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At least 19 recordsLinked to original sources
PubMed1998

Prilocaine-phenylephrine and bupivacaine-phenylephrine topical anesthetics compared with tetracaine-adrenaline-cocaine during repair of lacerations.

The effectiveness of two new topical anesthetics that do not contain cocaine (prilocaine-phenylephrine and bupivacaine-phenylephrine) was compared with that of tetracaine-adrenaline-cocaine (TAC) during laceration repair in children. This study was a prospective, randomized, double-blind trial conducted in the emergency department of a large children's hospital. Participants were 180 children 1 year of age or older with a laceration 5 cm or less in length that required suturing. Pain felt during suturing was scored by suture technicians, research assistants, parents, and patients 5 years of age and older using a visual analogue scale (VAS). There was no statistical difference demonstrated between the effectiveness of prilocaine-phenylephrine and that of TAC for any of the observer groups. A statistically significant difference was seen among anesthetics when comparing VAS scores of research assistants (P = .002), suture technicians (P = .006), and parents (P = .03), but not when comparing VAS ratings of patients (P = .07). Based on Tukey's post hoc test, these statistically significant differences were between TAC and bupivacaine-phenylephrine. When power analyses were performed using alpha = 0.05 and beta = 0.20, it was possible to detect a difference of 1.3 VAS units for each rater group. In conclusion, this study demonstrated the effectiveness and safety of prilocaine-phenylephrine and bupivacaine-phenylephrine. Prilocaine-phenylephrine statistically outperformed bupivacaine-phenylephrine and offers an effective alternative to TAC during laceration repair in children.

Adolescent↗
PubMed1990

Ocular pharmacokinetics and pharmacodynamics of phenylephrine and phenylephrine oxazolidine in rabbit eyes.

The aqueous humor concentration of phenylephrine and its corresponding mydriatic response were measured over time in New Zealand albino rabbit eyes following a 10-microliters topical instillation of a phenylephrine HCl viscous solution (10%) or a phenylephrine oxazolidine (prodrug) suspension in sesame oil (1 and 10%). The bioavailability of a 1% prodrug suspension in the rabbit eye (AUC of aqueous humor concentration vs time) was 30% lower than that of a 10% phenylephrine solution (P less than 0.1) with the exception that the peak time occurred 34 min earlier with the prodrug. A 10% prodrug suspension increased the aqueous humor bioavailability approximately eightfold but improved the mydriatic activity (AUC of mydriasis vs time) only fourfold. The pharmacokinetic parameters, apparent absorption, and elimination rate constants, of phenylephrine and the prodrug were determined from aqueous humor concentration-time and mydriasis-time profiles. The study showed that the kinetic parameters of phenylephrine estimated from its mydriasis profile do not accurately reflect the kinetics of drug distribution in the iris. These parameters also varied with the instillation of phenylephrine solution or prodrug suspensions. A mydriatic tolerance of the pupil response was apparent after the topical instillation of phenylephrine solution. The mydriatic tolerance may be due to the decrease in receptor number in the iris dilator muscle.

Absorption↗
PubMed1998

Comparison of the cardiovascular effects of 2.5% phenylephrine and 10% phenylephrine during ophthalmic surgery.

PURPOSE: The recommended concentration of topical phenylephrine for mydriasis is still a matter of debate. Our purpose was to compare the cardiovascular effects of 10% and 2.5% topical aqueous phenylephrine. METHODS: We carried out a double-masked randomised study on 54 consecutive patients undergoing routine local anaesthetic cataract extraction, comparing the effects on blood pressure and heart rate of either 2.5% or 10% topical aqueous phenylephrine in combination with 1% topical aqueous tropicamide in those with no history of cardiovascular disease. RESULTS: No difference was found in the rise in blood pressure produced by 2.5% and 10% topical aqueous phenylephrine. We also found no sustained changes in blood pressure or heart rate after instillation of either 2.5% or 10% topical aqueous phenylephrine. CONCLUSION: We recommend the routine use of 2.5% topical aqueous phenylephrine as a mydriatic agent during cataract surgery and acknowledge the role of 10% topical aqueous phenylephrine as an effective mydriatic agent in cases where 2.5% phenylephrine may not be so effective, such as in subjects with darkly pigmented irides.

Aged↗
PubMed1996

A comparative study of the efficacy of 2.5% phenylephrine and 10% phenylephrine in pre-operative mydriasis for routine cataract surgery.

