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PubMed1987

Reduction of phenylephrine drop size in infants achieves equal dilation with decreased systemic absorption.

We studied the effect of reducing eye drop size on the efficacy and systemic absorption of topical 2.5% phenylephrine hydrochloride in neonates and infants. Eleven neonates received an 8-microL drop volume in one eye and a 30-microL drop volume (commercial size) in the fellow eye. Mean pupillary dilation at 60 minutes was equivalent (4.86 mm vs 4.57 mm) for both eyes, respectively. The plasma phenylephrine level was determined for the two drop sizes in a second group of infants. Eight infants received an 8-microL drop volume in both eyes, while nine infants received a 30-microL drop volume in both eyes. The mean phenylephrine level at ten minutes was 0.9 ng/mL for the 8-microL drop group and 1.9 ng/mL for the 30 microL drop group. In neonates and infants, reducing the drop volume of topical phenylephrine may improve the risk-benefit ratio.

Absorption↗

PubMed2005

The transcriptional coactivator p300 plays a critical role in the hypertrophic and protective pathways induced by phenylephrine in cardiac cells but is specific to the hypertrophic effect of urocortin.

Anacardic acid is an alkylsalicylic acid obtained from cashew-nut-shell liquid, and is a potent inhibitor of p300 histone acetyl-transferase (HAT) activity. We have used anacardic acid to prevent the induction of hypertrophy in isolated neonatal rat cardiomyocytes. Hypertrophy was detected as an increase in cell size, the rearrangement of sarcomeres into a striated pattern, and the induction of embryonic genes beta-MHC and ANF. p300 inhibition was equally effective at preventing hypertrophy whether it was induced by treatment with the alpha1-adrenergic agonist, phenylephrine, or by treatment with urocortin, a member of the corticotrophin-releasing-factor family, which stimulates specific G protein-coupled receptors. Spiruchostatin A is a natural-product inhibitor of histone deacetylases (HDAC) similar to the depsipeptide FK228 molecule. We have recently synthesized spiruchostatin A and now show that, although HDACs act in opposition to HATs, spiruchostatin A has the same effect as anacardic acid, that is, it prevents the induction of hypertrophy in response to phenylephrine or urocortin. Pretreatment with either phenylephrine or urocortin reduced the extent of death observed after the exposure of isolated cardiomyocytes to simulated ischaemia and reoxygenation. Inhibition of p300 or HDAC activity eliminated the protection conferred by phenylephrine; however, it did not affect the protection conferred by urocortin. Therefore, it might eventually be possible to use chemical inhibitors such as these in a therapeutic setting to dissociate the protective effect and hypertrophic effect of urocortin, enhancing the survival of cardiomyocytes exposed to transient ischemia, while inhibiting the hypertrophic pathway that would otherwise be induced concurrently.

Anacardic Acids↗

PubMed1997

Effect of aging on norepinephrine and phenylephrine stimulated lactate production by white adipocytes.

We have recently demonstrated that adipose tissue can produce lactate independently of lipolysis in insulin-resistant rats and that lactate production depends on alpha 1-adrenergic stimulation. In this study, we have investigated the influence of aging on norepinephrine-and-phenylephrine-stimulated lactate production and glycerol production. We showed that basal and norepinephrine stimulated lactate production were significantly increased in adipocytes isolated from old vs. young rats (0.165 +/- 0.006 vs. 0.055 +/- 0.008 for basal and 0.567 +/- 0.026 vs. 0.277 +/- 0.019 mumol lactate/10(6) cells/15 minutes for norepinephrine-stimulated lactate production, respectively, p < 0.05). The sensitivity of lactate production to norepinephrine stimulation in adipocytes isolated from old rats was significantly decreased (EC50 = 523 +/- 63.7 vs. 46.7 +/- 6.34 nM, respectively, p < 0.05). Maximal lactate production obtained with norepinephrine and phenylephrine was not significantly different in either group (0.567 +/- 0.026 vs. 0.520 +/- 0.036 in old and 0.277 +/9 0.019 vs. 0 275 +/- 0.017 mumol/10(6) cell/15 minutes in young rats, respectively, ns). Lactate production by adipocytes isolated from old rats were significantly less sensitive to phenylephrine stimulation compared with young (EC50 = 3.67 +/- 1.16 vs. 0.07 +/- 0.01 nM, respectively, p < 0.05) indicating that the effects of aging on norepinephrine and phenylephrine stimulation were probably induced by a decreased number of alpha 1-adrenoceptors. The mechanism by which aging increases adipocyte responsiveness of lactate production has not yet been elucidated.

