (IOP) but the mechanism of action is poorly understood. However, its action as a vasoconstrictor suggests...
PURPOSE
Phenylephrine has been shown to affect intraocular pressure (IOP) but the mechanism of action is poorly understood. However, its action as a vasoconstrictor suggests possible effects on episcleral venous pressure (EVP). In this study, we evaluated the effect of phenylephrine on EVP and IOP in healthy subjects.
METHODS
Forty eyes of 20 subjects were included. Each subject received 3 drops of phenylephrine 2.5% in one eye at 1-minute intervals. The fellow eye served as control. Blood pressure, heart rate, and IOP and EVP of both eyes were measured at baseline, 15 minutes, and 60 minutes after instillation of phenylephrine. IOP was measured by pneumatonometry. EVP was assessed by using a computer-controlled episcleral venomanometer. Changes in IOP, EVP, blood pressure, and heart rate at 15 and 60 minutes were analyzed by paired t-tests.
RESULTS
IOP increased 15 minutes after instillation of phenylephrine in both treated (P = 0.001) and control eyes (P = 0.01) and returned to baseline at 60 minutes. The change in IOP at 15 minutes was not significantly different between the 2 groups. EVP in treated eyes was unchanged at 15 minutes (P = 0.8) but decreased significantly at 60 minutes (P < 0.001). In control eyes, there was no change in EVP at any time (P > 0.6). There were no significant changes from baseline in systolic and diastolic blood pressure and heart rate after instillation of phenylephrine.
CONCLUSIONS
IOP elevation associated with topical phenylephrine is not caused by an increase in EVP in healthy subjects. Instead, EVP decreases with phenylephrine, but the mechanism remains to be determined.
Topics: Administration, Topical; Adrenergic alpha-1 Receptor Agonists; Adult; Dose-Response Relationship, Drug; Female; Healthy Volunteers; Humans; Intraocular Pressure; Male; Middle Aged; Phenylephrine; Sclera; Venous Pressure; Young Adult
PubMed: 34617960
DOI: 10.1167/iovs.62.13.4 -
Journal of Clinical Monitoring and... Jun 2019
Topics: Animal Experimentation; Animals; Hemodynamics; Phenylephrine; Stroke Volume; Veins
PubMed: 30478524
DOI: 10.1007/s10877-018-0225-1 -
Journal of the American Heart... Sep 2023Background Pathological cardiac hypertrophy is a major cause of heart failure morbidity. The complex mechanism of intermolecular interactions underlying the pathogenesis...
Background Pathological cardiac hypertrophy is a major cause of heart failure morbidity. The complex mechanism of intermolecular interactions underlying the pathogenesis of cardiac hypertrophy has led to a lack of development and application of therapeutic methods. Methods and Results Our study provides the first evidence that TRAF4, a member of the tumor necrosis factor receptor-associated factor (TRAF) family, acts as a promoter of cardiac hypertrophy. Here, Western blotting assays demonstrated that TRAF4 is upregulated in cardiac hypertrophy. Additionally, TRAF4 deletion inhibits the development of cardiac hypertrophy in a mouse model after transverse aortic constriction surgery, whereas its overexpression promotes phenylephrine stimulation-induced cardiomyocyte hypertrophy in primary neonatal rat cardiomyocytes. Mechanistically, RNA-seq analysis revealed that TRAF4 promoted the activation of the protein kinase B pathway during cardiac hypertrophy. Moreover, we found that inhibition of protein kinase B phosphorylation rescued the aggravated cardiomyocyte hypertrophic phenotypes caused by TRAF4 overexpression in phenylephrine-treated neonatal rat cardiomyocytes, suggesting that TRAF4 may regulate cardiac hypertrophy in a protein kinase B-dependent manner. Conclusions Our results revealed the regulatory function of TRAF4 in cardiac hypertrophy, which may provide new insights into developing therapeutic and preventive targets for this disease.