It is common practice in many ophthalmic units to administer multiple applications of 10% phenylephrine in combination with an anti-cholinergic agent to ensure adequate pupil mydriasis prior to routine cataract surgery. Phenylephrine is a pure alpha-1 adrenoreceptor agonist known to produce marked systemic vasoconstriction and associated hypertension with occasional profound reflex bradycardia. Many reviews have suggested caution in the use of 10% phenylephrine in the elderly or hypertensive patient. In a prospective, randomised trial we have assessed pupil dilation comparing the efficacy of 10% phenylephrine (53 patients) versus 2.5% phenylephrine (62 patients). When administered in conjunction with 1% cyclopentolate four times over 1 hour pre-operatively, 2.5% phenylephrine was found to be as effective as 10% phenylephrine in the initiation and maintenance of mydriasis during both extracapsular and phacoemulsification cataract extraction.

Aged↗
PubMed2001

[Biochemical stress monitoring during cataract surgery; phenylephrine 10% shows no changes in serum-catecholamines in comparison with phenylephrine 5%].

BACKGROUND: There is a controversy about the concentration of topical phenylephrine recommended for diagnostic or therapeutic mydriasis. Phenylephrine 10% leads to a faster and more pronounced mydriasis but cardio-vascular side-effects like hypertension and arrhythmia have been reported. A maximal pupillary dilatation is a prerequisite for successful cataract surgery. The aim of this study was to evaluate the risk-benefit ratio of phenylephrine 10% in comparison to 5% in the daily practice of the cataract-surgery unit in our clinic by clinical assessment and monitoring of biochemical stress parameters. PATIENTS AND METHODS: 30 informed and consenting patients were randomly allocated to 2 groups of equal size. After a single application of 2 drops of phenylephrine 5% in group 1 and 10% in group 2 respectively and 1 drops of cyclopentolate 1% with neutral pupil (time 0), an ECG was recorded and blood pressure, pulse, oxygen-saturation and pupil size were measured. Simultaneously a blood-sample was taken and the serum-catecholamines adrenaline and noradrenaline were determined by HPLC (High Pressure Liquid Chromatography). These measurements were repeated after 5, 10 and 30 minutes. RESULTS: The mean pupil area after 30 minutes in group 1 was 31.97 (+/- 0.43) mm2 compared to 45.72 (+/- 0.39) mm2 in group 2. Our data showed no other significant variation between the groups: neither clinical monitoring nor catecholamine measurements showed concentration-dependent patterns in blood pressure development or serum levels. No systemic cardiovascular effects were observed. CONCLUSION: These results demonstrate that a controlled application of phenylephrine 10%--under observation of contraindications--yields no increased risk for the occurrence of cardio-vascular side-effects in comparison with phenylephrine 5%. Therefore, we recommend the use of phenylephrine 10% in the described dosage as routine medication for cataract surgery.

Aged↗
PubMed1995

The effects of phenylephrine 2.5% versus phenylephrine 10% on pupillary dilation in patients with diabetes.

PURPOSE: A prospective, double-blind study was conducted to compare the clinical efficacy of a combination of 1% tropicamide and 2.5% phenylephrine and a combination of 1% tropicamide and 10% phenylephrine for pupillary dilation in patients with diabetes. METHODS: Either 2.5% phenylephrine in one eye and 10% phenylephrine in the other eye, 2.5% phenylephrine in both eyes, or 10% phenylephrine in both eyes was administered to 127 consecutive patients with diabetes. All patients received 1% tropicamide in both eyes. RESULTS: There was no statistically significant difference in the amount of pupillary dilation between the three groups. CONCLUSION: As 2.5% phenylephrine may produce a lower incidence of side effects than the 10% concentration, we advise the use of the lower concentration, particularly among patients with diabetes, who already exhibit a higher prevalence of vascular disease and autonomic dysfunction.

Adolescent↗
PubMed1987

In vivo comparison of phenylephrine and phenylephrine oxazolidine instilled in the monkey eye.

