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PubMed2005

Phenylephrine to increase blood flow in the radial artery used as a coronary bypass conduit.

OBJECTIVE: The radial artery has more smooth muscle in its wall than the other arterial conduits and is known to be vasospastic. Because it is frequently necessary to use vasoconstrictors early after coronary bypass surgery we investigated the effects of phenylephrine on conduit flow in this setting. METHODS: Thirty patients undergoing coronary artery bypass with all arterial conduits in which the radial artery was used as a T-graft were randomly assigned to receive intravenous infusions of normal saline (n = 10); nitroglycerin, 0.5 microg x kg x min (n = 11); or nicardipine, 0.5 microg x kg x min (n = 9), beginning early in the operation. After discontinuation of cardiopulmonary bypass and achievement of stable hemodynamics, control measurements were obtained, and this was followed by phenylephrine infusion to achieve a 20% increase in mean arterial pressure, after which the measurements were repeated. RESULTS: Mean radial artery flow increased similarly in all groups: normal saline, 40% +/- 25%; nicardipine, 37% +/- 27%; nitroglycerin, 48% +/- 36% (P = .533). Comparable changes occurred in arterial pressure and systemic vascular resistance, whereas the cardiac index remained unchanged. CONCLUSION: Radial artery blood flow increases when the mean arterial pressure is increased with phenylephrine. There was no evidence of a conduit vasoconstrictive effect, which could limit or reduce conduit flow. Vasoconstriction with phenylephrine is appropriate to provide adequate perfusion pressure for radial artery grafts.

Blood Flow Velocity↗

PubMed2004

Effects of prostanoids on phenylephrine-induced contractions in the mesenteric vascular bed of rats with streptozotocin-induced diabetes mellitus.

The main aim of this study was to compare the vascular reactivity of the perfused (Krebs, 4 ml/min) mesenteric vascular bed (MVB) isolated from rats with streptozotocin (STZ)-induced diabetes of 8 weeks duration to that of the MVB from non-diabetic (ND) Wistar rats. There were no differences in basal perfusion pressure between the MVB isolated from STZ and ND rats. The addition of indomethacin to the perfusate increased the basal perfusion pressure in both ND (18.8 +/- 0.7 vs 29.4 +/- 3.7 mmHg, p < 0.05) and STZ rats (18.3 +/- 0.9 vs 27.2 +/- 2.6 mmHg, p < 0.05), suggesting the release of a vasodilator prostaglandin. Remotion of the endothelium did not affect this response, indicating that prostaglandin was released from vascular smooth muscle. The response to phenylephrine was reduced in STZ rats compared to ND rats (2.3 [1.6-3.8] vs 8.3 [3.5-19.4], ED50. [IC 95%]) and was not modified by removal of the endothelium or by perfusion of L-nitro-arginine (50 microM). In contrast, indomethacin was able to reduce the response to phenylephrine in ND but not in STZ rats (2.3 [1.6-3.8] vs 4.7 [3.2-6.0], ED50. [IC 95%], p=0.02), suggesting that the blunted response to phenylephrine observed in STZ was due to the abolition of the release of prostaglandin by vascular smooth muscle. In conclusion, experimental diabetes induction in the rat is followed by a reduction of the contractile effect of phenylephrine due to the lack of release of a vasoconstrictor prostaglandin from vascular smooth muscle.

Adrenergic alpha-Agonists↗

PubMed2004

Abnormal contralateral pain responses from an intradermal injection of phenylephrine in a subset of patients with complex regional pain syndrome (CRPS).

We have examined the effect of an intradermal injection of phenylephrine (1mg/0.1 ml), an alpha-1-adrenoceptor agonist in normal subjects, and patients with sympathetically-independent (SIP) and sympathetically-maintained pain (SMP). Normal subjects and SIP patients experienced only brief stinging pain, while subsets of both sympathectomized and non-sympathectomized SMP patients (6/9 and 4/8, respectively) experienced an additional abnormal pain response accompanied by mechano-allodynia around the injection site. Both the normal and abnormal pain response after intradermal phenylephrine are similar to those observed with intradermal norepinephrine. In contrast to previous reports in the literature, we found that three sympathectomized SMP patients (who, however, had failed to experience pain relief after surgical sympathectomy despite very good relief after sympathetic blocks) also experienced abnormal pain and mechano-allodynia when phenylephrine was injected to a limb contralateral to the symptomatic sympathectomized extremity. Abnormal pain response evoked by norepinephrine or phenylephrine injection in the ipsilateral symptomatic limb of SMP patients may be due to injury-evoked nociceptor responsiveness to catecholamines. However, such a response in contralateral asymptomatic limbs suggests an additional factor that more likely than not is of central origin and may or may not be related to sympathectomy and its success or failure to treat pain.