Topics: Mice; Animals; Rats; Proto-Oncogene Proteins c-akt; TNF Receptor-Associated Factor 4; Heart Failure; Phenylephrine; Cardiomegaly
PubMed: 37642020
DOI: 10.1161/JAHA.122.028185 -
Anesthesiology Dec 2002In our routine practice, we observed a reduced incidence of fetal acidosis (umbilical artery pH < 7.20) at cesarean delivery during spinal anesthesia when a combination... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
BACKGROUND
In our routine practice, we observed a reduced incidence of fetal acidosis (umbilical artery pH < 7.20) at cesarean delivery during spinal anesthesia when a combination of phenylephrine and ephedrine was used as first line vasopressor therapy, compared with using ephedrine alone.
METHODS
The study was randomized and double blind. It compared phenylephrine 100 microg/ml (phenylephrine group), ephedrine 3 mg/ml (ephedrine group), and phenylephrine 50 microg/ml combined with ephedrine 1.5 mg/ml (combination group), given by infusion, to maintain maternal systolic arterial pressure at baseline during spinal anesthesia for elective cesarean delivery.
RESULTS
Fetal acidosis was less frequent in the phenylephrine group (1 of 48) (P = 0.004) and less frequent in the combination group (1 of 47) (P = 0.005) than in the ephedrine group (10 of 48). The mean systolic arterial pressure was similar for the three groups: Phenylephrine group median 98% (IQR 94-103) of baseline, ephedrine group 100% (96-106) and combination group 101% (97-108) (P = 0.11). The mean heart rate was higher in the ephedrine group (median 107% [IQR 99-118] of baseline) than in the phenylephrine group (88% [82-98]) (P < 0.0001), or the combination group (96% [86-102]) (P < 0.0001). Nausea and vomiting were less frequent in the phenylephrine group (nausea 17%, vomiting 0%) than in the ephedrine group (nausea 66%, vomiting 36%) (P < 0.0001), or the combination group (nausea 55%, vomiting 18%) (P < 0.0001).
CONCLUSIONS
Giving phenylephrine alone by infusion at cesarean delivery was associated with a lower incidence of fetal acidosis and maternal nausea and vomiting than giving ephedrine alone. There was no advantage to combining phenylephrine and ephedrine because it increased nausea and vomiting, and it did not further improve fetal blood gas values, compared with giving phenylephrine alone.
Topics: Acidosis; Adrenergic alpha-Agonists; Adult; Anesthesia, Obstetrical; Anesthesia, Spinal; Blood Pressure; Cesarean Section; Double-Blind Method; Drug Therapy, Combination; Ephedrine; Female; Fetus; Humans; Infant, Newborn; Phenylephrine; Postoperative Nausea and Vomiting; Pregnancy
PubMed: 12459688
DOI: 10.1097/00000542-200212000-00034 -
BMC Complementary Medicine and Therapies Apr 2022Trans-cinnamaldehyde (TCA) is one of the main pharmaceutical ingredients of Cinnamomum cassia Presl, which has been shown to have therapeutic effects on a variety of...
BACKGROUND
Trans-cinnamaldehyde (TCA) is one of the main pharmaceutical ingredients of Cinnamomum cassia Presl, which has been shown to have therapeutic effects on a variety of cardiovascular diseases. This study was carried out to characterize and reveal the underlying mechanisms of the protective effects of TCA against cardiac hypertrophy.
METHODS
We used phenylephrine (PE) to induce cardiac hypertrophy and treated with TCA in vivo and in vitro. In neonatal rat cardiomyocytes (NRCMs), RNA sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were carried out to identify potential pathways of TCA. Then, the phosphorylation and nuclear localization of calcium/calmodulin-dependent protein kinase II (CaMKII) and extracellular signal-related kinase (ERK) were detected. In adult mouse cardiomyocytes (AMCMs), calcium transients, calcium sparks, sarcomere shortening and the phosphorylation of several key proteins for calcium handling were evaluated. For mouse in vivo experiments, cardiac hypertrophy was evaluated by assessing morphological changes, echocardiographic parameters, and the expression of hypertrophic genes and proteins.
RESULTS
TCA suppressed PE-induced cardiac hypertrophy and the phosphorylation and nuclear localization of CaMKII and ERK in NRCMs. Our data also demonstrate that TCA blocked the hyperphosphorylation of ryanodine receptor type 2 (RyR2) and phospholamban (PLN) and restored Ca handling and sarcomere shortening in AMCMs. Moreover, our data revealed that TCA alleviated PE-induced cardiac hypertrophy in adult mice and downregulated the phosphorylation of CaMKII and ERK.