The ocular and cardiovascular effects as well as aqueous humor and plasma concentrations of 10% phenylephrine HCl and 1% phenylephrine oxazolidine (prodrug) were compared in cynomolgus monkeys. A volume of 25 microliters of either drug was administered to one eye followed by blood pressure, pulse, and pupillary measurements at 10 min intervals up to 60 minutes. Careful slit lamp examinations of the anterior segment, indirect ophthalmoscopy of the vitreous and retina, and ERGs were performed at 60 minutes. Four plasma determinations of phenylephrine following administration of either drug were made between 5 and 60 minutes. Measurement of phenylephrine in aqueous humor was also determined at 60 minutes following all other measurements. The maximal pupillary dilation after administration of 1% prodrug (mean + s.d. = 4.4 + 0.5 mm, n = 12) was slightly greater than after administration of phenylephrine 10% (mean + s.d. = 3.9 + 0.8 mm, n = 12). The differences in pupillary diameter from 20 through 40 minutes were statistically greater for the prodrug. The greater pupillary diameter at the earlier times resulted in an onset of pupillary dilation approximately 15 minutes earlier for the 1% prodrug. There was no ocular toxicity from either drug. Neither drug resulted in any ERG changes compared to baseline. Significantly higher aqueous humor levels along with lower plasma levels were detected and found to be statistically different following administration of the 1% prodrug when compared to 10% phenylephrine.

Animals↗
PubMed1980

Mydriatic effect of phenylephrine 10% (aq) vs phenylephrine 2.5% (aq).

Pupil dilation from commercially available phenylephrine compounds was studied in a group of 11 subjects. Phenylephrine 10% (aq) did not produce significantly more mydriasis than phenylephrine 2.5% (aq) in the general population (P less than 0.05). This suggests that phenylephrine 2.5% can be used instead of phenylephrine 10% for diagnostic dilation.

Adult↗
PubMedDate not supplied

Ocular absorption and disposition of phenylephrine and phenylephrine oxazolidine.

The ocular bioavailability of phenylephrine oxazolidine (PO), a prodrug intended for rapid corneal penetration, was micronized and suspended in sesame oil (1 and 10 per cent) and compared in bioavailability to phenylephrine HC1 (PE) dissolved (10 per cent) in a buffered (pH 5.75), viscous (30 centipoise) vehicle. Cornea and aqueous humor of New Zealand rabbits were measured over time following 10 microliter instillation to the eye. Based upon AUC measurements, corneal and aqueous humor levels were approximately 6 and 8 times greater for 10 per cent PO versus 10 per cent PE, respectively. In addition, the ocular pharmacokinetic values were determined for PE applied in a constant concentration (1 per cent) to the cornea over 180 min to anesthetized rabbits. Cornea and aqueous humor were measured for drug content over time. Using moment analysis and an initial slope method, the absorption rate constant, ka, the steady state volume of distribution in the eye, Vss, and ocular clearance, Qe, were calculated. Values obtained for PE were 4.15 x 10(-5) min-1, 0.423 ml and 14.6 microliter min-1, respectively. The half-life for drug elimination ranged from 63-83 min depending on the tissue or route of administration.

Animals↗
PubMed1997

Improvement in oxygenation by phenylephrine and nitric oxide in patients with adult respiratory distress syndrome.

BACKGROUND: Inhaled nitric oxide (NO), a selective vasodilator, improves oxygenation in many patients with adult respiratory distress syndrome (ARDS). Vasoconstrictors may also improve oxygenation, possibly by enhancing hypoxic pulmonary vasoconstriction. This study compared the effects of phenylephrine, NO, and their combination in patients with ARDS. METHODS: Twelve patients with ARDS (PaO2/FIO2 180; Murray score 2) were studied. Each patient received three treatments in random order: intravenous phenylephrine, 50-200 micrograms/min, titrated to a 20% increase in mean arterial blood pressure; inhaled NO, 40 ppm; and the combination (phenylephrine+NO). Hemodynamics and blood gas measurements were made during each treatment and at pre- and posttreatment baselines. RESULTS: All three treatments improved PaO2 overall. Six patients were "phenylephrine-responders" (delta PaO2 > 10 mmHg), and six were "phenylephrine-nonresponders." In phenylephrine-responders, the effect of phenylephrine was comparable with that of NO (PaO2 from 105 +/- 14 to 132 +/- 14 mmHg with phenylephrine, and from 110 +/- 14 to 143 +/- 19 mmHg with NO), and the effect of phenylephrine+NO was greater than that of either treatment alone (PaO2 from 123 +/- 13 to 178 +/- 23 mmHg). In phenylephrine-nonresponders, phenylephrine did not affect PaO2, and the effect of phenylephrine+NO was not statistically different from that of NO alone (PaO2 from 82 +/- 12 to 138 +/- 28 mmHg with NO; from 84 +/- 12 to 127 +/- 23 mmHg with phenylephrine+NO). Data are mean +/- SEM. CONCLUSIONS: Phenylephrine alone can improve PaO2 in patients with ARDS. In phenylephrine-responsive patients, phenylephrine augments the improvement in PaO2 seen with inhaled NO. These results may reflect selective enhancement of hypoxic pulmonary vasoconstriction by phenylephrine, which complements selective vasodilation by NO.