Adipocytes↗

PubMed1994

Ras activity is required for phenylephrine-induced activation of mitogen-activated protein kinase in cardiac muscle cells.

The mitogen-activated protein (MAP) kinases are a family of kinases whose activity is implicated in a number of growth and differentiation responses. Recently, we and others have shown that these kinases are activated by agonists which induce cardiac muscle cell hypertrophy. Inhibition of MAP kinase activation prevents some of the phenotypes associated with phenylephrine-induced cardiac cell hypertrophy, indicating that this activation is of functional significance. In this communication, we show that active Ras can induce MAP kinase activation in cardiac muscle cells. In addition, phenylephrine-induced activation of the MAP kinases requires Ras activity since a dominant negative Ras mutant (Ala15Ras) and a Ras-blocking, Raf mutant (C4B Raf) prevent activation of the MAP kinase Erk2 by phenylephrine. These data indicate that phenylephrine signaling to the MAP kinases is mediated through Ras.

Animals↗

PubMed2002

Phenylephrine promotes phosphorylation of Bad in cardiac myocytes through the extracellular signal-regulated kinases 1/2 and protein kinase A.

Studies in non-cardiomyocytic cells have shown that phosphorylation of the Bcl-2 family protein Bad on Ser-112, Ser-136 and Ser-155 decreases its pro-apoptotic activity. Both phenylephrine (100 microM) and the cell membrane-permeating cAMP analog, 8-(4-chlorophenylthio)-cAMP (100 microM), protected against 2-deoxy-D-glucose-induced apoptosis in neonatal rat cardiac myocytes as assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). In cardiac myocytes, phenylephrine primarily stimulates the alpha-adrenoceptor, but, at high concentrations (100 microM), it also increases the activity of the cAMP-dependent protein kinase, protein kinase A (PKA) through the beta-adrenoceptor. Phenylephrine (100 microM) promoted rapid phosphorylation of Bad(Ser-112) and Bad(Ser-155), though we were unable to detect phosphorylation of Bad(Ser-136). Phosphorylation of Bad(Ser-112) was antagonized by either prazosin or propranolol, indicating that this phosphorylation required stimulation of both alpha(1)- and beta-adrenoceptors. Phosphorylation of Bad(Ser-155) was antagonized only by propranolol and was thus mediated through the beta-adrenoceptor. Inhibitor studies and partial purification of candidate kinases by fast protein liquid chromatography showed that the p90 ribosomal S6 kinases, p90RSK2/3 [which are activated by the extracellular signal-regulated kinases 1 and 2 (ERK1/2)] directly phosphorylated Bad(Ser-112), whereas the PKA catalytic subunit directly phosphorylated Bad(Ser-155). However, efficient phosphorylation of Bad(Ser-112) also required PKA activity. These data suggest that, although p90RSK2/3 phosphorylate Bad(Ser-112) directly, phosphorylation of this site is enhanced by phosphorylation of Bad(Ser-155). These phosphorylations potentially diminish the pro-apoptotic activity of Bad and contribute to the cytoprotective effects of phenylephrine and 8-(4-chlorophenylthio)-cAMP.

Animals↗

PubMed1990

The alpha 1-agonist phenylephrine inhibits voltage-gated Ca2(+)-channels in vascular smooth muscle cells of rabbit ear artery.