Complex Regional Pain Syndromes↗

PubMed2002

Adverse systemic effects from pledgets of topical ocular phenylephrine 10%.

PURPOSE: To report 11 cases of adverse systemic reactions to topical ocular application of phenylephrine 10% in pledget form and to discourage this method of treatment for hemostasis in laser assisted in-situ keratomileusis (LASIK) surgery and other ophthalmic uses. DESIGN: Observational case series. METHODS: The literature, reports provided to the spontaneous reporting system of the United States Food and Drug Administration and the National Registry of Drug-Induced Ocular Side Effects (Casey Eye Institute, Portland, Oregon) were reviewed. Age, sex, duration of therapy, other drugs the patient was taking, and systemic reactions are provided in the series of 11 cases with adverse systemic reactions. RESULTS: Eleven cases of adverse systemic reactions to topical ocular phenylephrine 10% applied in pledget form occurred in 8 male and 3 female patients with an age range from 1 to 76 years. All cases occurred after a single exposure, most patients noted systemic effects within minutes of phenylephrine application, and the adverse systemic reactions included severe hypertension, pulmonary edema, cardiac arrhythmia, cardiac arrest, and subarachnoid hemorrhage. CONCLUSIONS: We recommend ophthalmologists not use this method of phenylephrine application and believe it is contraindicated in ophthalmic surgery, especially when other medications may be used.

Adult↗

PubMed1993

The effect of reduced eyedrop size and eyelid closure on the therapeutic index of phenylephrine.

In this study we examined the relative effects of reducing eyedrop size (from 30 microliters to 10 microliters) and eyelid closure on the ocular efficacy and systemic absorption of 10% phenylephrine. Thirteen subjects participated in a quadruple crossover study that involved dilation with a 10-microliters and a 30-microliters drop of phenylephrine with and without eyelid closure. The 10-microliters drop was just as effective for pupillary dilation as the 30-microliters drop. Eyelid closure improved dilation for both drop sizes. Both eyelid closure and reducing the drug volume decreased systemic absorption of phenylephrine as measured by plasma concentration. When used together, eyelid closure and the smaller drop size reduced plasma concentration by 45%. The therapeutic index for 10% phenylephrine appears to be improved by using a 10-microliters drop followed by eyelid closure.

Absorption↗

PubMed1978

Phenylephrine provocative testing in the pigmentary dispersion syndrome.

Forty-nine patients with bilateral pigmentary dispersion syndrome (abnormal accumulation of pigment in the anterior chamber, principally from the posterior layers of the iris), including 31 patients with pigmentary glaucoma, underwent 10% phenylephrine testing in one eye for evaluation of liberation of pigment floaters into the anterior chamber and the influence of phenylephrine on the intraocular pressure. Ten patients with pigmentary glaucoma developed a 3+ to 4+ pigment response, but only two demonstrated a pressure rise greater than 2 mm Hg. The highest pressure rise observed was 7 mm Hg. Nine patients with pigmentary dispersion syndrome but without glaucoma also developed a 3+ to 4+ pigment response, but none of these had a pressure rise. The incidence of pigment liberation was higher in older patients and in pigmentary glaucoma patients receiving topical antiglaucoma therapy at the time of testing. The extent of iris transillumination did not correlate with the grade of phenylephrine-induced pigment liberation. Two pigmentary glaucoma patients, who did not liberate pigment or have a pressure rise when tested with phenylephrine, did exhibit spontaneous or exercise-induced liberations of pigment into the anterior chamber, with marked rises of intraocular pressure and obstruction of aqueous outflow.