Adult↗
PubMed1995

The role of capacitative Ca2+ influx in the alpha 1B-adrenoceptor-mediated contraction to phenylephrine of the rat spleen.

1. The mechanism of contraction to phenylephrine in the rat spleen (mediated via alpha 1B-adrenoceptors) has been studied in functional experiments. 2. The concentration-dependent contraction of the rat spleen to cumulative additions of phenylephrine (pD2 4.8 +/- 0.1) was not significantly reduced by the selective protein kinase C (PKC) inhibitor, calphostin C (10(-6)M) or potentiated by the DAG kinase inhibitor, R59022 (10(-6) M). 3. Contraction of the rat spleen in normal Krebs solution containing Ca2+ (2.5 mM) to a single concentration of phenylephrine (3 x 10(-4) M) produced a maximal response consisting of an initial phasic component and a more slowly developing tonic component. However in Ca(2+)-free Krebs solution (containing EGTA), phenylephrine (3 x 10(-4)M) produced only a phasic contraction which was reduced to 46 +/- 3% maximum response to phenylephrine in normal Krebs solution. 4. In some tissues after the contraction to phenylephrine (3 x 10(-4) M) in Ca(2+)-free Krebs solution (containing EGTA), the phenylephrine was washed out and the tissue was allowed to recover. After 2 h, upon addition of Ca2+ (2.5 mM) to the Krebs solution (EGTA now removed) a tonic contraction developed in the tissue (97 +/- 4% maximum response to phenylephrine). 5. Cyclopiazonic acid produced a tonic contraction of the rat spleen with a maximum effect at 10(-5) M (202 +/- 8% maximum response compared with that to phenylephrine). The contraction to CPA (10(-5) M) was reduced in Ca(2+)-free Krebs solution containing EGTA (30 +/- 4% of the maximum response to phenylephrine). One hour after the end of the contraction in Ca(2+)-free Krebs solution (EGTA now removed), upon addition of Ca2+ (2.5 mM) to the Krebs solution a tonic contraction developed in the tissue (263 +/- 12% maximum response to phenylephrine). 6 In Ca2+-free Krebs solution, after the spleen had been incubated with cyclopiazonic acid for 30 min,the subsequent contraction to phenylephrine (3 x 10-4 M) was reduced from 46+/-3% to 9+/-2%maximum response to phenylephrine.7 Cumulative contractions to phenylephrine and the contraction to cyclopiazonic acid (10-5 M) in the spleen were not significantly affected by nifedipine (10-6 M). The non-selective Ca2+channel blocker,SK&F 96365 (3 x 10-5 M) reduced the maximum response for the cumulative additions of phenylephrine to 35+/-1% and the contraction to CPA (10-5 M) from 202+/-8% to 108+/-8% maximum response to phenylephrine.8 The tyrosine kinase inhibitors genistein (3 x 10-5 M and tyrphostin 23 (10-4 M), reduced the maximum response to phenylephrine in the spleen to 51+/-4% and 44+/-5% respectively and the maximum contraction to cyclopiazonic acid (3 x 10-6 M) in the spleen from 132 +/- 6% to 82 +/-5% and 80 +/- 7% maximum response to phenylephrine respectively without affecting contractions to K+.9 In conclusion, these results are consistent with the contraction of the rat spleen to phenylephrine consisting of an initial phasic contraction due to release of intracellular Ca2+ and a larger tonic contraction due to capacitative Ca2+ influx through non-voltage-gated Ca2+ channels and which may involve a tyrosine kinase. This suggests that inositol triphosphate but not diacylglycerol is involved in the contraction.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1990

Phenylephrine-induced antinociception: investigations of potential neural and endocrine bases.