The effects of the alpha 1-agonist phenylephrine on the voltage-gated Ca2(+)-entry in vascular smooth muscle cells has been studied by measuring the agonist-induced changes of [Ca2+]i in K(+)-depolarized tissues. These changes have been estimated from the changes in fluorescence of the Ca2(+)-indicator fura-2, or have been assessed from the changes in 86Rb-efflux rate through Ca2(+)-activated K(+)-channels. Phenylephrine increases the force development in K(+)-depolarized tissues, but reduces [Ca2+]i and inhibits the 86Rb-efflux rate. However, in the presence of the Ca2(+)-entry blocker verapamil, phenylephrine increases both force development and [Ca2+]i. It is concluded that phenylephrine inhibits voltage-gated Ca2(+)-channels, and also induces an influx of calcium by activating a verapamil-insensitive pathway.

Animals↗

PubMed1984

Effects of (-)-phenylephrine on force of contraction in the presence of cocaine and hydrocortisone in cat papillary muscle.

The positive inotropic effect of (-)-phenylephrine, in the presence of propranolol, was studied after inhibition of neuronal and extraneuronal uptake in isolated papillary muscles from reserpine-pretreated cats. An inhibition of extraneuronal uptake with hydrocortisone influenced the effect of (-)-phenylephrine neither when present alone nor in the presence of cocaine (additional inhibition of neuronal uptake). An inhibition of neuronal uptake with cocaine caused a small but significant increase in the potency of (-)-phenylephrine. We conclude that in cat ventricular cardiac muscle the extraneuronal compartment is apparently neither a "site of loss" nor a "site of gain" for (-)-phenylephrine with respect to force of contraction.

Animals↗

PubMed1999

[Clinical use of mydriasis with 10% phenylephrine and its antagonism by 0.5% dapiprazole].

BACKGROUND: Dapiprazole hydrochloride is an alpha-1-adrenergic inhibitor that anticipates the mydriatic effect of phenylephrine in dilator muscle receptors in a competitive way. The aim of this study was to determine for which indications for mydriasis pupil dilation by phenylephrine alone is sufficient and if the reversal by dapiprazole is convenient and the practical. MATERIAL AND METHOD: In 286 eyes of 147 outpatients, the pupil was dilated for fluorescein angiography-FLA (100 eyes of 50 patients), examination of the fundus-Fd (99 eyes of 52 patients), central argon laser coagulation-cALC) (64 eyes of 32 patients), peripheral argon laser coagulation-pALC (16 eyes of 9 patients) and Nd:YAG capsulotomy (7 eyes of 4 patients) with phenylephrine 10% eyes drops, followed by reversal by dapiprazole 0.5%. The width and mobility of the pupil were tested at intervals of 10 min. When mydriasis by phenylephrine was insufficient, tropicamide was applied additionally. RESULTS: In 98% of FLA with scanning laser ophthalmoscope, 75% of cALC, 76% of Fd, 62% FLA with fundus camera and 38% of pALC, mydriasis could be reached that was sufficient for the indication. Diabetics showed significantly more sluggish pupil mobility (t1/2: P < 0.05 mydriasis, P < 0.005 reversal). The mean duration after using dapiprazole until reaching the starting value (+/- 1 mm) of the pupil was 44.3 +/- 26.3 min. In 86% of the examined eyes, the pupil reached its starting value within 1 h. The subjective degree of satisfaction with the application of dapiprazole was "satisfied" to "very satisfied" (5.4 +/- 1.4 points on a scale from 1 to 7 points). DISCUSSION AND CONCLUSION: In fundus examination, fluorescein angiography by a laser scanner, diagnostic retinal examination and central laser coagulation, the combination phenylephrine/dapiprazole was most suitable. In our opinion, the combination is less suitable for peripheral argon laser coagulation and fluorescein angiography using a fundus camera.

Adolescent↗

PubMed1994

Systolic time intervals after phenylephrine administration for early stratification of patients after acute myocardial infarction.