Adult↗

PubMed1995

The effect of phenylephrine on Müller muscle. A blepharogram study of eyelid motion.

PURPOSE: The blepharogram technique is used to study the effect of a drug on blinking. The authors show that ocular instillation of phenylephrine, a stimulant of Müller muscle of the eyelid, accelerates the up phase of the blink. METHODS: Motion of a tiny search coil glued to the eyelid moving in a weak magnetic field modifies an induced alternating current which is amplified and used to display the position of the upper eyelid in degrees on the ordinate of a graph with time in milliseconds on the abscissa. The graph is called a blepharogram. Blepharogram studies and individual blink analysis show the effect of phenylephrine on eyelid motion (blinking). RESULTS: Instillation of phenylephrine accelerated the up phase of the blink in all ten experimental subjects. In 65% of subjects, phenylephrine also produced or increased newly described N and M blepharogram patterns. CONCLUSION: This is the first instrumental detection of the effect of a pharmacologic agent on eyelid motion. The blepharogram technique provides insight into eyelid physiology and can be used to study any neuromuscular condition that affects eyelid motion.

Adult↗

PubMedDate not supplied

Erythrodermia to pseudoephedrine in a patient with contact allergy to phenylephrine.

BACKGROUND: Phenylephrine and pseudoephedrine are sympathomimetic drugs belonging to the phenylamine family. Adverse cutaneous effects associated with these drugs have been reported but, in view of their frequent use, appear to be rare. The very close chemical structures of these drugs could explain potential cross-reactions among them but the results reported in the literature are controversial. CASE REPORT: An 18-year-old woman developed blepharoconjunctivitis after application of phenylephrine and tropicamide eye drops. Four years after this reaction, she took 1 tablet of Narine (pseudoephedrine and loratadine) and 3-4 hours later developed a generalized erythrodermic reaction. Cutaneous biopsy revealed hydropic changes in the basal layer and, in the dermis, moderate edema with slight perivascular lymphocyte and eosinophil infiltrates. Patch tests with European standard series, commercial eye drops, tropicamide, phenylephrine, pseudoephedrine and other sympathomimetic agents were applied to the patient's back. After 47 and 96 hours, only the patches with pseudoephedrine and phenylephrine were positive. CONCLUSIONS: We believe that our patient has presented two different reactions with different clinical outcome and histopathology, which are unlikely to be due to cross-reactivity between the drugs involved. We have found no similar coincidences reported int the literature.

Adolescent↗

PubMed1999

Denervation supersensitivity to phenylephrine in guinea-pig vas deferens in vivo and in vitro: functional studies on alpha1-adrenoceptors.

The objective was to estimate alterations in adrenergic receptor sites of guinea pig vas deferens, in vivo and in vitro, induced by chronic denervation. The denervation process induced an increased sensitivity (3-fold at the EC50 level) without alteration in the maximum response to phenylephrine in vitro. The sensitivity alteration was characterized by the decrease in the dissociation constant of phenylephrine for alpha-adrenoceptor [K(A): normal tissue 3.50 (0.75-16.21) x 10(-5) and denervated tissue 0.43 (0.11-1.67) x 10(-5) M, p < 0.05] without changing the dissociation constant of prazosin. A decrease in pD'2 value for phenylephrine-phenoxybenzamine, probably due to a qualitative rather than a quantitative alteration in the alpha-adrenoceptor, was also shown in vitro [pD'2: normal tissue (8.2776+/-0.0402) and denervated tissue (8.0051+/-0.0442), p < 0.05]. No change in sensitivity and maximum response to phenylephrine was observed in vivo after denervation, although an increased resistance of vas deferens to phenoxybenzamine blockade has been evidenced in this condition.

Adrenergic Agonists↗

PubMed1999

Preconditioning prevents the negative inotropic action of phenylephrine in rat isolated stunned papillary muscle.