Acute hypertensive states can produce antinociception, largely via unknown mechanisms. The aim of the present series of experiments was to examine potential hormonal and neural bases of analgesia induced by i.v. infusion of the pressor (hypertensive) agent phenylephrine. All rats were implanted with right jugular and left carotid cannulae for phenylephrine infusion and blood pressure/heart rate monitoring, respectively, and were tested approximately 24 h later in the unanesthetized state. The tail-flick test was used to measure responsivity prior to, during, and after phenylephrine infusion. Potential adrenal and pituitary contributions to phenylephrine-induced antinociception were examined, respectively, by physical disruption of adrenal blood flow and pharmacological suppression of pituitary activation. Acute block of all adrenal hormones, via closure at the time of testing of pre-implanted adrenal ligatures, did not block phenylephrine antinociception. However, pharmacological suppression of pituitary activation via pretreatment with the synthetic glucocorticoid dexamethasone abolished phenylephrine antinociception. Intriguingly, dexamethasone had no noticeable effect on urination prior to phenylephrine administration, yet only dexamethasone-treated rats exhibited copious urination during phenylephrine infusion. This suggests that the hypertensive agent phenylephrine releases vasopressin from the posterior pituitary terminals of the paraventricular hypothalamus (PVH) in a dexamethasone-suppressible manner, possibly via the known baroreceptor-nucleus tractus solitarius (NTS)-PVH link. Since (1) bilateral lesions of the spinal cord dorsolateral funiculus (DLF) were shown in the current study to abolish phenylephrine antinociception, (2) PVH is known to send vasopressinergic projections to the spinal cord via the DLF, and (3) intrathecal vasopressin produces antinociception via V1-like vasopressin receptors, the effect of an intrathecal V1 vasopressin antagonist was tested on phenylephrine-induced antinociception. The V1 vasopressin antagonist blocked phenylephrine antinociception, suggesting that phenylephrine antinociception may be mediated by a baroreceptor-NTS-PVH-DLF circuit leading to vasopressin release at spinal levels.

Adrenal Glands↗
PubMed1976

Relationship between the level of cAMP and the contractile force under stimulation of alpha- and beta-adrenoceptors by phenylephrine in the isolated rabbit papillary muscle.

The time course of changes of the level of 3',5'-cyclic AMP (cAMP) and of the tension developed under stimulation of alpha- and beta-adrenoceptors by phenylephrine was investigated in the isolated rabbit papillary muscle. Furthermore the dose-response relationships for increases of cAMP and of developed tension elicited by phenylephrine were determined. 1. A submaximally effective concentration of phenylephrine (10(-5) M) increased significantly the level of cAMP of the papillary muscle at 15 and 30 s by 45 and 36% respectively; the level of cAMP returned to the control value at 60 s after the administration. The developed tension increased significantly not before 45 s and reached its maximal level at 180 s. 2. When alpha-adrenoceptors were blocked by phentolamine (10(-6) M), the positive inotropic effect of phenylephrine was decreased significantly but the increase of cAMP induced by phenylephrine was not reduced. In the presence of phentolamine the increase of cAMP induced by phenylephrine lasted longer than in the control experiments. 3. The effects of phenylephrine (10(-5) M) both on the level of cAMP and the developed tension mediated via stimulation of beta-adrenoceptors in the presence of phentolamine were enhanced by the phosphodiesterase inhibitor papaverine throughout the course of responses. 4. Phenylephrine produced an increase in developed tension as well as in cAMP. The corresponding dose-response curves run parallel to each other but differed by about 1.5 log units whereby the developed tension was evoked by lower concentrations. Phentolamine (10(-6) M) shifted the curve for the positive inotropic action by about 1.5 log units but did not affect that for increase in cAMP. Therefore, in the presence of the alpha-adrenolytic drug phentolamine the difference between both curves became smaller so that both curves were superimposed. Papaverine (10(-5) M) shifted the whole curve for cAMP upwards and enhanced the maximal contractile response to phenylephrine mediated by stimulation of beta-adrenoceptors. 5. The present results indicate that the positive inotropic action of phenylephrine in lower concentrations (less than 10(-5) M) induced by stimulation of alpha-adrenoceptors is independent of the level of cAMP. The positive inotropic action of the higher concentrations of phenylephrine induced via stimulation of beta-adrenoceptors was preceded by an accumulation of cAMP; the inhibition of the cAMP phosphodiesterase activity by papaverine enhanced the actions of phenylephrine both on the level of cAMP and on the contractile force.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1991

Depolarization-induced influx of sodium in response to phenylephrine in rat atrial heart muscle.