This study was designed to assess the usefulness of the changes in left ventricular (LV) systolic time intervals after phenylephrine administration for detecting high-risk patients soon after acute myocardial infarction by correlation with the angiographic and ventriculographic findings. The procedure was performed in 76 consecutive patients (group I) on the fourth postinfarction day and in 12 normal subjects (group II) free of coronary artery disease. In 20 patients with LV ejection fraction < or = 40% (subgroup IA) the preejection period (PEP)/LV ejection time (ET) ratio increased from 0.410 +/- 0.107 to 0.535 +/- 0.102 (p = 0.01) after phenylephrine, whereas in the remaining 56 patients (subgroup IB) with LV ejection fraction > 40% and in the 12 normal subjects the PEP/LVET increased nonsignificantly. Of patients with LV ejection fraction > 40% a subset of 20 patients was distinguished with proximal stenosis in both left anterior descending and either a dominant right or left circumflex coronary artery (subset IB-a). In these the PEP/LVET increased from 0.347 +/- 0.056 to 0.445 +/- 0.019 (p = 0.0001) after phenylephrine, whereas in the remaining 36 patients (subset IB-b) without proximal lesions in 2 main arteries the PEP/LVET increased nonsignificantly. In conclusion, the PEP/LVET response to phenylephrine administration early after acute myocardial infarction is a precise, safe, noninvasive bedside method for early stratification of these patients.

Adult↗

PubMed1994

Effect of pre-treating rat atria with potassium channel blocking drugs on the electrical and mechanical responses to phenylephrine.

Action potential duration (APD) and systolic developed tension (SDT) were recorded from electrically paced rat atria before, during and after treatment with phenylephrine in vitro. Phenylephrine caused a prolongation of APD and an increase in SDT, the magnitude of which depended upon the frequency of pacing of the atria. Effects very similar to those elicited by phenylephrine were produced by exposing the atria to 4-aminopyridine, 3,4-diaminopyridine, CsCl, amantadine or sparteine. Atria that had been pre-treated with any of the latter five compounds showed a diminished responsiveness when subsequently treated with maximally effective concentrations of phenylephrine, and vice versa. These findings are consistent with blockade of potassium ion channels being responsible for the observed responses to all of the above agents.

4-Aminopyridine↗

PubMed1976

Biochemical and mechanical effects of phenylephrine on the heart.

Injections of phenylephrine into isolated perfused guinea pig hearts increased cyclic AMP and phosphorylase a. Reserpine pretreatment or propranolol decreased or abolished the phenylephrine-induced biochemical changes without affecting the contractile response. Phentolamine, on the other hand, shifted the phenylephrine dose-response curve for contractility to the right without affecting the other parameters. The biochemical effects of phenylephrine are apparently due to the release of noradrenaline while the contractile effect is mediated directly through stimulation of alpha-adrenoceptors.

Animals↗

PubMed1983

Antisecretory effects of berberine with morphine, clonidine, L-phenylephrine, yohimbine or neostigmine in pig jejunum.

The effects of berberine alone or in combination with morphine, clonidine, L-phenylephrine or yohimbine were compared in Escherichia coli heat-stable enterotoxin (ST)-exposed ligated jejunal loops in 2 week old pigs. In addition, net water and electrolyte fluxes in normal jejunal loops were measured in the presence of neostigmine, morphine, clonidine, L-phenylephrine or yohimbine alone or in combination with berberine. Berberine, morphine, clonidine and L-phenylephrine each reduced the net secretion of water and electrolytes induced by ST (P less than 0.05). A significant enhancement of antisecretory effect was observed only with the combination of berberine and L-phenylephrine. Yohimbine or neostigmine augmented the net loss of water and electrolytes produced by ST. Yohimbine did not block the antisecretory action of berberine. In normal jejunum, there was no significant difference in water and ion absorption between adrenergic or opiate agonists alone and their combination with berberine. Neostigmine reversed absorption to net secretion in normal jejunum and this effect was significantly reduced by berberine. The anti-secretory action of berberine appears similar to that of alpha 2-adrenergic agonists, opiates, and anticholinergic agents.

Animals↗

PubMed1995

Identification of alpha 1-adrenoceptor subtypes involved in the antinatriuretic response to intrarenal infusion of phenylephrine.