The aim of the present study was to establish a model of ischemic preconditioning of rat isolated papillary muscle and to investigate its effect on the simulated ischemia-induced disturbances in contractility and responsiveness to isoproterenol and phenylephrine. Experiments were performed in rat left ventricle papillary muscle. The following parameters were measured: force of contraction (Fc), velocity of contraction (+dF/dt), velocity of relaxation (-dF/dt), time to peak contraction (ttp), and relaxation time at the level of 10% of total amplitude (tt10). After 60 min of simulated ischemia induced by the perfusion of isolated tissues with no-substrate solution aerated by 95% N2/5% CO2, all of the measured parameters were markedly decreased. There was not complete recovery of Fc, +dF/dt and -dF/dt after 60 min of reperfusion. Positive inotropic action of isoproterenol does not differ before and after simulated ischemia. In contrast, phenylephrine induces a positive inotropic action in non-treated, but a significant negative one in simulated ischaemia/reperfusion treated preparations. The latter effect of phenylephrine was reversed by chloroethylclonidine (CEC), a selective blocker of alpha1b-adrenoceptor, but not by WB-4101, a selective blocker of alpha1a-adrenoceptor. Ischemic preconditioning of rat isolated cardiac tissue induced by the 5 min perfusion with no-substrate solution, aerated by 95% N2/ 5% CO2, in the presence of fast electrical pacing (BCL shortened from 2000 ms to 700 ms) and 10 min reperfusion, significantly improves a recovery of the contractility and prevents phenylephrine negative inotropic action.

Adrenergic alpha-Antagonists↗

PubMed1998

Effects of epinephrine and phenylephrine on QT interval dispersion in congenital long QT syndrome.

OBJECTIVES: Measurement of QT interval dispersion during pharmacologic adrenergic stimulation was used to assess the effect of alpha- and beta-adrenergic stimulation on arrhythmic vulnerability in familial long QT syndrome (LQTS). BACKGROUND: Nonhomogeneity in the ventricular action potential duration causes electrical instability leading to life-threatening ventricular arrhythmias and is markedly increased in LQTS. QT interval dispersion measured from the electrocardiogram (ECG) can be used as an index of nonhomogeneous ventricular repolarization. METHODS: Sixteen symptomatic patients with LQTS and nine healthy control subjects were examined at baseline and during epinephrine (mainly beta-adrenergic agonist, 0.05 microg/kg body weight per min) and phenylephrine infusions (alpha-adrenergic agonist, mean 1.4 microg/kg per min). QT interval dispersion was determined from a 12-lead ECG as interlead range and coefficient of variation measured to the end (QTend) and apex (QTapex) of the T wave. RESULTS: At baseline QTend dispersion was greater in patients with LQTS compared with control subjects (mean [+/-SD] 68+/-34 vs. 36+/-7 ms, p=0.001). QTend dispersion was markedly increased in patients with LQTS by use of epinephrine (from 68+/-34 to 90+/-36 ms, p=0.002), but remained unchanged in control subjects. Phenylephrine did not affect QT dispersion in either group (all p=NS). Atrial pacing to achieve comparable heart rates during baseline and epinephrine and phenylephrine infusions did not influence the magnitude of QT dispersion in either group. QTapex dispersion analysis gave congruent results. CONCLUSIONS: Epinephrine but not phenylephrine increased QT dispersion, suggesting that beta-adrenergic stimulation provokes arrhythmias in patients with LQTS by aggravating nonhomogeneity of ventricular repolarization, whereas alpha-adrenergic stimulation is less important for arrhythmic vulnerability. The results also suggest that rapid pacing may not reduce vulnerability to arrhythmias in congenital LQTS.

Action Potentials↗

PubMed1999

Effects of age and hypertension on cardiac responses to the alpha1-agonist phenylephrine in humans.

Both aging and hypertension decrease the responsiveness of several receptor systems. The purpose of this study was to investigate the effect of aging versus hypertension on the blood pressure (BP), heart rate, and left ventricular (LV) responses to the alpha1-agonist phenylephrine in humans. Fourteen young (age, 21-40 years; range, 30+/-1 years; mean +/- SEM), and 18 older (age, 50-73 years; range, 60+/-1 years) healthy volunteers, as well as 10 young (age, 30-39 years; range, 36+/-1 years) and 15 older (age, 50- 64 years; range, 58+/-1 years) hypertensive subjects were studied. Phenylephrine was administered at four incremental rates for 8 min each. Cardiac responses were assessed by echocardiography. Phenylephrine caused twofold larger increases in systolic BP in young and older hypertensives and older normotensives, compared with young normotensives, but similar decreases in heart rate in all four groups. Younger normotensive subjects exhibited the largest decreases in stroke volume index, ejection fraction, and cardiac index in response to phenylephrine, despite similar increases in end-systolic stress for all groups. There is an age- and hypertension-related decrease in reflex vagal restraint in response to alpha1-adrenoceptor stimulation in humans, which leads to significant attenuation of the decrease in heart rate as well as in LV function in response to a pressor stimulus, and presumably therefore to enhanced systolic BP responses relative to young normotensive subjects.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Phenylephrine and norepinephrine increase dopamine transporter ligand binding in striatum.