1. The effects of alpha 1-adrenoceptor stimulation on transmembrane potential, currents and ion fluxes were investigated in multicellular preparations and/or single cells obtained from the left atrium of rat hearts. 2. In multicellular preparations, phenylephrine caused a concentration-dependent positive inotropic effect, an increase in action potential duration, and a decrease in resting potential; the effects were antagonized by phentolamine. 3. In the presence of phenylephrine (100 mumol/1), two levels of resting potential were observed when the preparations were, alternately, electrically stimulated or kept at rest (-74 +/- 1 mV during activity and -62 +/- 4 mV at rest; mean +/- S.E.M.; n = 9). 4. In resting preparations, the depolarization in response to phenylephrine was eliminated in low-Na+ solution (12 mmol/l) and antagonized by tetrodotoxin (10 mumol/l). 5. The phenylephrine-induced depolarization was also seen in nominally Ca(2+)-free solution and in the presence of (-)-devapamil (1 mumol/l). 6. The alkylating agent N-ethyl-maleimide (30 mumol/l) abolished the depolarizing effect of phenylephrine. 7. Phorbol 12,13-dibutyrate (10 mumol/l) also abolished the depolarizing effect of phenylephrine. 8. Phenylephrine caused a significant increase of 22Na+ uptake in resting preparations and of 45Ca2+ uptake in beating preparations. 9. The depolarizing effect of phenylephrine was also observed in single atrial myocytes. Steady-state membrane currents in response to 500 ms depolarizing and hyperpolarizing voltage clamp steps were decreased. The cross-over of I-V curves under control and test conditions was at about -70 mV. The effects of phenylephrine were antagonized in the presence of phentolamine. 10. After suppression of potassium currents by substitution of CsCl for internal and external KCl ([KCl]o), phenylephrine had no effect on membrane currents. 11. In conclusion, we presume the following sequence of events in response to phenylephrine in rat atrial heart muscle. First, the stimulation of alpha 1-adrenoceptors decreases the K+ conductance thereby producing a depolarization in the presence of an inward current. Second, the change of the membrane potential in the depolarizing direction induces a TTX-sensitive Na+ window current which further propels the depolarization. Third, the increase in Na+ influx may increase Ca2+ influx by activating the Na(+)-Ca2+ exchange in mechanism. The greater influx of Ca2+ may contribute to the positive inotropic effect in response to phenylephrine.

Action Potentials↗
PubMed1997

Effect of phenylephrine infusion on atrial electrophysiological properties.

OBJECTIVE: To determine the effect of changes in autonomic tone induced by phenylephrine infusion on atrial refractoriness and conduction. DESIGN: Left and right atrial electrophysiological properties were measured before and after a constant phenylephrine infusion designed to increase sinus cycle length by 25%. SUBJECTS: 20 patients, aged 53 (SD 6) years, undergoing electrophysiological study for investigation of idiopathic paroxysmal atrial fibrillation (seven patients) or for routine follow up after successful catheter ablation of supraventricular tachycardia (13 patients). MAIN OUTCOME MEASURES: Changes in left and right atrial effective refractory periods, atrial activation times, and frequency of induction of atrial fibrillation. RESULTS: Phenylephrine (mean dose 69 (SD 18) mg/min) increased mean blood pressure by 22 (12) mm Hg (range 7 to 44) and lengthened sinus cycle length by 223 (94) ms (20 to 430). Left atrial effective refractory period lengthened following phenylephrine infusion from 250 (25) to 264 (21) ms (P < 0.001) but there was no significant change in right atrial effective refractory period: 200 (20) v 206 (29), P = 0.11. There was a significant relation between the effect of phenylephrine on sinus cycle length and on right atrial refractoriness (r = 0.6, P = 0.005) with shortening of right atrial refractoriness in patients with the greatest prolongation in sinus cycle length. During phenylephrine infusion, the right atrial stimulus to left atrial activation time at the basic pacing cycle length of 600 ms was unchanged, at 130 (18) v 131 (17) ms, but activation delay with a premature extrastimulus increased: 212 (28) v 227 (38) ms, P = 0.002. Atrial fibrillation was induced by two of 58 refractory period measurements at baseline and by 12 of 61 measurements during phenylephrine infusion (P < 0.01). Phenylephrine increased the difference between left and right atrial refractory periods by 22.8 (19.4) ms in the five patients with induced atrial fibrillation after phenylephrine compared to 0.9 (16.2) ms in the 13 patients without induced atrial fibrillation after phenylephrine infusion (P = 0.02). CONCLUSIONS: Phenylephrine infusion increased left atrial refractoriness and intra-atrial conduction delay following a premature right atrial extrastimulus. Induction of atrial fibrillation during phenylephrine infusion was associated with non-uniform changes in atrial refractoriness. These data support the concept that changes in autonomic tone may precipitate atrial fibrillation in susceptible individuals.

Adult↗