It is reported that alpha 1-adrenoceptors located in the renal vasculature and renal tubules play a major role in mediating antinatriuretic response to renal nerve stimulation as well as to the infusion of alpha 1-adrenoceptor agonist. In the present study intrarenal infusion of alpha 1-adrenoceptor agonist phenylephrine (0.25 microgram/kg/min) to Inactin-anesthetized Sprague-Dawley rats produced approximately 50% reduction in urine output, Na+ excretion and glomerular filtration rate without causing significant alterations in mean blood pressure, heart rate and fractional Na+ excretion. These changes were completely abolished by prior intrarenal infusion of prazosin (0.5 microgram/kg/min for 30 min). In separate groups of experiments, the animals received either a selective irreversible alpha 1A-adrenoceptor antagonist, SZL-49 [1-(4-amino-6,7-dimethoxy-2-quinazolinyl)-4-(2-bicyclo[2,2,2]octa-2,5- diene-2-carbonyl)piperazine], or an alpha 1B-adrenoceptor antagonist, chloroethylclonidine, intrarenally prior to phenylephrine infusion. Neither SZL-49 nor chloroethylclonidine alone significantly altered glomerular filtration rate and renal electrolyte excretion. However, SZL-49 (0.15 microgram/kg/min), but not chloroethylclonidine (50 micrograms/kg/min), completely abolished phenylephrine-induced changes in urine output, Na+ excretion and glomerular filtration rate. These results demonstrate that phenylephrine decreases urine output and Na+ excretion, mainly due to a reduction in glomerular filtration rate resulting from activation of alpha 1A-adrenoceptors, and that proximal tubular alpha 1A- or alpha 1B-adrenoceptors do not appear to contribute to this response.

Adrenergic alpha-Agonists↗

PubMed1996

Vascular alpha 1D-adrenoceptors have a role in the pressor response to phenylephrine in the pithed rat.

In rats, the pressor response to intravenous (i.v.) phenylephrine is mediated by vascular alpha 1A- and alpha 1B-adrenoceptors, but the role of alpha 1D-adrenoceptors is uncertain. These studies evaluated the effect of a selective alpha 1D-adrenoceptor antagonist, BMY 7378 (8-[2-[4-(2- methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspirol[4,5]decane-7,9-dio ne 2HCl), on the pressor effect to i.v. phenylephrine (alpha 1A/B/D-adrenoceptor agonist) and (R)A-61603 (alpha 1A-adrenoceptor agonist; N-[5-(4,5-dihydro-1 H-imidazol-2yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-l -yl] methanesulfonamide HBr) in pithed rats. Pretreatment with BMY 7378 (0.1-1 mg/kg) competitively antagonized the phenylephrine pressor response, but not the (R)A-61603 pressor curve. At 10 mg/kg, BMY 7378 antagonized the (R)A-61603 response, indicating the non-selective blockade of alpha 1A-adrenoceptors. These findings demonstrate that i.v. phenylephrine can activate vascular alpha 1D-adrenoceptors in the pithed rat.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1983

Effect of phenylephrine on pyruvate dehydrogenase activity in rat hepatocytes and its interaction with insulin and glucagon.

In isolated rat hepatocytes phenylephrine promotes a rapid increase in the amount of pyruvate dehydrogenase present in its active form (PDHa). This action is mediated by alpha 1-adrenergic receptors and is not observed in Ca2+-depleted hepatocytes. It is mimicked by the Ca2+ ionophore A23187. No changes in metabolites known to affect PDH activity are measured 3 min after addition of phenylephrine. Glucagon also increases PDHa, its action is additive to that of phenylephrine. The action of phenylephrine on PDHa could be explained by an increase in mitochondrial free Ca2+.

Animals↗

PubMed1991

Contractile responses of rat aorta to phenylephrine and serotonin, and aging.