PURPOSE: 8-(2-[18F]fluoroethyl)-2 beta-carbomethoxy-3beta-(4-chlorophenyl)nortropane ([18F]FECNT) is a radiotracer for positron emission tomography (PET) used to trace the location and binding potential (BP) of the dopamine transporter (DAT). We tested the hypothesis that adrenergic receptor agonists increase the BP of [18F]FECNT for the DAT. PROCEDURES: Anesthetized monkeys were scanned twice to determine the ligand BP at baseline and during administration of phenylephrine (3-6 microg/kg/min) or norepinephrine (0.5-1 microg/kg/min). Standard immunohistochemistry and immunoblot analyses were performed in rats to determine if the quantity of DAT changed with phenylephrine. [18F]FECNT uptake in human embryonic kidney (HEK) cells, stably transfected with DAT cDNA, was measured by gamma scintillation counting during phenylephrine. RESULTS: The PET measured BP of [18F]FECNT increased by 50% and 45% during the phenylephrine and norepinephrine infusion, respectively. The immunohistochemistry and immunoblot analyses did not show a difference in total DAT. CONCLUSION: Adrenergic agonists increase the BP of [18F]FECNT in monkey striatum.

Adrenergic Agonists↗

PubMed1998

The effect of phenylephrine and pilocarpine on pupil size and aqueous flare intensity in patients with diabetes mellitus.

PURPOSE: The aqueous flare intensity and pupillary size were studied before and after instillation of 10% phenylephrine and 4% pilocarpine in eyes with diabetes mellitus (DM). METHODS: Twenty-three patients with DM type I were compared with 30 age-matched controls, and 25 patients with DM type II were compared with 30 age-matched controls. Patients with DM were divided into two groups: 1) with mild-moderate nonproliferative diabetic retinopathy (NPDR), and 2) with advanced diabetic retinopathy (DR) which includes moderate-severe, severe NPDR and proliferative DR. The aqueous flare intensity and the horizontal diameter of the pupil were measured before and 60 minutes after topical instillation of 10% phenylephrine and 60 min after topical administration of 4% pilocarpine. RESULTS: Degree of induced mydriasis after phenylephrine instillation was not significantly different between diabetic groups and controls. Significantly less pronounced miosis was observed after stimulation of cholinergic receptors by pilocarpine in eyes with mild-moderate NPDR with DM type II and in eyes with advanced DR with DM type I and type II when compared to controls (p<0.05). Phenylephrine decreased flare intensity in all groups without a significant difference between groups. Pilocarpine instillation increased flare intensity in all groups as compared to flare intensity before any treatment. Also, a significantly smaller increase in flare intensity in eyes with advanced retinopathy in both DM type I and type II was found when compared to controls (p<0.05). CONCLUSION: Pharmacological response to cholinergic stimulation on pupil size and flare intensity is weaker in advanced stages of DR.

Administration, Topical↗

PubMed1984

Beta adrenoceptor antagonism and pressor response to phenylephrine.

Patients on beta-blockers may experience a potentially harmful blood pressure rise after topical alpha-adrenoceptors such as phenylephrine. The presumed mechanism for this enhanced pressor responsiveness is unopposed alpha-adrenoceptor activity. This possibility has been investigated in 12 patients with hypertension by infusing increasing intravenous doses of phenylephrine after 2 wk on propranolol, metoprolol, or placebo within a randomized, double-blind, crossover study design. Mean (+/- SE) phenylephrine doses required to increase systolic blood pressure by 25 mm Hg were 4.8 +/- 0.7, 4.7 +/- 0.8, and 5.3 +/- 0.9 microgram/kg on propranolol, metoprolol, and placebo; these differences are not significant. Baroreceptor-mediated decreases in heart rate during phenylephrine infusion were in the same range, 15.8, 15.6, and 17.4 mm Hg on propranolol, metoprolol, and placebo, over baseline heart rate values. In these 12 patients with hypertension, beta-blockade did not induce any appreciable enhancement of alpha-adrenoceptor activity, suggesting that patients with hypertension who receive beta-blockers do not have enhanced pressor responsiveness.