CONCLUSION
TCA has a protective effect against PE-induced cardiac hypertrophy that may be associated with the inhibition of the CaMKII/ERK pathway.
Topics: Acrolein; Animals; Calcium; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cardiomegaly; MAP Kinase Signaling System; Mice; Myocytes, Cardiac; Phenylephrine; Rats; Ryanodine Receptor Calcium Release Channel
PubMed: 35468773
DOI: 10.1186/s12906-022-03594-1 -
The Journal of Veterinary Medical... Nov 2013To determine dose-dependent cardiovascular effects of dobutamine and phenylephrine during anesthesia in horses, increasing doses of dobutamine and phenylephrine were...
To determine dose-dependent cardiovascular effects of dobutamine and phenylephrine during anesthesia in horses, increasing doses of dobutamine and phenylephrine were infused to 6 healthy Thoroughbred horses. Anesthesia was induced with xylazine, guaifenesin and thiopental and maintained with sevoflurane at 2.8% of end-tidal concentration in all horses. The horses were positioned in right lateral recumbency and infused 3 increasing doses of dobutamine (0.5, 1.0 and 2.0 µg/kg/min) for 15 min each dose. Following to 30 min of reversal period, 3 increasing doses of phenylephrine (0.25, 0.5 and 1.0 µg/kg/min) were infused. Cardiovascular parameters were measured before and at the end of each 15-min infusion period for each drug. Blood samples were collected every 5 min during phenylephrine infusion period. There were no significant changes in heart rate throughout the infusion period. Both dobutamine and phenylephrine reversed sevoflurane-induced hypotension. Dobutamine increased both mean arterial blood pressure (MAP) and cardiac output (CO) as the result of the increase in stroke volume, whereas phenylephrine increased MAP but decreased CO as the result of the increase in systemic vascular resistance. Plasma phenylephrine concentration increased dose-dependently, and these values at 15, 30 and 45 min were 6.2 ± 1.2, 17.0 ± 4.8 and 37.9 ± 7.3 ng/ml, respectively.
Topics: Anesthetics, Inhalation; Animals; Blood Pressure; Cardiac Output; Cardiotonic Agents; Cardiovascular System; Dobutamine; Dose-Response Relationship, Drug; Heart Rate; Horses; Male; Methyl Ethers; Phenylephrine; Sevoflurane
PubMed: 23832627
DOI: 10.1292/jvms.13-0104 -
European Journal of Pharmacology Jul 2023A role for mitochondrial fission in vascular contraction has been proposed based on the vasorelaxant activity of the dynamin (and mitochondrial fission) inhibitors...
A role for mitochondrial fission in vascular contraction has been proposed based on the vasorelaxant activity of the dynamin (and mitochondrial fission) inhibitors mdivi-1 and dynasore. However, mdivi-1 is capable to inhibit Ba currents through Ca1.2 channels (I), stimulate K1.1 channel currents (I), and modulate pathways key to the maintenance of vessel active tone in a dynamin-independent manner. Using a multidisciplinary approach, the present study demonstrates that dynasore, like mdivi-1, is a bi-functional vasodilator, blocking I and stimulating I in rat tail artery myocytes, as well as promoting relaxation of rat aorta rings pre-contracted by either high K or phenylephrine. Conversely, its analogue dyngo-4a, though inhibiting mitochondrial fission triggered by phenylephrine and stimulating I, did not affect I but potentiated both high K- and phenylephrine-induced contractions. Docking and molecular dynamics simulations identified the molecular basis supporting the different activity of dynasore and dyngo-4a at Ca1.2 and K1.1 channels. Mito-tempol only partially counteracted the effects of dynasore and dyngo-4a on phenylephrine-induced tone. In conclusion, the present data, along with previous observations (Ahmed et al., 2022) rise caution for the use of dynasore, mdivi-1, and dyngo-4a as tools to investigate the role of mitochondrial fission in vascular contraction: to this end, a selective dynamin inhibitor and/or a different experimental approach are needed.
Topics: Rats; Animals; Mitochondrial Dynamics; Dynamins; Niacinamide; Phenylephrine
PubMed: 37179045
DOI: 10.1016/j.ejphar.2023.175786