1. The potency (pD2 value) of phenylephrine increased with age from 3 to 10 weeks, but decreased thereafter from 10 to 80 weeks, while the affinity (pKA value) of phenylephrine to alpha 1-adrenoceptors did not alter with aging. 2. The potency (pD2 value) of serotonin did not alter with aging. 3. There is no significant difference between slopes of regression lines between a cytosolic free Ca2+ level ([Ca2+]i) and tension in the presence of phenylephrine in aorta strips from 10- and 60-week-old rats, suggesting that the sensitivity of contractile system to Ca2+ did not alter with aging. 4. Effect of ryanodine on the transient increase of [Ca2+]i and the followed sustained contraction induced by phenylephrine or serotonin in Ca2+ free solution did not alter with aging.

Aging↗

PubMedDate not supplied

Phenylephrine in the prevention of hypotension following spinal anesthesia for cesarean delivery.

STUDY OBJECTIVE: Phenylephrine and ephedrine were compared in the prevention of maternal hypotension following spinal anesthesia for elective cesarean delivery. DESIGN: Randomized, double-blind trial. SETTING: Obstetric suite at a university-affiliated hospital. PATIENTS: Sixty healthy patients electively scheduled for cesarean delivery under spinal anesthesia. INTERVENTIONS: Patients were randomly assigned to receive either ephedrine (n = 29) in 10 mg intravenous (IV) bolus injections or phenylephrine (n = 31) in 80 microgram IV bolus injections to maintain systolic blood pressure (SBP) above 100 mmHg. MEASUREMENTS AND MAIN RESULTS: Maternal venous, umbilical artery, and umbilical vein blood gases were measured, and neonatal Apgar scores and Early Neonatal Neurobehavior Scale scores were assessed. In the ephedrine group, umbilical artery pH was 7.28 +/- 0.01 (mean +/- SEM), umbilical artery partial pressure of carbon dioxide (PCO2) was 56.6 +/- 1.4 mmHg, and umbilical artery base deficit was 2.2 +/- 0.04 meq. In the phenylephrine group, umbilical artery pH was 7.32 +/- 0.01, umbilical artery PCO2 was 52.1 +/- 1.3 torr, and umbilical artery base deficit was 0.38 +/- 0.35 meq. There were significant differences between the groups in mean umbilical artery pH, PCO2, and base deficit, although all values obtained were within normal limits. There were no significant differences between the groups in the remaining acid-base values, neonatal Apgar scores, Early Neonatal Neurobehavior Scale scores, or frequency of maternal nausea and vomiting. CONCLUSIONS: Phenylephrine is as effective as ephedrine in the treatment of maternal hypotension, and when used in small incremental bolus injections, it appears to have no adverse neonatal effects in healthy, nonlaboring parturients.

Anesthesia, Obstetrical↗

PubMed2005

Hemodynamic effects of spinal anesthesia and simultaneous intravenous bolus of combined phenylephrine and ephedrine versus ephedrine for cesarean delivery.

BACKGROUND: Hypotension following spinal anesthesia for cesarean delivery can produce adverse maternal symptoms and neonatal acid-base effects. Single-agent prophylaxis, most notably with ephedrine, does not reliably prevent spinal anesthesia-induced hypotension; recently, however, the prophylactic use of phenylephrine with ephedrine as an infusion was observed to be effective. We postulated that this combination, when given as an intravenous bolus for prophylaxis and rescue treatment, could be similarly effective. METHOD: Forty-three term parturients were randomized to receive a bolus of ephedrine 10 mg +/- phenylephrine 40 microg (groups E and EP, respectively) simultaneously with spinal anesthesia. Hypotension was defined as a systolic blood pressure below 100 mmHg or a decrease of 20% from a baseline value. Rescue boluses comprised of ephedrine 5 mg +/- phenylephrine 20 microg. RESULTS: For groups E and EP, respectively, the incidence of hypotension was 80% vs. 95% (P=0.339), with the mean number of rescue boluses being 3.85+/-3.7 and 3.05+/-1.7 and the mean umbilical artery pH being 7.246+/-0.081 vs. 7.244+/-0.106. All comparisons were not significant (NS). CONCLUSION: The combination of ephedrine and phenylephrine given as an intravenous bolus at the doses selected is not superior to ephedrine alone in preventing or treating hypotension in healthy parturients undergoing cesarean delivery.

Adult↗