Adult↗

PubMed2001

Suppression of K(+)-induced hyperpolarization by phenylephrine in rat mesenteric artery: relevance to studies of endothelium-derived hyperpolarizing factor.

In intact mesenteric arteries, increasing [K(+)]o by 5 mM hyperpolarized both endothelial and smooth muscle cells. Subsequent exposure to 10 microM phenylephrine depolarized both cell types which were then repolarized by a 5 mM increase in [K(+)]o. In endothelium-denuded vessels, increasing [K(+)]o by 5 mM hyperpolarized the smooth muscle but K(+) had no effect after depolarization by 10 microM phenylephrine. On subsequent exposure to iberiotoxin plus 4-aminopyridine, the repolarizing action of 5 mM K(+) was restored. In endothelium-intact vessels exposed to phenylephrine, pretreatment with a gap junction inhibitor (gap 27) reduced K(+)-mediated smooth muscle repolarization without affecting the endothelial cell response. It is concluded that phenylephrine-induced efflux of K(+) via smooth muscle K(+) channels produces a local increase in [K(+)]o which impairs repolarization to added K(+). Thus, studies involving vessels precontracted with agonists which increase [K(+)]o maximize the role of gap junctions and minimize any contribution to the EDHF pathway from endothelium-derived K(+).

4-Aminopyridine↗

PubMed1994

Effect of phenylephrine on the compartmentation of inorganic phosphate in perfused rat liver during gluconeogenesis and urea synthesis: a 31P-n.m.r.-spectroscopic study.

The transport of Pi between the cytosol and the mitochondria was investigated in perfused rat liver stimulated with phenylephrine and metabolic precursors of glucose and urea: pyruvate, lactate, NH4+ and ornithine. The relative concentrations of phosphorus metabolites in the liver were measured by 31P-n.m.r. spectroscopy. When added simultaneously, phenylephrine and the precursors induced a decrease in the Pi level which in 4-5 min reached a new steady state at 73% of the control level. After 5 min or more of stimulation the ATP level had also decreased. When the stimulation ended, Pi and ATP returned to their initial levels within 15 min. In mitochondria isolated after 5 min of stimulation, Pi was increased more than 2-fold as compared with control mitochondria and, in addition, an accumulation of Pi from the perfusion buffer into the liver was observed. Phenylephrine by itself did not cause any significant changes in the ATP or Pi levels, whereas the glucose and urea precursors in the absence of phenylephrine induced a 9% decrease in Pi, while ATP remained constant. The Pi content of mitochondria isolated under these conditions was not significantly increased as compared with control mitochondria. These results showed that Pi accumulated into the mitochondria by a mechanism possibly involving exchange for malate, and that a major part of the intramitochondrial Pi was invisible by n.m.r.

Adenosine Triphosphate↗

PubMed1983

The effect of phenylephrine upon arterial pressure, carotid sinus radius and baroreflex sensitivity in the conscious greyhound.

1. A method for recording carotid sinus diameter in conscious dogs has been developed, using an ultrasound transit time technique. We have used this method to measure the distensibility of the carotid sinus in resting animals, and we have investigated the effect of injecting the vasoactive drug phenylephrine on the mechanical behaviour of the sinus wall. 2. Baroreflex sensitivity was measured in the dogs by the usual method of relating the slowing of the heart to the transient pressure rise induced by the injections of phenylephrine. 3. We have shown that phenylephrine directly reduces the radius of the carotid sinus during the measurements of baroreflex sensitivity. At a dose of 2-4 micrograms/kg, phenylephrine has an enhancing effect on the baroreflex response, possibly resulting from a modification of baroreceptor output.

Animals↗